[摘 要] 目的：探讨健脾复胃颗粒（JPFWG）通过调控IL-6/JAK/STAT3信号通路对胃癌前病变（PLGC）大鼠胃黏膜损伤的干 预效果及其作用机制。方法：采用MNNG联合复合因素造模法建立PLGC模型大鼠，随机分为6组（20只/组）：空白组（未处理）、 模型组（给予生理盐水）、维酶素组（0.05 g/mL维酶素）、JPFWG低剂量组（JPFWG-L，0.088 g/mL）、JPFWG中剂量组（JPFWG-M， 0.176 g/mL）、JPFWG高剂量组（JPFWG-H，0.351 g/mL）。各治疗组大鼠分别给予相应药物处理12周后，麻醉处死动物并取胃组 织标本。采用H-E染色法观察胃黏膜的病理变化，通过免疫组化、qPCR和WB法检测胃黏膜组织中IL-6介导的JAK/STAT3信号 通路相关因子（包括IL-6、JAK、STAT3）及其下游靶基因c-Myc、cyclin D1的 mRNA和蛋白的表达水平。结果：与模型组相比，维 酶素组和JPFWG-L、JPFWG-M、JPFWG-H组大鼠胃黏膜炎性细胞浸润均减少，病理状态改善以JPFWG-H组最明显；IL-6、JAK1、 STAT3蛋白表达显著降低（P < 0.05或P < 0.01）；维酶素组和JPFWG-H组大鼠胃黏膜组织中c-Myc、cyclin D1的 mRNA和蛋白表 达均显著降低（P < 0.05或P < 0.01）。结论：JPFWG能够改善PLGC大鼠胃黏膜的组织病理变化，其机制可能是通过调控IL-6/ JAK/STAT3信号通路，进而下调c-Myc、cyclin D1的表达，从而阻断炎-癌转化过程。

[Abstract] Objective: To explore the intervention effect of Jianpifuwei granule (JPFWG) on gastric mucosal injury in rats with precancerous lesions of gastric cancer (PLGC) by regulating the IL-6/JAK/STAT3 signaling pathway and its mechanism. Methods: The PLGC model rats were established by MNNG combined with composite factors, and randomly divided into 6 groups (20 rats/group): the blank group (untreated), model group (treated with normal saline), Weimeisu group (0.05 g/mL Weimeisu), JPFWG low-dose group (JPFWG-L，0.088 g/mL), JPFWG medium-dose group (JPFWG-M，0.176 g/mL) and JPFWG high-dose group (JPFWG-H， 0.351 g/mL). After being treated with Weimeisu and different doses of JPFWG for 12 weeks, the animals were anesthetized and sacrificed, and the gastric tissues were collected. The pathological changes of gastric mucosa were observed by H-E staining, and the expression levels of IL-6-mediated JAK/STAT3 signaling pathway factors (including IL-6, JAK and STAT3) and the mRNA and proteins of their downstream target genes c-Myc and cyclin D1 in gastric mucosal tissues were detected by immunohistochemistry, qPCR and WB. Results: Compared with that in the model group, the gastric mucosal inflammatory cell infiltration was reduced in the Weimeisu group and the low, medium, and high dose groups of JPFWG; pathological condition was improved, most obviously in the high dose group of JPFWG; The protein expressions of IL-6, JAK1 and STAT3 decreased significantly (P < 0.05 or P < 0.01). The expressions of mRNA and proteins of c-Myc and cyclin D1 in the gastric mucosal tissues of the rats in the Weimeisu group and JPFWG-H group decreased significantly (P < 0.05 or P < 0.01). Conclusion: JPFWG can improve the histopathological changes of gastric mucosa in rats with PLGC, and its mechanism may be down-regulating the expressions of c-Myc and cyclin D1 through regulating IL-6/JAK/STAT3 signal pathway, thus blocking inflammation-cancer transformation process.

宁夏回族自治区科技厅自然基金（No. 2021AAC03410）；宁夏卫健委课题（No. 2022-NWKY-038）