目的 基于Toll样受体4（Toll-like receptor 4，TLR4）/髓样分化因子88（myeloid differentiation primary response 88，MyD88）介导的核因子-κB（nuclear factor-κB，NF-κB）通路探讨首荟通便胶囊对幽门螺杆菌Helicobacter pylori感染人胃黏膜上皮细胞GES-1诱导的炎症反应的影响。方法 构建幽门螺杆菌诱导GES-1细胞炎症模型，设置对照组、模型组及首荟通便胶囊（80、160、320 μg/mL）组，给予首荟通便胶囊干预后，检测细胞上清液中一氧化氮（nitric oxide，NO）水平；流式细胞术检测细胞凋亡及活性氧（reactive oxygen species，ROS）水平；ELISA测定白细胞介素-1β（interleukin-1β，IL-1β）水平；qRT-PCR检测IL-1β的mRNA表达；Western blotting检测TLR4/MyD88/NF-κB信号通路相关蛋白表达。结果 与模型组比较，首荟通便胶囊显著降低NO释放量、细胞凋亡率、ROS和IL-1β水平（P＜0.05、0.01、0.001），下调IL-1β的mRNA表达（P＜0.001），并抑制TLR4、MyD88、p-NF-κB/NF-κB的蛋白表达水平（P＜0.05、0.01）。结论 首荟通便胶囊可通过抑制TLR4/MyD88介导的NF-κB通路活化，减轻氧化应激损伤，减少促炎因子生成，从而缓解幽门螺杆菌感染诱导的GES-1细胞炎症反应。

Objective To explore the effect of Shuhui Tongbian Capsule (首荟通便胶囊) on inflammatory response induced by Helicobacter pylori infection in human gastric epithelial GES-1 cells based on Toll-like receptor 4 (TLR4)/myeloid differentiation primary response 88 (MyD88) mediated nuclear factor-κB (NF-κB) pathway. Methods H. pylori induced GES-1 cells inflammation model was constructed, control group, model group and Shouhui Tongbian Capsule (80, 160, 320 μg/mL) groups were set up. After intervention with Shouhui Tongbian Capsule, the level of nitric oxide (NO) in supernatant was detected. Flow cytometry was used to detect cell apoptosis and reactive oxygen species (ROS) level. ELISA was used to measure the level of interleukin-1β (IL-1β). qRT-PCR was used to detect the mRNA expression of IL-1β. Western blotting was used to detect the expressions of TLR4/MyD88/NF-κB signaling pathway related proteins. Results Compared with model group, Shouhui Tongbian Capsule significantly reduced NO release, cell apoptosis rate, ROS and IL-1β levels (P < 0.05, 0.01, 0.001), down-regulated IL-1β mRNA expression (P < 0.001), and inhibited the protein expression levels of TLR4, MyD88 and p-NF-κB/NF-κB (P < 0.05, 0.01). Conclusion Shouhui Tongbian Capsule could alleviate the inflammatory response of GES-1 cells induced by H. pylori infection by inhibiting the activation of TLR4/MyD88 mediated NF-κB pathway, reducing oxidative stress damage, and decreasing the production of pro-inflammatory factors.

R285.5

泰山产业领军人才（tscx202306086）