31 March 2026, Volume 46 Issue 2

  

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  Hmbox1 promotes pyroptosis of cardiomyocyte through PI3K/Akt signaling pathway to aggravate myocardial ischemia-reperfusion injury

  WANG Tao, SHAO Lili, QI Weigang, WANG Yangui

  2026, 46(2): 137-143.

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  This study aims to investigate whether homeobox containing 1 (Hmbox1) promotes cardiomyocyte pyroptosis and aggravates myocardial ischemia-reperfusion injury (MIRI) through the PI3K/Akt signaling pathway. 24 SD rats were randomly divided into the sham operation group, the model group, the sh-NC group (lentivirus blank vector), and the sh-Hmbox1 group (lentivirus vector containing sh-Hmbox1), with 6 rats in each group. Mice of the sh-NC group and sh-Hmbox1 group were injected with corresponding lentiviral vectors 48 h before modeling. Except for the sham-operation group, the MIRI model was established by ligating the left anterior descending branch of the coronary artery through thoracotomy in the other three groups. Left ventricular function indexes ( left ventricular end-diastolic diameter ［LVEDD］, left ventricular end-systolic diameter ［LVESD］, left ventricular ejection fraction ［LVEF］, and left ventricular fractional shortening ［LVFS］) were measured by echocardiography 24 h after modeling. The levels of serum myocardial injury markers (creatine kinase-MB ［CK-MB］, cardiac troponin I ［cTnI］, lactate dehydrogenase ［LDH］) and inflammatory factors (IL-18, IL-1β) were detected by ELISA. Immunohistochemistry （IHC） was used to detect the level of Hmbox1 positive cells. Western blotting was used to detect the expressions of p-PI3K/PI3K, p-Akt/Akt, NOD-like receptor family pyrin domain-containing protein 3 (NLRP3), cleaved-Caspase-1, and GSDMD-N. The levels of oxidative stress (reactive oxygen species ［ROS］ and malondialdehyde ［MDA］) were detected by commercial kits. The results showed that, compared to the sham-operation group, the model group showed evident myocardial inflammatory cell infiltration and loose arrangement of myocytes. The levels of LVEDD, LVESD, serum CK-MB, cTnI, LDH, IL-18, and IL-1β were significantly higher in the model group than those in the sham operation group. The levels of ROS, MDA, Hmbox1 positive cells, and protein expressions of NLRP3, cleaved-Caspase-1, and GSDMD-N  in cardiac tissue were increased, while the protein expressions of p-PI3K/PI3K and p-Akt/Akt  were decreased. The values of LVEF and LVFS were reduced (all P<0.05). Compared to those of the sh-NC group, the morphology of cardiomyocytes in the sh-Hmbox1 group was improved, and the infiltration of inflammatory cells was significantly reduced. The sh-Hmbox1 group also showed decreased values of LVEDD and LVESD, along with levels of CK-MB, cTnI, LDH, IL-18, and IL-1β in serum, levels of ROS, MDA, Hmbox1 positive cells, and protein expressions of NLRP3, cleaved-Caspase-1, and GSDMD-N in cardiac tissue. On the other hand, the values of LVEF and LVFS, as well as the protein expressions of p-PI3K/PI3K and p-Akt/Akt, were significantly increased (all P<0.05). The results of this study show that knockdown of Hmbox1 inhibits cardiomyocyte pyroptosis by promoting the PI3K/Akt signaling pathway, resulting in alleviation of MIRI.  This may provide a new target for clinical treatment and prevention of MIRI.
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  Qianjin Weijing Decoction alleviates acute lung injury in septic rats via the NF-κB/NLRP3 signaling pathway-mediated pyroptosis

  CHEN Hui, WANG Pei, XU Junru, ZHANG Yan, CHENG Feng, ZHOU Tingting

  2026, 46(2): 144-150.

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  This study aims to explore the effect of Qianjin Weijing Decoction on acute lung injury in sepsis rats through pyroptosis mediated by NF-κB/NOD-like receptor family pyrin domain-containing protein 3(NLRP3) signaling pathway. Rat model of sepsis was established by cecal ligation. Rats were randomly divided into the model group, the low-dose, medium-dose and high-dose Qianjin Weijing Decoction groups, and the Qianjin Weijian Decoction + phorbol 12-myristate 13-acetate (PMA; NF-κB signaling pathway activator) group, with 12 rats in each group. An other 12 rats from the same cohort without cecal ligation were assigned as the sham operation group. The lung index and water content of lung tissue were measured. The pathological changes of lung tissue were observed by H-E staining, and the relevant scoring was calculated. The pyroptosis of lung tissue was detected by immunofluorescence staining. The levels of inflammatory factors in serum were detected by ELISA. The expressions of NF-κB/NLRP3 signaling pathway related proteins were detected by Western blotting. The results showed that compared to those of the sham operation group, the lung index, water content of lung tissue, score of lung injury, relative fluorescence intensity of NLRP3, levels of serum IL-1β, IL-18, and TNF-α, expressions of phosphorylated NF-κB p65 (p-NF-κB p65)/NF-κB p65, NLRP3 and cleaved Caspase -1 (C-Caspase-1) protein in lung tissue were all increased in the model group (P<0.05). Compared to those of the model group, the lung index, water content of lung tissue, score of lung injury, relative fluorescence intensity of NLRP3, levels of serum IL-1β, IL-18, and TNF-α, expressions of p-NF-κB p65/NF-κB p65, NLRP3 and C-Caspase-1 in lung tissue were all decreased in the medium-dose and high-dose Qianjin Weijing Decoction groups (P<0.05). The treatment of PMA reversed the above effects of Qianjin Weijing Decoction. This study shows that Qianjin Weijing Decoction may inhibit pyroptosis by down-regulating the NF-κB/NLRP3 signaling pathway, thus alleviate acute lung injury in sepsis rats.
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  Analysis of intestinal differential metabolites in patients with irritable bowel syndrome

  LING Pengyun, LI Dan, CAI Linli, CHEN Mengying, HUANG Yuanlan

  2026, 46(2): 151-159.

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  In this study, a widely targeted metabolomics (liquid chromatograph-mass spectrometer ［LC-MS］) approach was used to qualitatively and quantitatively analyze the gut microbiota metabolites between individuals with irritable bowel syndrome (IBS) and healthy controls and to compare the differential metabolites between the two groups. 30 patients with irritable bowel syndrome (IBS) admitted to PLA Naval Medical Center from January 2023 to September 2023 were selected as the study subjects. After exclusion based on inclusion/exclusion criteria, 8 remaining cases were assigned to the IBS group, while 8 healthy individuals matched by sex and age during the same period served as the control group. Fecal samples were frozen at  immediately after collection, and IL-1β, IL-6, and TNF-α were detected by ELISA. LC-MS was used to analyze the difference and enrichment of the extracts. The results showed that the levels of IL-1β (P<0.001), IL-6 (P<0.001), and TNF-α (P<0.05) in the IBS group were significantly higher than those in the control group. LC-MS analysis identified 46 different metabolites between the IBS group and the control group. These metabolites included 10 classes, mainly amino acids and their derivatives, nucleotides and their derivatives, organic acids and their derivatives, lipids, flavonoids, lignans and coumarins, alkaloids, vitamins and their derivatives, and steroid hormones, accounting for 87% of all metabolites detected. Further hierarchical cluster analysis and principal component analysis (PCA) demonstrated clear separation between the two sample groups. Screening of differential metabolites and pathway analysis revealed that these metabolites were primarily enriched in amino acid-related pathways, including valine, leucine, and isoleucine biosynthesis and degradation, aminoacyl-tRNA biosynthesis, and tryptophan metabolism pathways. Amino acids and their derivatives, such as valine, leucine, tryptophan, arginine, and methionine, are key metabolites for antioxidation and inhibition of inflammatory response, and may be involved in the occurrence and development of psychological stress symptoms such as insomnia and anxiety. Therefore, quantitative evaluation of differential metabolites and Kyoto encyclopedia of genes and genomes (KEGG) enrichment analysis are helpful to explore the pathogenesis of IBS from the perspective of amino acid metabolism, and lay a foundation for preventing and treating physiological and psychological stress of soldiers.
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  Ligustrazine modulates intestinal flora in atherosclerotic rats by regulating the TLR4/MyD88/NF-κB signaling pathway

  ZHAO Kun, LIU Ming, JI Wenyan, ZHANG Lu

  2026, 46(2): 160-168.

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  To study the effect of ligustrazine on intestinal flora in atherosclerosis (AS) rats by regulating the TLR4/myeloid differentiation factor 88 (MyD88)/ NF-κB signaling pathway, SD rats were randomly separated into the control group, the model group, the low-dose ligustrazine group the high-dose ligustrazine group, and the high-dose ligustrazine+LPS group. The AS model was established by feeding high-fat diet combined with vitamin D3 injection. After intervention with ligustrazine and TLR4 activator LPS, body weight and the levels of low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C), total cholesterol (TC), and triglyceride (TG) in blood lipids were measured. H-E staining was used to detect the morphology of thoracic aorta, liver and kidney tissues. Oil Red O staining was used to detect the plaque formation of thoracic aorta tissue. Myeloperoxidase (MPO) immunofluorescence staining was used to detect inflammatory cell infiltration of thoracic aorta tissue. 16S rRNA sequencing was used to detect changes in gut microbiota. ELISA was applied to determine the levels of serum endothelin-1 (ET-1), ICAM-1, GM-CSF and TNF-α. Western blotting was used to detect the expressions of TLR4/MyD88/NF-κB signaling pathway related proteins in thoracic aortic tissue. The results showed that compared to those of the control group, the LDL-C, TG and TC levels, proportion of thoracic aortic plaque area and MPO positivity ratio, Ace and Chao1 indexes, relative abundance of Proteobacteria, Escherichia and Coprococcus, ET-1, ICAM-1, GM-CSF and TNF-α levels, TLR4 and MyD88 protein expressions, p-NF-κB p65/NF-κB p65 of the model group were significantly increased (P<0.05), while the HDL-C level, Shannon index, relative abundance of Bacteroidetes and Lactobacillus were significantly reduced (P<0.05). Ligustrazine could improve the aforementioned pathological changes in AS model rats, with a stronger effect at higher dosage. LPS reversed the improvement effect of ligustrazine on the aforementioned pathological changes in AS model rats. This study suggests that ligustrazine improves gut microbiota composition in AS rats by reducing the activity of the the TLR4/MyD88/NF-κB signaling pathway, thereby alleviating arterial tissue damage.
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  Exploring the role of sevoflurane in regulating M1 polarization of macrophages through glycometabolism reprogramming for anti-colon cancer effects

  LIU Zhuo, WANG Tai, HE Zilu, LIU Shouyou

  2026, 46(2): 169-177.

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  This study investigates the effects of sevoflurane on the growth of colon cancer cell line CT26 and the M1 polarization of macrophages. RAW264.7 macrophages were divided into the negative control group, the model group (LPS-induced M1 polarization), the sevoflurane groups of different concentrations (1%, 2%, 4%), and the 2% sevoflurane+2-deoxy-D-glucose (2-DG; the glycolysis inhibitor) group. Conditioned media from these macrophages culture was co-cultured with CT26 cells, and divided into the control group (CT26 alone), the model group (CT26 with media from LPS-treated macrophages), the sevoflurane groups of different concentrations (CT26 co-cultured with macrophage media with 1%, 2%, 4% sevoflurane treatment), and the 2% sevoflurane + 2-DG group (CT26 co-cultured with conditioned macrophage media treated with 2% sevoflurane + 2-DG). A mouse tumor xenograft model was established and divided into the model group, the 2% sevoflurane group, the 2% sevoflurane + 2-DG group, and the macrophage-depleted + 2% sevoflurane group. Western blotting was used to detect the expressions of CD86, inducible nitric oxide synthase (iNOS), and glycolysis marker proteins including pyruvate dehydrogenase kinase 1 (PDK-1), hexokinase 2 (HK2), lactate dehydrogenase A (LDHA), and hypoxia-inducible factor 1α (HIF-1α). Levels of TNF-α, IL-6, and IL-12 were measured by ELISA. The results showed that compared to that in the control group, the proliferation ability of CT26 cells was inhibited in the sevoflurane group. Sevoflurane treatment increased the proportion of M1 macrophages and the expressions of glycolysis marker proteins. Conditioned media from sevoflurane-treated macrophages inhibited CT26 cell proliferation and colony formation, and the effect was attenuated by 2-DG. In the mouse tumor xenograft model, 2% sevoflurane reduced tumor volume and increased the proportion of M1 macrophages, glycolysis protein levels, and inflammatory cytokine levels in tumor tissue, which were counteracted by 2-DG. Depleting macrophages weakened the anti-tumor effect of sevoflurane compared to the 2% sevoflurane group. In conclusion, sevoflurane may inhibit colon cancer cell growth by modulating macrophage glycolysis to promote M1 polarization.
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  miR-21 aggravates allergic rhinitis by disrupting Treg/Th17 immune balance via inhibiting the PTEN/Akt signaling pathway

  FENG Qiaolei, ZHANG Cheng

  2026, 46(2): 178-184.

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  To investigate how miR-21 affects the balance between Treg and Th17 by regulating the phosphatase and tensin homolog deleted on chromosome 10 (PTEN)/Akt signaling pathway, which promotes the pathological process of allergic rhinitis (AR),  rats were randomly divided into 4 groups: the control group, the AR group, the negative control (NC) inhibitor group ( AR rats transfected with NC inhibitor ), and the miR-21 inhibitor group ( AR rats transfected with miR-21 inhibitor ) , with 10 rats in each group. The expression of miR-21 in nasal mucosa, behavioral symptom score, pathological changes of nasal mucosa, the proportion of Treg and Th17, the levels of IL-10, IL-6, IL-17, and IgE in serum, and the expressions of PTEN/Akt signaling pathway related proteins were measured. The results showed that compared to those of the control group, the expression of miR-21, symptom score, Th17 ratio, IL-6, IL-17 and IgE levels, p-PI3K/PI3K and p-Akt/Akt ratios in the AR group and the NC inhibitor group were significantly increased (P<0.05). The proportion of Treg , IL-10 level and PTEN protein expression  decreased significantly (P<0.05). Compared to those of the AR group and the NC inhibitor group, the miR-21 expression level, symptom score, Th17 ratio, IL-6, IL-17 and IgE levels, p-PI3K/PI3K and p-Akt/Akt retios in the miR-21 inhibitor group were significantly reduced (P<0.05), while the proportion of Treg, IL-10 level and PTEN protein expression increased significantly (P<0.05). The study suggests that miR-21 may play an important role in the pathogenesis of AR by inhibiting the PTEN/Akt signaling pathway, thereby regulating Treg/Th17 immune balance and effectively inhibiting inflammatory response. 
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  Kaempferol regulates the inflammatory response and synovial function in acute gouty arthritis rats

  ZHAO Xiaoyan, LI Zhipeng, XU Kang

  2026, 46(2): 185-191.

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  To explore the impacts of kaempferol on inflammatory response and synovial function in acute gouty arthritis rats, SD rats were assigned to the control group, the model group, the colchicine group (0.3 mg/kg), the low-dose kaempferol group (25 mg/kg), the medium-dose kaempferol group (50 mg/kg), and the high-dose kaempferol group (100 mg/kg). Except for the control group, rats were orally administered the specified drug once a day for 7 consecutive days. Establishment of the acute gouty arthritis model started on the 5th day after administration. The gait of rats, the joint inflammation index, and the degree of joint swelling of rats in each group were measured. Levels of IL-8, IL-17, and IL-37 in the serum and TNF-α, IL-1β, and IL-6 in the joint fluid were detected using ELISA. H-E staining was used to observe the morphology of synovial tissue in the ankle joints. Western blotting was used to detect proteins in the MAPK/NF-κB/activator protein-1 (AP-1) pathway in the synovial tissue. Compared with the control group, the model group showed edema in the synovial tissue and more infiltration of inflammatory cells. The gait score, joint inflammation index, joint swelling score, and the protein expressions of IL-8, IL-17, IL-37, TNF-α, IL-1β, IL-6, p-p38, p-JNK, p-NF-κB p65, and AP-1 were all elevated (P<0.05).  Compared with the model group, the colchicine and kaempferol groups showed improvement in all the indicators mentioned above (P<0.05). However, there was no significant difference in the above indicators between the high-dose kaempferol group and the colchicine group (P>0.05).  Our findings suggest that kaempferol may improve the inflammatory response and synovial function in rats with acute gouty arthritis by inhibiting the MAPK/NF-κB/AP-1 pathway.
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  Effect of lncRNA ZFAS1 on hypoxia/reoxygenation-induced cardiomyocyte injury by targeting the miR-525-5p/HIF1αN axis

  ZHANG Yichao, LI Jianlong, ZHAO Yansha, TIAN Xixi, HAN Siliang

  2026, 46(2): 192-198.

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  The aim of this study is to investigate the impact of long non-coding RNA (lncRNA) zinc finger protein antisense 1 (ZFAS1) on hypoxia/reoxygenation (H/R)-induced cardiomyocyte injury through the miR-525-5p/hypoxia-inducible factor 1α inhibitor (HIF1αN) axis. Injury of cardiomyocyte H9c2 was induced by H/R, and the treated cells were divided into the control group, the H/R group, the H/R+shZFAS1 group (H/R treatment after transfection with shZFAS1), the H/R+negative control (shNC) group (H/R treatment after transfection with shNC), the H/R+shZFAS1+miR-525-5p inhibitor group (H/R treatment after co-transfection with shZFAS1 and co-incubation with miR-525-5p inhibitor), and the H/R+shZFAS1+inhibitor NC group (H/R treatment after co-transfection with shZFAS1 and co-incubation with  inhibitor NC). Commercialized kits were applied to detect levels of malondialdehyde (MDA), superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), IL-6, and TNF-α. Flow cytometry was used to detect cell apoptosis rate, qRT-PCR was used to detect the expressions of miR-525-5p, lncRNA ZFAS1, and HIF1αN mRNA in each group. Western blotting was used to detect the expressions of HIF1αN, B-cell lymphoma 2（Bcl-2）, and Bcl-2-associated X protein (Bax）. Dual-luciferase reporter assay was applied to verify the targeting between miR-525-5p and lncRNA ZFAS1 or HIF1αN. The results showed that compared to those of the control group, the expressions of Bcl-2 and miR-525-5p, the levels of SOD and GSH-Px in the H/R group were significantly decreased, and the expressions of HIF1αN, Bax protein, lncRNA ZFAS1, HIF1αN mRNA, cell apoptosis rate, levels of IL-6, TNF-α, and MDA were significantly increased (all with P＜0.05). Compared to those of the H/R+shNC group, the expressions of Bcl-2 and miR-525-5p, the levels of SOD and GSH-Px in the H/R+shZFAS1 group were significantly increased, while the expressions of HIF1αN, Bax protein, lncRNA ZFAS1, HIF1αN mRNA, cell apoptosis rate, levels of IL-6, TNF-α, and MDA were significantly decreased (all with P＜0.05). Compared to those of the H/R+shZFAS1+inhibitor NC group, the expressions of Bcl-2 and miR-525-5p, the levels of SOD and GSH-Px in the H/R+shZFAS1+miR-525-5p inhibitor group were significantly decreased, whereas the expressions of HIF1αN, Bax protein, HIF1αN mRNA, cell apoptosis rate, levels of IL-6, TNF-α, and MDA were significantly increased (all with P＜0.05). The dual-luciferase reporter assay verified that miR-525-5p targeted lncRNA ZFAS1 and HIF1αN. In conclusion, interfering with lncRNA ZFAS1 expression can alleviate H/R-induced cardiomyocyte injury by regulating the miR-525-5p/HIF1αN axis.
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  Detection and clinical analysis of antinuclear antibodies in autoimmune disease patients in Enshi area

  KANG Jun, ZHOU Long, YANG Nianan, YU Peijuan, SU Linchong, HUANG Xia

  2026, 46(2): 199-203.

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  The study aims to investigate the positive distribution and clinical diagnostic value of anti-nuclear antibody (ANA) in autoimmune disease (AID) and non-AID patients in Enshi area. 8 653 suspected AID patients were collected. Indirect immunofluorescence (IIF) assay was used to detect ANA and linear immunoassay (LIA) to detect ANA spectrum. Based on clinical data, the overall positive rates of ANA and ANA spectrum, the positive distribution in different age groups and diseases, as well as their clinical value were analyzed. The results showed that the overall positive rates of ANA and ANA spectrum were 14.77% and 13.20%, respectively. The positive rates in the ≥40, 30-39  and ≤29 age groups were (15.50%, 13.75%), (14.71%, 13.31%), and (9.92%, 9.44%), respectively. Among the positive ANA cases, 45.54% were AID and 54.46% were non-AID. The specific antibodies with higher positive rates in the ANA test were Ro52 antibody,  centromere protein B (CENPB) antibody, and Sjogren's syndrome antigen B (SSB) antibody with positive rates of 7.62%, 6.99%, 2.44%, and 2.08% respectively. Both ANA and ANA spectrum can be positive in AID and non-AID cases.  Timely screening of ANA and ANA spectrum is beneficial for the diagnosis, differential diagnosis, and early intervention of AID and non-AID.
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  Profile and analysis of sIgE in children from western Shenzhen

  2026, 46(2): 204-210.

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  he purpose of this study is to investigate the distribution of allergens in children with positive serum specific IgE (sIgE) for allergens in the western part of Shenzhen based on the data from the Shenzhen Baoan women's and children's Hospital. A retrospective analysis was conducted on allergen detection data and related clinical records. The results showed that with increasing age, both the types and numbers of positive allergen tests in children showed a linear upward trend, and the number of multiple positive allergen-sIgE (≥2) also increased linearly.  The top five  inhalant allergens were Dermatophagoides pteronyssinus (27.87%), Dermatophagoides farinae (26.85%), dust mite (26.68%), cat dander (6.41%), and Blomia tropicalis (5.86%). The positive rates were significantly higher in male children than in female children (P< 0.05).The top five food allergens were cow's milk (17.50%), egg white (15.28%), cashew (8.24%), crab (4.76%), and  shrimp (3.59%). Except for egg white,  sIgE positivity to the other four allergens was significantly higher in male children than in females (all P<0.05). The sIgE positivity rates for milk and egg  white decreased progressively with age (P<0.001). Sensitization to Dermatophagoides pteronyssinus, Dermatophagoides farinae, dust mite, and cat dander peaked during summer months, whereas Blomia tropicalis sensitization reached its highest level in spring, with all seasonal variations being statistically significant (P<0.001).  The level of sIgE positivity is related to the age and gender of the children. Overall, the sIgE positivity rate is higher in male than in female children, and with increasing age, the spectrum of sIgE-positive allergens expands significantly, and the proportion of multiple positivity shows a linear increase.
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  Exploring the neuroprotective effect and mechanism of picrosideⅡ on traumatic brain injury mice by the Shh/Gli1 signaling pathway

  ZHAO Gang, ZHANG Guodong, WANG Lixiang, ZHANG Jiaqi, CHENG Zhenguo

  2026, 46(2): 211-217.

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  The study aims to investigate the neuroprotective effect of picrosideⅡ (PIC Ⅱ) on traumatic brain injury (TBI) in mice by regulating the sonic hedgehog (Shh)/glioma-associated oncogene homolog 1 (Gli1) signaling pathway. A TBI mouse model was constructed and TBI mice were assigned to the model (TBI) group,  the low-dose PIC Ⅱ(L-PIC Ⅱ; 6.25 mg/kg) group, the medium-dose PIC Ⅱ (M-PIC Ⅱ; 12.50 mg/kg) group, the high-dose PIC Ⅱ(H-PIC Ⅱ; 25.00 mg/kg) group, and the high-dose PIC Ⅱ+cyclophosphamide (25.00 mg/kg H-PIC Ⅱ+15.00 mg/kg Shh/Gli1 signaling pathway inhibitor cyclophosphamide) group, with 12 mice each. Another 12 mice were used as the sham group. The modified neurological severity score (mNSS), Morris water maze (MWM) experiment, and brain water content were measured. ELISA was used to detect inflammatory factors and oxidative stress levels. H-E staining was used to observe pathological changes in hippocampal tissue. Western blotting was used to detect the proteins related to the Shh/Gli1 signaling pathway. The results showed that the hippocampal tissue structure in the sham group was normal. The cell arrangement of hippocampal tissue in the TBI group was disordered, and nerve cells exhibited nuclear condensation. Compared to those of the sham group, the mNSS, IL-6, TNF-α, IL-1β, malondialdehyde (MDA) levels and brain water content in the TBI group increased significantly (P<0.05), the escape latency was prolonged (P<0.05), the number of crossing platform attempts was reduced (P<0.05), and the levels of superoxide dismutase (SOD), Shh and Gli1 protein expression were significantly decreased (P<0.05). Compared to those of the TBI group, the above indicators were improved in the L-PIC Ⅱ group, M-PIC Ⅱ group and H-PIC Ⅱ group, while the results of the H-PIC Ⅱ+cyclophosphamide group were opposite to those of the H-PIC Ⅱ group. This study suggests that the neuroprotective effect of PIC Ⅱ in TBI mice may be achieved by activating the Shh/Gli1 signaling pathway.
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  Myricetin promotes fracture healing in rats with traumatic fractures by regulating the BMP-2/Runx2 signaling pathway

  WANG Bin, SHI Zhiyuan, LI Derong, YU Jinwei

  2026, 46(2): 218-226.

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  To explore the effect of myricetin on fracture healing in rats with traumatic fractures by the regulation of the bone morphogenetic protein 2 (BMP-2)/Runt-related transcription factor 2 (Runx2) signaling pathway, SD rats were randomly divided into 5 groups (n=12): the sham-operated group, the model group, the low-dose myricetin treatment group, the medium-dose myricetin treatment group, and the high-dose myricetin treatment group. Microcomputer tomography (Micro-CT) was used to assess fracture healing and bone microstructure parameters. H-E staining was conducted to evaluate morphological changes in femoral tissue. Commercial kits were used to measure the levels of calcium, phosphorus, osteocalcin (OCN), alkaline phosphatase (ALP), type Ⅰ procollagen amino-terminal propeptide (P1NP), typeⅠcollagen C-terminal telopeptide (CTX-Ⅰ), typeⅡcollagen C-terminal telopeptide (CTX-Ⅱ), inducible nitric oxide synthase (iNOS), TNF-α, and IL-6. qRT-PCR and Western blotting were used to detect the BMP-2, Runx2 mRNA and protein expressions, respectively. The results showed that compared to the sham-operated group, the model group showed severely damaged morphology and trabecular bone structure of femoral tissue, reductions of serum calcium, phosphorus, OCN levels, and ALP activity（P<0.001）, and increase of P1NP, CTX-Ⅰ, CTX-Ⅱ, TNF-α, IL-6, and iNOS levels (P<0.001). The BMP-2 and Runx2 mRNA and protein expressions in femoral tissue significantly decreased (P<0.001), while the mRNA levels of TNF-α, IL-6, and iNOS  significantly increased (P<0.001). Compared to the model group, myricetin dose-dependently improved the morphology of femoral tissue and the structure of trabecular bone, enhanced the serum levels of calcium, phosphorus, OCN, and ALP activity(P<0.05), lowered P1NP, CTX-Ⅰ, CTX-Ⅱ, TNF-α, IL-6, and iNOS levels (P<0.05). It also upregulated the mRNA and protein expressions of BMP-2 and Runx2 (P<0.01), while downregulated the mRNA of TNF-α, IL-6, and iNOS (P<0.05). These findings suggest that myricetin promotes the fracture healing of traumatic fractures in rats, possibly through the modulation of the BMP-2/Runx2 signaling pathway.
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  dectin-1 regulates lung tissue inflammatory injury and M1-type macrophage infiltration in sepsis-induced ALI mice

  QI Wenmei, WANG Honghu

  2026, 46(2): 227-236.

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  To analyze the effects of dendritic cell-associated C-type lectin-1 (dectin-1) on inflammatory injury and M1 macrophage infiltration in lung tissue of mice with sepsis-induced acute lung injury (ALI), differentially expressed genes were analyzed in lung tissues of normal or sepsis-induced ALI mice in PRJNA899441 dataset. The correlations with inflammatory factors IL-1β, IL-6, TNF-α, and the abundance of various immune cell infiltrations were analyzed. Male C57BL/6 mice underwent cecal ligation and puncture surgery to establish a sepsis-induced ALI mouse model, which was divided into the sham group, the model group, the adeno-associated virus (AAV) short hairpin RNA (shRNA)-negative control (NC) group (AAV-sh-NC group), and the AAV-sh-dectin-1 group. The infection efficiency of AAV was evaluated by fluorescence microscope. Lung tissue pathological injury was observed by H-E staining. ELISA was used to measure the levels of inflammatory factors IL-1β, IL-6, and TNF-α in lung tissues. Transcriptome analysis was performed on lung tissues of the AAV-sh-NC and AAV-sh-dectin-1 groups to obtain differentially expressed genes, which were then subjected to Gene Ontology (GO) enrichment and Kyoto Encyclopedia of Genes and Genomes (KEGG) signaling pathway enrichment analyses. Double immunofluorescence staining was used to measure the positive staining rates of the lung epithelial cell marker SP-C and the M1 macrophage marker CD86. Western blotting was used to determine the protein expressions of dectin-1 and NF-κB in lung tissues. The results showed that in the PRJNA899441 dataset, dectin-1 level was significantly higher in the lung tissues of ALI mice than in normal lung tissues, and dectin-1 level was positively correlated with IL-1β, IL-6, and TNF-α levels. Compared to the AAV-sh-NC group, the AAV-sh-dectin-1 group showed reduced dectin-1 protein expression, decreased inflammatory factors TNF-α, IL-6, and IL-1β, and mitigated lung tissue pathological injury. Transcriptome analysis combined with GO enrichment results revealed that inhibiting dectin-1 was associated with reduced M1 macrophage infiltration. KEGG signaling pathway enrichment assay indicated that inhibiting dectin-1 affected the NF-κB signaling pathway. The lung tissue of ALI mice in the AAV-sh-dectin-1 group showed reduced percentage of CD86-positive staining (indicating M1 macrophage infiltration), increased SP-C positive staining rate, and decreased NF-κB activity. The above results suggest that inhibition of dectin-1 suppresses the release of inflammatory factors in the lung tissues of mice with sepsis-induced ALI, as well as the activation of the NF-κB signaling pathway, which reduces M1 macrophage infiltration and attenuates sepsis-induced lung injury.
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  The dual role of FASLG/FAS in tumor development: from apoptosis regulation to immune escape

  HU Ming, REN Jianye, LU Jialing, DENG Jianqing, ZHANG Hongyu

  2026, 46(2): 237-243.

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  The FAS ligand (FASLG)/FAS exhibits dynamic dual functions in tumors: on one hand, it activates the Caspase cascade through the death-inducing signaling complex (DISC) to induce apoptosis of tumor cell; on the other hand, under microenvironmental stress, it drives immune escape via the NF-κB/MAPK pathway. Currently, the dual role of the FASLG/FAS has become a hot topic in cancer research, but the underlying mechanisms remain elusive, particularly regarding its expression and clinical translation strategies across different types of tumors. This review summarizes the latest research progress on the FASLG/FAS in tumor development and progression, focusing on its dual functions in apoptosis regulation and immune escape, and discusses how related research can provide new insights and methods for cancer treatment. By discussing current literature, this review aims to offer a new perspective on FAS signaling regulation in the tumor microenvironment and to promote its potential applications in targeted therapy.
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  Research progress on the role and mechanisms of efferocytosis in SLE pathogenesis

  LI Wanyang, LI Nan, QIAN Cheng

  2026, 46(2): 244-249.

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  Systemic lupus erythematosus (SLE) is an autoimmune disease characterized by an increase in auto-antibodies, with complex clinical manifestations and limited therapeutic efficacy. Efferocytosis, the physiological process of apoptotic cell clearance, plays a pivotal role in maintaining immune homeostasis. Defective efferocytosis is associated with the pathogenesis of SLE by exposing self-antigens, triggering inflammatory responses, and promoting auto-antibody production. The molecular mechanisms of SLE-associated efferocytosis impairments include elevated “find-me” signals, aberrant expression and distribution of phosphatidylserine (“eat-me” signals) and its receptors, formation of antibodies against phosphatidylserine and its receptors, upregulation of “don't-eat-me” signals, and deficiencies in key enzymes or receptors essential for phagocytic engulfment and digestion. This review concludes current advances on the pathogenic role of efferocytosis defects in SLE and the underlying molecular pathways, providing new directions for future clinical diagnosis and drug development of SLE.
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  Research progress of therapeutic hepatitis B vaccine based on whole Saccharomyces cerevisiae cells

  BIAN Guanglin, GAO Yinfeng, MA Wenqiao, SUI Ping, JING Yu, WANG Yan, FU Jiangping, ZHANG Ruifeng

  2026, 46(2): 250-254.

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  Hepatitis B virus (HBV) infection is a major global public health issue that poses a serious threat to human health. Current treatment regimens have limited efficacy, thus there is an urgent need to develop novel therapeutic strategies. Saccharomyces cerevisiae has emerged as a research hotspot for therapeutic vaccine platform, due to its ability to efficiently express exogenous proteins and its natural adjuvant components, which activates the immune system and enhances antigen-specific responses. Developed  on this platform, GS-4774 is a therapeutic hepatitis B vaccine using inactivated Saccharomyces cerevisiae cells expressing HBV antigens. Clinical studies have demonstrated that GS-4774 exhibits good safety and tolerability in healthy volunteers and can induce HBV-specific T-cell responses, verifying its potential as a therapeutic vaccine for chronic HBV infection. However, GS-4774 fails to significantly reduce serum hepatitis B surface antigen (HBsAg) level in patients with chronic HBV infection and show clear therapeutic benefits. This indicates that its immunogenicity and treatment regimens still need optimization. This review summarizes the research progress on whole-yeast-cell-based HBV therapeutic vaccines, analyzes the core issues of such vaccines represented by GS-4774, and proposes optimization strategies based on immunological research. This review provides references for promoting research and development in the field while broadening clinical therapeutic approaches for chronic HBV infection.
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  Current status and prospects of sapovirus research

  ZHANG Longlong, QI Juan, LIU Zhen, PU Xiuying

  2026, 46(2): 255-261.

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  This review systematically and comprehensively summarizes the current research status of sapovirus, including epidemiological characteristics, molecular evolution mechanisms, advances in detection technology, infection immune mechanisms, prevention and control strategies, as well as vaccine development challenges, to reveal current achievements and limitations and provide scientific basis for future prevention and vaccine development. This review discusses gene sequence of the main structural protein VP1 of popular strains GⅠ.1 and GⅠ.2 in recent years. Molecular evolution analysis and protein structure analysis of their consensus genes reveals that the GⅠ.1 type is more prone to gene mutations and recombination. In term of infection mechanism, instead of dependent on histo-blood group antigens (HBGA), the virus relies on bile acid to promote intestinal replication. In addition, virus tropism is limited to small intestinal epithelial cells. Finally, the development of sapovirus vaccine is limited by the elusive receptor binding mechanism and the lack of in vitro culture system. Although virus like particle (VLP) technology has the potential to induce antibody responses, it lacks effective model validation.
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  Advances in hematological toxicity following CAR-T  therapy in hematologic malignancies

  ZHANG Jiaze, LU Ying, PEI Renzhi, WANG Tiantian

  2026, 46(2): 262-268.

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  Chimeric antigen receptor T-cell (CAR-T) therapy has demonstrated significant efficacy in the treatment of hematologic malignancies, but it is accompanied by a variety of adverse effects. Hematological toxicity is among the most common and important factors that affect the prognosis of patients, including the development of anemia, lymphopenia, neutropenia and thrombocytopenia. This review comprehensively discusses the clinical manifestations and factors influencing the hematological toxicity of CAR-T therapies, highlighting the complex interplay between the disease burden, the patient's immune status and the characteristics of the CAR-T product. Concurrently, this review discusses the prediction and assessment of hematological toxicity of CAR-T therapy in hematologic malignancies, highlighting tailored approaches to mitigate severe and long-term hematological toxicity. These management strategies underscore the need for targeted interventions to manage hematological toxicity of CAR-T therapy in hematologic malignancies without compromising CAR-T efficacy. Optimised management of hematological toxicity of CAR-T therapy in hematologic malignancy could improve patient outcomes, reduce medical expenses and increase the accessibility of treatment.