Exploring the Effect of Jianpi Qinghua Tang on Helicobacter pylori-Induced Damage to Gastric Mucosal Epithelial Cells based on the SOCS3/TLR4/NF-κB Pathway
HE Zixiong1, SUN Meiyu2, YAN Yuerong3*
This study explores the effect of CM (Jianpi Qinghua Tang) on Hp (Helicobacter pylori)-induced damage to gastric mucosal epithelial cells based on the SOCS3 (suppressor of cytokine signaling 3)/TLR4 (Toll-like receptor 4)/NF-κB (nuclear factor kappa-B) pathway. Normal cultured gastric mucosal epithelial cells GES-1 were designated as the control group, and Hp-induced cell damage model was established. They were assigned into model group, CM group (120 μg/mL CM), CM+sh-NC group (120 μg/mL CM+transfection of sh-NC), and CM+sh-SOCS3 group (120 μg/mL CM+transfection of sh-SOCS3) according to different treatment methods. qRT-PCR and Western blot were applied to detect the transfection efficiency of SOCS3. MTT and colony formation assays were applied to detect cell proliferation in each group. ELISA was applied to detect the expression of IL-1β (interleukin- 1β), IL-6, and TNF-α (tumor necrosis factor-α) of cells in various groups. Flow cytometry was applied to detect apoptosis of cells in various groups. Western blot was applied to detect the expression of Bcl-2, Bax, TLR4, NF-κB, and SOCS3 proteins of cells in each group. The results showed that compared with the control group, the survival rate, clone number, the expression of Bcl-2, and SOCS3 in the model group reduced, and the apoptosis rate, the expression of Bax, TLR4, NF-κB, IL-1β, IL-6, and TNF-α increased (P<0.05). Compared with the model group, the survival rate, clone number, the expression of Bcl-2, and SOCS3 in the CM group increased, and the apoptosis rate, the expression of Bax, TLR4, NF-κB, IL-1β, IL-6, and TNF-α reduced (P<0.05). Compared with the CM group or CM+sh-NC group, the survival rate, clone number, the expression of Bcl-2, and SOCS3 in the H-CM+sh-SOCS3 group reduced, and the apoptosis rate, the expression of Bax, TLR4, NF-κB, IL-1β, IL-6, and TNF-α increased (P<0.05). In conclusion, CM can inhibit the secretion of inflammatory factors in Hp-induced GES-1 cells, suppress cell apoptosis, and thereby alleviate damage to gastric mucosal epithelial cells. Its mechanism may be related to the activation of the SOCS3/TLR4/NF-κB pathway.
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