30 March 2025, Volume 45 Issue 2

  

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  Eosinophils in obesity and obesity-associated disorders

  HU Ya-nan, WANG Ke-fan, LU Li-ming, Svetoslav Chakarov

  2025, 45(2): 89.

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  In recent years, the prevalence of obesity has been steadily increasing, yet our understanding of the precise cellular and molecular mechanisms underlying obesity remains limited. The excessive accumulation of adipocytes during the process of obesity leads to a series of low-grade inflammation and has numerous effects on overall physiological function. This review focuses on the significant role of eosinophils in the progression of obesity and related metabolic disturbances, eosinophil generation and development, as well as their recruitment in adipose tissue (AT), and discusses the interaction between the microenvironment of AT and eosinophils. Understanding the detailed characteristics of eosinophils in the AT microenvironment will be beneficial for better exploiting their potential in the treatment of obesity.
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  The effect of plumbagin on neuronal damage in epileptic rats through regulating AMPK/CREB/BDNF signaling pathway

  REN Guang-wei, GENG Biao, LI Ming-wei, WANG Hai-min, LIANG Xiao-yan

  2025, 45(2): 96.

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  To investigate the effect of plumbagin (PL) on neuronal damage in epileptic rats by regulating adenosine-monophosphate-activated protein kinase (AMPK)/cAMP-responsive element-binding protein (CREB)/brain-derived neurotrophic factor (BDNF) signaling pathway, a rat epilepsy model was established by intraperitoneal injection of lithium chloride and pilocarpine. The model rats were randomly divided into model group, low-, medium- and high-dose PL groups (1, 5, and 10 mg/kg, respectively), and inhibitor group (10 mg/kg PL+20 mg/kg AMPK/CREB/BDNF signaling pathway inhibitor Compound C). Rats injected with the equal volume of physiological saline were set as control group. After successful modeling, each group received intraperitoneal injection of corresponding drugs, once a day for 21 consecutive days. The seizure status of rats in each group was evaluated according to the Racine grading standard; Brain waves of rats in each group were observed by electroencephalogram (EEG) and  Morris water maze experiment was applied to evaluate the cognitive and memorial functions. H-E staining was applied to observe the pathological damage of hippocampal tissues and TUNEL staining was applied to observe the apoptosis of rat neural cells. ELISA was applied to detect the levels of IL-6, IL-1β, and TNF-α in the hippocampus of rats in each group. Western blotting was used to detect the expression of proteins regarding the AMPK/CREB/BDNF signaling pathway in hippocampal tissues. Compared to those of the control group, the Racine grading, seizure frequency and duration of rats in the model group were all increased, along with the amplitude, total duration and frequency of the EEG waveform increased. The number of platform crossings and target quadrant activity time were reduced, and the escape latency prolonged. The rats hippocampal tissue structures were seriously damaged, neurons were loosely and badly arranged, with obvious edema and inflammatory cells infiltration. The apoptosis rate of neural cells, IL-6, IL-1β, and TNF-α levels were increased.  The expression levels of p-AMPK/AMPK, p-CREB/CREB, and BDNF proteins were significantly decreased (all with P＜0.05). Compared to those of the model group, the Racine grading, seizure frequency and duration of rats in the low-, medium-, and high-dose PL groups were decreased and the amplitude, total duration and frequency of the EEG waveform was decreased. The number of platform crossings and target quadrant activity time were increased, and the escape latency was shortened. The rats hippocampal structures damage was alleviated to certain extent, the cells were ordered, whose nuclear membrane was relatively clear, with few inflammatory cells infiltration. The apoptosis rate of neural cells, IL-6, IL-1β, and TNF-α levels were decreased. The expression levels of p-AMPK/AMPK, p-CREB/CREB, and BDNF proteins were significantly increased (all with P＜0.05). Compared to those of the high-dose PL group, the changes in the above indicators of rats in the inhibitor group were significantly reversed (all with P＜0.05). In conclusion, PL may activate the AMPK/CREB/BDNF signaling pathway, reduce neuronal apoptosis, inhibit inflammatory responses, and relieve neuronal damage in epileptic rats, thus exerting neuro-protective effects in epileptic rats.
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  Allergen regulates the pathogenesis of allergic rhinitis and asthma syndrome by modulating plasma levels of IL-18, IL-18BPa, and IL-18Rα

  WANG Jun-ling, ZHAN Meng-meng, DU En-ming, WANG Ling, HE Shao-heng, QIN Bing-yu

  2025, 45(2): 104.

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  This study aimed to investigate the expression levels of IL-18, IL-18 binding protein a (IL-18BPa), and IL-18 receptor α (IL-18Rα) in plasma CD4⁺ T cells and Th2 of patients with allergic rhinitis and asthma syndrome (ARA) and how allergen regulated their expressions. To this end, blood samples of ARA patients and healthy control subjects were collected, and the expression levels of IL-18, IL-18BPa, and IL-18Rα in CD4⁺ T cells and Th2 were determined by flow cytometry. Plasma levels of  total IL-18 (tIL-18) and total IL-18BPa (tIL-18BPa) were measured by ELISA, and the level of free IL-18 (fIL-18) was calculated. The level of IL-4 was examined by Bioplex system, and the correlations between fIL-18 and IL-4, and the percentage of Th2 were further analyzed. Our data showed that the proportions of IL-18⁺ cells in CD4⁺ T cells and Th2 were increased in ARA patients, and  house dust mite extract (HDME) induced rising IL-18 expression in Th2 of ARA patients. Plasma levels of IL-4, tIL-18, and fIL-18 were increased in ARA patients, and the level of fIL-18 was moderately correlated with levels of IL-4 and the proportion of Th2 in ARA patients. In conclusion, allergen may be involved in the pathogenesis of ARA by inducing elevated expression of IL-18 in Th2.
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  Expression level of serum soluble CD39 in patients with hepatitis B-related liver diseases and its clinical significance

  ZHANG Qian-ge, MA Hai-xia, CHEN Kai-yong, CAO Lei, LIU Ying, GONG Yan-ping, JIANG Ting-wang, YANG Wen-yan

  2025, 45(2): 111.

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  The study aims to investigate the serum soluble CD39 (sCD39) levels and explore its clinical significance in patients with hepatitis B-related liver diseases. A total of 134 patients with hepatitis B infection were selected for this study, including 46 patients with chronic hepatitis B (CHB), 56 patients with hepatitis B liver cirrhosis (HBLC), 32 patients with hepatocellular carcinoma (HCC), and additional 42 healthy controls (HC). The serum sCD39 levels were detected by ELISA. Additionally, the activities of aspartate transaminase (AST) and alanine transaminase (ALT) were measured by a biochemical analyzer. The expressions of serum AFP, hyaluronic acid (HA), and laminin (LN) were determined by the chemiluminescence method. qRT-PCR was employed to detect the HBV DNA content in serum. Furthermore, the liver fibrosis 4 factor (FIB-4) index, model for end-stage liver disease (MELD) score, AST-to-platelet ratio index (APRI), and modified PAGE-B (mPAGE-B) score were calculated. The differential expressions of serum sCD39 of HBV patients at different stages were measured and Spearman analysis was used to examine the correlation between sCD39 and various clinical indicators. The value of sCD39 in the diagnosis of HCC was evaluated by ROC curve analysis. The results showed that the sCD39 level in the HCC group was the highest and significantly different from that of all other groups (P<0.01). Importantly, the level of sCD39 in patients with liver injury（ALT＞40 U/L）was significantly higher than those without liver injury (ALT≤40 U/L, P<0.001). sCD39 was positively correlated with AST,ALT, AFP, LN, HA, APRI, FIB-4 index (P<0.001), and the MELD score (P=0.016). The AUC of serum sCD39 for the diagnosis of HCC was 0.743. The AUC of AFP combined with sCD39 was 0.894. The study suggests that sCD39 detection may be valuable for prognosis assessment in HBLC patients and for diagnosis of hepatitis B-related HCC. Therefore, sCD39 may serve as a potential diagnostic biomarker for HCC.
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  Alleviating effect of boneset total flavonoids on endometrial inflammatory lesion in ovariectomized osteoporotic rats

  FANG Hong, LONG Feng, LU Lin

  2025, 45(2): 118.

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  The aim of this study was to explore the effect and possible mechanism of total flavonoids of rhizomadrynariae (TFRD) on endometrial damage and cell apoptosis in ovariectomized osteoporotic rats. Postmenopausal osteoporosis (PMOP) rat model was established by ovariectomy. The SD rats were randomly divided into 4 groups: the sham-operation group, the model group, the TFRD treatment group, and the positive drug (estradiol valerate) group. The latter two groups were daily gavaged with 108 mg/(kg·d) TFRD or 0.21 mg/(kg·d) estradiol valerate tablet from the 7th day after operation and treated for 12 weeks. H-E staining was used to observe the pathological morphology of rat femur and uterus tissues. Apoptosis of endometrial cells was evaluated by TUNEL staining. Western blotting was used to detect caspase-3 expression in uterus. ELISA was used to quantify levels of IL-6, TNF-α, and estradiol (E2) in the uterus tissues. Estrogen receptor alpha (ESR1) expression of uterus was detected by immunohistochemistry. Compared to the sham-operation group, the model group showed pathological injury of femur tissues and pathological changes in the uterus tissues. Apoptosis of endometrial cells was increased, along with elevated expressions of caspase-3, IL-6, and TNF-α, while the E2 and ESR1 expressions were decreased (all with P＜0.01). Compared to the model group, the TFRD, and positive drug treatment groups exhibited improved pathological changes in rat femur tissues and uterus. Apoptosis of endometrial cells and the protein levels of caspase-3, IL-6, and TNF-α were significantly decreased, while the expression levels of E2 and ESR1 were increased (all with P＜0.01). Therefore, TFRD can effectively alleviate endometrial injury and apoptosis in PMOP rats, and the mechanism may involve the regulation of E2 and the inhibition of the expression of inflammatory factors IL-6 and TNF-α.
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  lncRNA USP2-AS1 regulates the proliferation, apoptosis, and epithelial-mesenchymal transition of non-small cell lung cancer cells via the miR-299-3p/MMP2 axis

  SHU De-jun, SHEN Yu-guang, ZHOU Wei-fu, LU Xun, TANG Ji-yang

  2025, 45(2): 125.

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  The aim of this study is to explore the effect of lncRNA USP2-AS1 on the proliferation, apoptosis and epithelial-mesenchymal transition (EMT) of non-small cell lung cancer (NSCLC) cells through regulating the miR-299-3p/matrix metalloproteinase 2 (MMP2) axis. si-NC, si-USP2-AS1, si-USP2-AS1+inhibitor NC, and si-USP2-AS1+miR-299-3p inhibitor were transfected into A549 cells, respectively, and cells were defined into corresponding groups. Untreated A549 cells were defined as the NC group. qRT-PCR was applied to detect the expressions of lncRNA USP2-AS1 and miR-299-3p in normal human lung epithelial cell line BEAS-2B and A549 cells. CCK-8 assay was used to evaluate the proliferative activity and flow cytometry was used to examine the apoptosis rate of A549 cells.Transwell assay was used to measure the invasion and migration of A549 cells. Western blotting was used to examine the levels of E-cadherin (Ecad), N-cad, vimentin and MMP2 in A549 cells, and dual-luciferase reporting gene assay was used to detectthe interactions of lncRNA USP2-AS1, miR-299-3p and MMP2. Xenograft on nude mice was used to evaluate the growth of tumor cells in vivo. The results showed that compared to those of the BEAS-2B cells, the levels of lncRNA USP2-AS1 and MMP2 in A549 cells were significantly up-regulated (both P＜0.05) while the expression of miR-299-3p was significantly down-regulated (P＜0.05). Compared to those of the NC group and the si-NC group, the proliferative activity, the cell number of migration and invasion, the level of lncRNA USP2-AS1, and the protein levels of N-cad and vimentin in A549 cells in the si-USP2-AS1 group were all significantly decreased (all with P＜0.05) while the apoptosis rate of A549 cells, the expression of miR-299-3p, and the protein level of E-cad were all significantly increased (all with P＜0.05). Compared to those of the NC group and sh-NC group, the graft volume and mass in the sh-USP2-AS1 group were significantly decreased (all with P＜0.05). Inhibition of miR-299-3p expression weakened the effect of lncRNA USP2-AS1 silencing on the inhibition of the proliferation, migration, invasion, and tumor growth of A549 cells, as well as the stimulation of apoptosis. lncRNA USP2-AS1 negatively regulated the miR-299-3p/MMP2 axis. In conclusion, lncRNA USP2-AS1 silencing may down-regulate MMP2 expression through up-regulating miR-299-3p, thereby affecting the proliferation, apoptosis, migration, invasion, and EMT of A549 cells.
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  Mechanistic study of Nandina domestica Thunb in gouty arthritis treatment based on network pharmacology and experimental verification

  LIU Dao-zhong, FENG Jia, ZHANG Zong-xing, JIANG Lu, XIAO Ting, LIU Yi, LI Wei-yi, BAO Zhuo-ma, YUAN Lin

  2025, 45(2): 134.

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  This study aimed to explore the potential mechanism of Nandan bamboo in the treatment of gouty arthritis (GA) by combining network pharmacology and experimental research. Procedures: (1) The pharmacological active ingredients of Nandina domestica Thunb were identified by literature review. The corresponding drug targets were explored by SwissTarget and TargetNet databases. OMIM and GeneCards databases were used to screen for GA disease-related targets. The overlapping targets of the two analyses were imported into the STRING platform for protein-protein interaction (PPI) network analysis to find out the core targets. Cytoscape 3.10.1 software was used to draw the “disease-drug-pathway-target” network to screen for the key active ingredients of Nandina domestica Thunb for the treatment of GA. GO function and KEGG pathway enrichment analysis were performed using online bioinformatics analysis and visualization cloud platform. (2) GA inflammatory cell model was established by stimulation of THP1-derived macrophages using LPS in combination with monosodium urate (MSU). Cells were coincubated with different concentrations of drugs for 24 h. CCK8 assay was used to detect the cell toxicity of Nandina domestica Thunb extract and ELISA was used to detect the IL-1β level in supernatant. RT-qPCR was used to detect the expressions of TLR2/NF-κB signaling pathway related genes and the relative expression of NLRP3 mRNAs. Western blotting was used to detect the NF-κB, NLRP3, and IL-1β protein expressions. The results showed that (1) A total of 309 drug interacting targets, 776 disease-related targets, and 30 common targets were identified. The key bioactive molecules included caffeic acid and biapigenin, and the core disease targets included TNF, PTGS2, RELA (NF-κB p65), SIRT1, and SYK. The key targets were mainly involved in inflammatory signaling pathways such as NF-κB pathway and NOD-like receptor pathway; (2)The CCK8 assay showed that the concentration of Nandina domestica Thunb had no significant effect on cell viability at 37.5, 75 or 150 μg/mL. Compared to those of the control group, the IL-1β level in the cell supernatant, the mRNA expressions of TLR2, myeloid differentiation factor 88 (MYD88), TNF receptor-associated factor 6 (TRAF6), TGF-β-activated activated kinase 1 (TAK1), inhibitor α of κB kinase (IKKα), NF-κB, NLRP3, and IL-1β, and the protein expressions of NF-κB, NLRP3, and IL-1β in the model group were significantly increased (all with P＜0.05). Compared to those of the model group, the level of IL-1β in the cell supernatant, the mRNA expressions of TLR2，MYD88，TRAF6，TAK1，IKKα，NF-κB，NLRP3  and IL-1β, and the protein expressions of NF-κB, NLRP3, and IL-1β in the Nandina domestica Thunb extract treated groups were all significantly decreased（all with P＜0.05）. In conclusion, Nandina domestica Thunb extract can reduce the production and release of inflammatory factors through regulating the TLR2/NF-κB signaling pathway and inhibiting the activation of NLRP3 inflammasome, making it a treatment for GA.
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  Cinnamaldehyde regulates the intestinal immune function in rats with acute pancreatitis via the RhoA/ROCK signaling pathway

  ZHANG Yu, ZHAO Na-na, WU Wei-min

  2025, 45(2): 143.

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  The aim of this study is to investigate the effect of cinnamaldehyde on intestinal immune function in rats with acute pancreatitis (AP) and its regulation on the Ras homolog gene family member A(RhoA)/Rho-associated coiled-coil protein kinase (ROCK) signaling pathway. Rats were randomly divided into the sham operation group, the model group, the cinnamaldehyde group, the RhoA/ROCK signaling pathway activator lysophosphatidic acid (LPA) group, and the cinnamaldehyde+LPA group, with 15 rats in each group. Except for those in the sham operation group, rats were injected with sodium taurocholate into the pancreatic duct to establish the AP model. Subsequently, corresponding drugs were administered once a day for 2 weeks. ELISA was used to detect the levels of IL-1, TNF-α, and myeloperoxidase (MPO), and H-E staining was used to observe the histomorphology of mesenteric lymph nodes (MLN). The levels of NOD-like receptor family pyrin domain-containing protein 3(NLRP3）and apoptosis-associated speck-like protein（ASC）were detected by immunofluorescence staining. The proportion of Treg and the Th1/Th2 ratio were analyzed by flow cytometry. Western blotting was used to detect the expressions of RhoA/ROCK signaling pathway proteins. The results showed that the structure of lymph nodes in the sham operated group was basically normal, while those of the model group showed an increased number and thickened cortical area. Compared to those of the sham operation group, the levels of IL-1, TNF-α, MPO, the numbers of NLRP3 and ASC positive cells, the ratios of CD4⁺CD25⁺Foxp3⁺, CD4⁺, Treg, Th1, Th1/Th2 ratio, and the protein levels of RhoA and phosphorylated ROCK(p-ROCK)/ROCK in the model group significantly increased (P<0.05), while the level of Th2 significantly decreased (P<0.05).The cinnamaldehyde treatment greatly improved the above indicators, while the LPA treatment had the opposite effect of the cinnamaldehyde treatment and diminished the beneficial effect of cinnamaldehyde on the intestinal immune function in AP rats. In conclusion, cinnamaldehyde may improve the intestinal immune function of AP rats by inhibiting RhoA/ROCK signaling pathway.
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  lncRNA PVT1 upregulates KLF12 by competing with miR-484 to promote the progression of cervical cancer via the IL-6/STAT3 signaling pathway

  BAO Ke-yong, WANG Dong, BAO Li-hong, ZHANG Li, ZHANG Xue, TAO Xiao-yu, GAO Han

  2025, 45(2): 151.

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  The aim of this study is to investigate the effects of long non-coding RNA (lncRNA) plasmacytoma variant translocation 1 (PVT1) on the proliferation, apoptosis, migration, and invasion of cervical cancer cells, and its regulation on miR-484 and Krüppel-like factor 12(KLF12), as well as the IL-6/ STAT3 signaling pathway. qRT-PCR was used to detect the expressions of lncRNA PVT1, miR-484, and the mRNA expression of KLF12 in cervical cancer tissue and cell lines. Double luciferase assay was used to detect the relationship between lncRNA PVT1, miR-484, and KLF12. Upon transfection of Sh-PVT1, Sh-PVT1+antagomir, or Sh-PVT1+antagomir+pcDNA3.1, the proliferation, apoptosis, migration, and invasion of cells were examined. The in vivo tumor growth and metastasis were also measured. Western blotting was used to detect the expression of KLF12, B-cell lymphoma 2 (Bcl-2), and Bcl-2-associated X protein (Bax) in each group of tumor cells and mouse tumor tissue. Immunohistochemistry was used to detect the expression of IL-6, phosphorylated JAK2(p-JAK2), and phosphorylated STAT3 (p-STAT3) in cells and mouse tumor tissue. The results showed that the expressions of lncRNA PVT1 and KLF12 were significantly increased in cervical cancer tissue and cervical cancer cell lines, while the expression of miR-484 was significantly decreased (P＜0.05). Double luciferase assay confirmed the targeted regulation of lncRNA PVT1 on the expression of miR-484 which in turn regulated the expression of KLF12. Inhibiting lncRNA PVT1 significantly inhibited the proliferation, migration, and invasion of cervical cancer cells, induced cell apoptosis, downregulated the expressions of KLF12, Bcl-2, IL-6, p-JAK2, and p-STAT3, and upregulated the expression of Bax (P＜0.05). However, antagomir could partially relieve the suppression of inhibition of lncRNA PVT1 in cervical cancer progression, while pcDNA3.1 partially restored the suppression of inhibition of lncRNA PVT1 in cervical cancer progression. Therefore, this study suggests that in cervical cancer, lncRNA PVT1 upregulates KLF12 by endogenous competition with miR-484 to promote the proliferation, migration, and invasion of cervical cancer cells, inhibit apoptosis, promote the growth and metastasis of tumor cells, and the malignant progression of cervical cancer in vitro, which may be related to the activation of IL-6/STAT3 signaling pathway.
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  Engeletin increased oxygen-glucose deprivation/reoxygenation-induced neuron autophagy through regulating the PINK1/Parkin signaling pathway

  TIAN Xin-li, SHANGGUAN Jun-fa, CHEN Li-ping, LI Xiao-gang

  2025, 45(2): 164.

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  The aim of this study was to investigate the effect of engeletin (Eng) on the autophagy of neurons induced by oxygen-glucose deprivation/reoxygenation (OGD/R) by the PTEN-induced kinase 1 (PINK1)/Parkin signaling pathway. The mouse hippocampal neuron HT22 cell line was used as the study object to establish an OGD/R-induced cell damaged model. HT22 cells were grouped into the model group (OGD/R group), the low-, medium- and high-dose Eng groups (Eng-L, -M, -H groups, with 1, 5, 10 mmol/L Eng, respectively), the si-PINK1 NC+Eng-H group, the si-PINK1+Eng-H group, and blank group (control group). The cell viability, cell apoptosis, reactive oxygen species (ROS) level, the cell levels of glutathione peroxidase (GSH-Px), malondialdehyde (MDA), and superoxide dismutase (SOD),the changes of mitochondrial membrane potential, cell autophagy level, the expressions of PINK1, Parkin (E3 ubiquitin ligase), microtubule-associated protein 1 light chain 3 (LC3), ubiquitin-binding protein p62, and caspase3 were evaluated using appropriate methods. The results showed that compared to those of the control group, the viability of HT22 cells, the GSH-Px, the SOD levels, the mitochondrial membrane potential, the cell autophagy level, the ratio of LC3-Ⅱ/LC3-Ⅰ, and the protein expressions of PINK1 and Parkin in the OGD/R group were significantly decreased (all with P＜0.05), whereas the apoptosis rate, the caspase3 protein expression, ROS, MDA levels, and p62 protein expression all significantly increased (all with P＜0.05). Compared to those of the OGD/R group, the viability of HT22 cells, the GSH-Px, SOD levels, the mitochondrial membrane potential, the cell autophagy level, the ratio of LC3-Ⅱ/LC3-Ⅰ, and the protein expressions of PINK1 and Parkin in the Eng-L、-M and -H groups were significantly increased (all with P＜0.05) while the apoptosis rate, the caspase3 protein expression, ROS, MDA levels and the p62 protein expression all significantly decreased (all with P＜0.05). Compared to the Eng-H group, si-PINK1+Eng-H treatment reversed the effect of Eng-H on the enhancement of autophagy of HT22 cells, and aggravated cell injury and apoptosis. In conclusion, we have firstly demonstrated that Eng can up-regulate the expression of PINK1/Parkin signaling pathway, and alleviate OGD/R-induced neuronal damage through the mitochondrial autophagy pathway.
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  Tenuifoliside A alleviates depressive symptoms in postpartum depression rats by regulating Treg/Th17 balance and the ERK1/2/BDNF signaling pathway

  ZHU Chang-wei, WANG Pei-pei, GE Hai-yan

  2025, 45(2): 172.

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  To evaluate the effect and mechanism of tenuifoliside A (TFSA) on postpartum depression (PPD), this study randomly divided rats into 5 groups: sham group, PPD group, PPD+25TFSA group, PPD+50TFSA group and PPD+100TFSA group, with 12 rats in each group. After model establishment, rats in sham group and PPD group were administrated daily with 2 mL 1% dimethyl sulfoxide (DMSO) solution by gavaging, while rats in PPD+25TFSA group, PPD+50TFSA group and PPD+100TFSA group were intragastrically infused daily with 25, 50 and 100 mg/kgTFSA dissolved in 2 mL 1% DMSO,respectively, for 28 days. The depressive symptoms of rats were evaluated by sucrose preference test and open field test. The levels of inflammatory markers (TNF-α and IL-1β) and oxidative stress markers ［malondialdehyde (MDA) and superoxide dismutase (SOD)］ in rat hippocampus were measured by commercial kits following manufacturer's instructions. The protein expression levels of brain-derived neurotrophic factor (BDNF), extracellular signal-regulated kinase 1/2 (ERK1/2) and p-ERK1/2 in rat hippocampus were detected by Western blotting. The results showed that compared to those of the sham group, the sucrose preference rate, horizontal activity fraction and vertical activity fraction in PPD group were all decreased, while the contents of TNF-α and IL-1β in hippocampus increased in the PPD group, accompanied by increased MDA and decreased SOD level and proportion of Treg and Treg/Th17 ratio. PPD group also exhibited increased proportion of Th17 in peripheral blood and decreased relative expression of BDNF protein and relative phosphorylation level of ERK1/2 in hippocampus (P<0.05). Compared to those of the PPD group, sucrose preference rate, horizontal activity fraction and vertical activity fraction in PPD+25TFSA group, PPD+50TFSA group and PPD+100TFSA group all increased while TNF-α and IL-1β content decreased. TFSA also caused decreased MDA level, increased SOD level, increased proportion of Treg and Treg/Th17 ratio in peripheral blood, decreased proportion of Th17 in peripheral blood, and increased relative expression of BDNF protein and the relative phosphorylation level of ERK1/2 in hippocampus (P<0.05). Taken together, TFSA effectively improves the depressive symptoms of PPD rats, and the mechanism may include the regulation of T cell immunity and activation of the ERK1/2/BDNF signal pathway. 
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  Therapeutic effect of paeoniflorin on chronic atrophic gastritis ratsthrough regulating the IL-6/STAT3 signaling pathway

  MAO Wei-ling, LIANG Rong-zhen, JI Zhen-liao, FANG Xiang-yu

  2025, 45(2): 179.

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  The aim of this study was to investigate the therapeutic effect of paeoniflorin (PF) on chronic atrophic gastritis (CAG) rats through regulating the IL-6/STAT3 signaling pathway. A total of 84 SD rats were randomly divided into 6 groups (14 rats/group): the control group, the model group, the low-dose PF group (5 mg/kg), the medium-dose PF group (15 mg/kg), the high-dose PF group (30 mg/kg), and the activator group (IL-6 activator, recombinant rat IL-6 protein ［rIL-6］ 0.05 mg/kg+30 mg/kg PF). CAG rat model was established by N-methyl-N′-nitro-N-nitrosoguanidine (MNNG) compound method. After successful model establishment, the rats in each group were intraperitoneally injected with corresponding drugs, once a day for 8 weeks. The general condition and weight change of rats were observed during modeling and drug administration. After respective drug administration, the gastric mucosal ulcer index (UI) was calculated according to the Cuth method. The histopathology of gastric mucosa was observed by H-E staining. TUNEL staining was used to observe the apoptosis of gastric mucosa cells and the levels of serum IL-6, IL-1β, IL-4, and TNF-α were detected by ELISA. Western blotting was applied to detect the expressions of anti-apoptosis factor B cell lymphoma 2 (Bcl-2), Bcl-2-associated X protein (BAX), and IL-6/STAT3 signaling pathway proteins in gastric mucosa. Compared to that of the control group, the pathological damage of gastric mucosa in the model group was more serious, the body mass of rats, and the expression level of Bcl-2 protein in gastric mucosa decreased significantly while the UI, apoptosis index of gastric mucosa cells, the levels of IL-6, IL-1β, IL-4, TNF-α in serum, and the expressions of BAX, IL-6, p-STAT3/STAT3 in gastric mucosa tissues all increased significantly (all with P＜0.05). Compared to that of the model group, the pathological damage of gastric mucosa of rats in each PF dosage group was alleviated.The body weight and the expression of Bcl-2 protein in gastric mucosa of rats increased significantly while the UI, apoptosis index of gastric mucosa cells, the levels of IL-6, IL-1β, IL-4, TNF-α in serum, and the expression levels of BAX, IL-6, p-STAT3/STAT3 in gastric mucosa tissues decreased significantly in a dose-dependent manner (all with P＜0.05). IL-6 activator rIL-6 could diminish the beneficial effect of high-dose PF on the pathological damage of gastric mucosa in CAG rats (all with P＜0.05). In conclusion, PF may play a role in relieving pathological damage of gastric mucosa by reducing inflammatory responses and cell apoptosis in CAG rats through inhibiting the IL-6/STAT3 signaling pathway.
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  Research progress of local intestinal mucosal humoral immunity in inflammatory bowel disease

  WU Xin-yu, CHEN Ke, WANG Xiao-yun

  2025, 45(2): 185.

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  Inflammatory bowel disease (IBD) is a chronic relapsing intestinal inflammatory disease, including ulcerative colitis (UC) and Crohn's disease (CD). Although the etiology of IBD remains unknown, it is well accepted that factors including heredity, intestinal environment, bacterial infection and dysregulated immunity may contribute to the onset. A number of guidelines in China and abroad have pointed out that basal plasmacytosis is an important pathological indicator of IBD diagnosis, and the aggregation value of plasma cells in the middle and lower mucosa is much higher than that of other lymphocytes. It was also observed that plasma cell aggregation disappeared in the intestinal tissue of IBD patients in remission after treatment with biologics. Therefore, it is speculated that the B cell-plasma cell axis in humoral immunity is an important path in the pathophysiology of IBD. However, the underlying mechanism remains unclear. This review summarizes the progress on the roles of humoral immunity of the intestinal mucosa in the pathogenesis of IBD.
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  Application of single-cell RNA sequencing in autoimmune diseases

  HOU Xian-liang, LIU Zhen-yu, HU Zi-peng, XU Yu-jiao, LIAO Song-bai

  2025, 45(2): 190.

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  Single-cell RNA sequencing (scRNA-seq) is a novel technigue for high-throughput sequencing analysis of the whole transcriptome to elucidate the gene status of monocells. It is an important research method to investigate the heterogeneity of cells and the underlying mechanisms as well as help to identify novel cell subpopulations. In addition, it provides insight into the molecular underpinnings of disease pathogenesis, evolution, and drug resistance. This technology has quickly developed in recent years and has accumulated a significant amount of research data. This review summarizes the advances of scRNA-seq  and its usage on autoimmune diseases in order to provide a theoretical framework for the application of this technology in immunology and  related fields as well as diagnosis and management of diseases.
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  The important role of mast cell-derived mediators in the activation of the NLRP3 inflammasome during allergic inflammatory response

  PAN Yue-yue, SHU Wen, YIN Yue, CUI Ze-lin, LIAO Huan-jin

  2025, 45(2): 198.

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  As an integral component of the innate immune system,mast cells (MC) are ubiquitously distributed throughout the skin and mucosal tissues. Upon activation by exogenous or endogenous stimuli, these cells rapidly secrete intracellular mediators, including cytokines, proteases, and lipids, thereby playing a crucial role in the defense against bacterial, viral, and parasitic infections, as well as in mediating allergic inflammatory responses. The NOD-like receptor family pyrin domain-containing protein 3 (NLRP3) inflammasome is a critical element of innate immunity, significantly contributing to the body's defense against bacterial and viral infections, and allergen-induced inflammatory responses. Furthermore, it represents a promising therapeutic target for the treatment of various inflammatory diseases.While mast cells and NLRP3 are both integral to the processes underlying allergic inflammatory responses, the mechanisms governing mast cell activation, NLRP3 activation and expression, as well as the regulatory interactions between these components in the context of allergic inflammation remain inadequately elucidated. This review systematically summarizes and discusses the role of mast cell activation and the mediator releasing in modulating NLRP3 activation and expression in the context of allergic inflammatory responses. The objective is to elucidate the mechanisms by which mast cells regulate allergic inflammation, thereby enhancing the comprehensive understanding of the signaling pathways involved in allergic inflammatory responses. This review aims to provide a theoretical foundation for the development of anti-inflammatory treatment strategies and combination therapies.
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  Research progress on the regulation of macrophage polarization by succinate-SUCNR1 axis in inflammatory and fibrotic diseases

  TIAN Qi, CHANG Kai-kai, YI Xiao-fang

  2025, 45(2): 203.

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  The field of immunometabolism has made significant advances in elucidating the regulation of cellular metabolism on the phenotype and function of immune cells. Succinate is a metabolite of the tricarboxylic acid cycle that plays a critical role as a 'hormone-like' signaling molecule beyond its metabolic function. The macrophages (Mφ) are the hub for immune response, affecting the onset and progression of metabolic diseases associated with inflammation. The polarization of Mφ is shaped by metabolites, which contribute to various disease states and can even lead to metabolic dysfunction in tissues. Succinate has been demonstrated to regulate Mφ phenotype through several mechanisms, promoting or inhibiting inflammatory responses based on environmental factors. Consequently, it is regarded as a key regulator of Mφ function. This review aims to provide an overview of the most recent research on the modulation of Mφ phenotype by succinate-succinate receptor 1 (SUCNR1) axis in inflammatory and fibrotic diseases.
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  Research progress on the effect of mast cells on the occurrence and development of immune-related diseases

  CHEN Zi-tong, YAO Yi-chen, YANG Zheng-zhe, CAO Tian-ze, CHEN Guang-jie

  2025, 45(2): 211.

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  Mast cells are innate immune cells, and matured mast cells are distributed throughout the body, mainly near blood vessels and nerves. Upon stimulation by IgE and other stimuli, degranulation process of mast cells occurs through acascade of signal transduction, releasing inflammatory factors and various cytokines. Mast cells therefore have complicated proinflammatory and immunoregulatory effects. This review focuses on the influence of mast cells on allergic diseases including the promotion of diseases through degranulation, immunoregulation and neuro-immune regulation, highlights the importance of mast cells in autoimmune diseases, discusses their immunoregulatory function in various organs and tissues and their dual effect to autoimmune diseases.
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  Research progress of the inhibitory receptors on T-cell exhaustion in coronavirus disease 2019

  LI Meng-qing, ZHANG Fang-xiong, TANG Jia-tao, FU Qiang

  2025, 45(2): 218.

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  The coronavirus disease 2019 (COVID-19) continues to affect the health of people around the world. The severe acute respiratory syndrome coronavirus 2(SARS-CoV-2) spreads through the respiratory tract and interacts with the immune system to cause a variety of clinical symptoms of COVID-19. Innate and adaptive immunity both play a role in resisting virus infection. However, in some cases, T cells enter a state of exhaustion even when the body elicits the immune response. Multiple inhibitory receptors expressed on the cell surface are regarded as important factors in suppressing the T cell effector function. This review briefly introduces the mode of SARS-CoV-2 infection and the changes of host immune response. In addition, it systematically summarizes the research progress of inhibitory receptors including PD-1, T-cell immunoglobulin and mucin domain-containing protein 3 (TIM-3), lymphocyte-activation gene 3 (LAG-3), and CTLA-4 on T-cell exhaustion during COVID-19.
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  Research progress on the therapeutic effect of T cell immunotherapy in acute myeloid leukemia

  HURILE Bateer, SU Li-de, LI xin

  2025, 45(2): 223.

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  Acute myeloid leukemia (AML) is a malignant hematological disease characterized by the clonal proliferation of myeloid progenitor cells and high heterogeneity. The development and progression of AML are closely associated with alterations in T cell phenotype and function. These changes can lead to aberrancies in the T cell population, ultimately resulting in immune dysfunction ofthe body. In recent years, researchers have utilized the anti-tumor activity of T cells in the treatment of AML, and it has been observed that the functional recovery of T cells in patients exerts a pronounced inhibitory effect on leukemia cells. At present, T cell immunotherapy for AML includes tumor infiltrating lymphocyte (TIL) therapy, bispecific antibody-recruited T cell therapy, immune checkpoint inhibitor (ICI) therapy, chimeric antigen receptor T-cell (CAR-T) therapy, and tumor-specific receptor gene-transduced T cell (TCR-T) therapy. This review comprehensively summarizes recent domestic and international advancements in T cell immunotherapy research, offering anoverview of the therapeutic efficacy and mechanisms of T cell immunotherapy on AML. The objective is to elucidate new potential strategies for the clinical treatment of AML.
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  Research progress on the relationship between neutrophil extracellular trap and adaptive immune cell imbalance

  YANG Kang-jie, LU Yong-liang, E Wei-jian

  2025, 45(2): 230.

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  A special defense mode of neutrophils has been found in recent years, i.e. the neutrophil extracellular trap (NET), which can resist the invasion of pathogens to a certain extent. However, excessive amount of NET will cause pathological inflammation and immune disorders. Studies have confirmed that NET is highly correlated with the imbalance of adaptive immune cells and plays an important role in adaptive immunity. This review briefly summarizes the composition, formation mechanisms, and functional detection of NET, and focuses on the research progress on the relationship between NET and adaptive immune cell imbalance. This review will promote a clear understanding of NET and provide a theoretical basis for revealing the pathogenesis of related diseases, developing disease monitoring and treatment protocols, as well as identifying therapeutic targets.
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  Research progress on the role of inflammatory markers in peripheral blood and cerebrospinal fluid on inflammation-related neuropsychiatric diseases

  YAO Peng-hao, CHEN Hui-ling, CAO Xia

  2025, 45(2): 236.

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  Inflammatory responses play an important role in neuropsychiatric disorders, and the relationship between the levels of inflammatory markers in peripheral blood or cerebrospinal fluid (CSF) and neuropsychiatric diseases has been extensively studied in recent years. This review summarizes the recent advances in this field. Studies have shown that many inflammatory markers are vital in the pathogenesis, progression, and prediction of neuropsychiatric diseases. By detecting changes in the levels of different inflammatory markers in peripheral blood and CSF, it is possible to better understand the relationship between neuropsychiatric disorders and inflammatory responses, and to provide reliable guidance for the diagnosis and treatment of the diseases. This review discusses the research progress on the role of inflammatory markers in peripheral blood and CSF on inflammation-associated neuropsychiatric disorders, which may provide evidence and ideas for research concerning the diseases.
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  The role of TIM family proteins in virus infections

  LU Zheng-mei, PAN Yong, XU Li-yun, LI Shi-bo

  2025, 45(2): 243.

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  Phosphatidylserine (PS) receptors are important molecules expressed on the surface of host cells and involved in two main biological processes: clearance of apoptotic cells and facilitation of the entry of enveloped viruses into host cells to ease infection. In recent years, there has been research interest in PS receptors, particularly as members of the human T-cell immunoglobulin and mucin structural domain (TIM) gene family. This review describes the structure of TIM family proteins and their role in viral entry into host cells to shed light on the latest advance of TIM gene family research in viral infections.