LAN Jingsheng, HUANG Youyi, LI Donghua, BAN Chaolian, QIN Ziqing, TANG Meiyan, CHEN Liquan, LI Nini, WEN Lina
Current Immunology. 2026, 46(1): 24-33.
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This study aims to elucidate the inhibitory effects and underlying mechanisms of allicin on fibrosis in mouse cardiac fibroblasts (CF) through long non-coding RNA (lncRNA) maternally expressed gene 3 (MEG3). Mouse CFs were isolated and cultured, and an in vitro fibrosis model of CFs was established. The fibrotic CFs were treated with allicin at concentrations of 10, 20, and 40 μg/L to evaluate the protective effect of allicin on CF injury. Subsequently, cells were transfected with the sh-lncRNA MEG3 plasmid or the sh-lncRNA NC plasmid. The cells were divided into the control group, the model group, the allicin group, the sh-lncRNA MEG3 group, the sh-lncRNA NC group, the allicin + sh-lncRNA MEG3 group, and the allicin + sh-lncRNA NC group. CCK-8 assay was used to evaluate cell proliferation, flow cytometry was employed to assess cell apoptosis, and qRT-PCR was conducted to measure the expression changes of matrix metalloproteinase (MMP)-2, MMP-3, MMP-9, lncRNA MEG3, and inflammatory cytokines (IL-8, IL-6, IL-1β). Western blotting was used to detect the expressions of alpha-smooth muscle actin (α-SMA), collagen type Ⅰ (COL1), collagen type Ⅲ (COL3), and proteins involved in the NF-κB signaling pathway (NF-κB p65, p-NF-κB p65, inhibitor of κB ［IκB］ , and p-IκB). The results showed that compared to the control group, the model group showed enhanced cell proliferation (P<0.01), reduced apoptosis rate (P<0.01), upregulated lncRNA MEG3 levels (P<0.01), and increased mRNA levels of MMP-2, MMP-3, MMP-9, as well as IL-8, IL-6, and IL-1β (P<0.01). After allicin treatment, cell proliferation was inhibited (P<0.01), apoptosis rate increased (P<0.01), and the mRNA levels of MMP-2, MMP-3, MMP-9, as well as IL-8, IL-6, and IL-1β were downregulated (P<0.05) in a dose-dependent manner. In addition, allicin downregulated the protein expressions of α-SMA, COL1, and COL3, as well as the p-NF-κB p65/NF-κB p65 ratio (P<0.01), while upregulating the p-IκB/IκB ratio (P<0.01) in the CFs fibrosis model. Compared to the model group, both the sh-lncRNA MEG3 group and the allicin group showed similar trends. Moreover, the combined treatment of allicin and sh-lncRNA MEG3 generated stronger inhibitory effect on CF injury than of sh-lncRNA MEG3 alone. This study suggests that allicin exerts a protective effect against fibrosis induced CF injury by downregulating lncRNA MEG3, thereby inhibiting the NF-κB pathway to suppress CFs proliferation, and reduce the levels of MMPs, inflammatory cytokines, and collagen deposition proteins.
