【目的】探讨吴茱萸次碱对幽门螺杆菌 （Hp） 诱导的慢性萎缩性胃炎 （CAG） 的治疗作用及其潜在机制。 【方法】采用Hp 诱导CAG大鼠模型。将造模成功的大鼠随机分为模型组，吴茱萸次碱低、中、高剂量组。另设12只大鼠作为正常组。记录 各组大鼠治疗前后体质量变化；采用苏木精-伊红 （HE） 染色进行胃黏膜组织病理分析；采用酶联免疫吸附分析 （ELISA） 检测 胃黏膜上清中肿瘤坏死因子α （TNF-α） 、白细胞介素6 （IL-6） 、白细胞介素10 （IL-10） 等炎性因子水平；应用实时荧光定量聚 合酶链反应 （RT-qPCR） 技术检测胃黏膜组织诱导型一氧化氮合酶 （iNOS） 、分化簇86 （CD86） 、精氨酸酶1 （Arg-1） 、甘露糖受 体（CD206）mRNA表达水平；蛋白免疫印迹（Western Blot）法检测胃黏膜组织核因子 κB（NF-κB）通路相关蛋白表达。 【结果】 与正常组比较，模型组胃黏膜上皮结构紊乱，固有层腺体减少，大量炎症细胞浸润，胃黏膜组织评分显著升高，胃 黏膜上清TNF-α、IL-6、IL-10水平，胃黏膜iNOS、CD86 mRNA表达水平及磷酸化核因子κB抑制蛋白α （p-IκBα） 、磷酸化 核因子κB p65亚基 （p-p65） 蛋白水平显著升高，胃黏膜Arg-1、CD206 mRNA水平显著降低，差异均有统计学意义 （P＜ 0.05） ；与模型组比较，吴茱萸次碱中、高剂量炎性细胞浸润减少，细胞排列趋于规则，固有层腺体增多，胃黏膜组织评分 显著降低，TNF-α、IL-6、IL-10水平，iNOS、CD86 mRNA表达水平及p-p65、p-IκBα蛋白表达显著降低，Arg-1、CD206 mRNA表达显著升高，差异均有统计学意义 （P＜0.05） ，且呈剂量依赖性。 【结论】吴茱萸次碱能够通过调控巨噬细胞极化改 善Hp诱导的CAG，减轻炎症反应，其机制可能与下调p-p65、p-IκBα表达进而抑制NF-κB通路的活化有关。

Objective To investigate the therapeutic effects and underlying mechanisms of rutaecarpine on Helicobacter pylori （Hp） -induced chronic atrophic gastritis （CAG） . Methods An Hp-induced CAG rat model was established. Successfully modeled rats were randomly divided into model group，low-dose rutaecarpine group， medium-dose rutaecarpine group，and high-dose rutaecarpine group，with 12 rats in each group. An additional 12 rats served as the normal control group. Body mass changes were recorded before and after treatment. Gastric mucosal histopathology was analyzed using hematoxylin-eosin （HE） staining. Levels of inflammatory cytokines （TNF-α，IL-6，IL-10） in gastric mucosal supernatants were measured by enzyme-linked immunosorbent assay （ELISA） . mRNA expression levels of inducible nitric oxide synthase （iNOS）， cluster of differentiation 86 （CD86） ，arginase 1 （Arg-1） ，and mannose receptor （CD206） in gastric mucosal tissues were detected by real- time quantitative polymerase chain reaction （RT-qPCR） . Protein expression levels of nuclear factor κB （NF-κB） pathway-related proteins were determined by Western Blot. Results Compared with the normal group，the model group exhibited disorganized gastric mucosal epithelium，reduced glandular structures in the lamina propria， significant inflammatory cell infiltration，and elevated gastric mucosal histopathology scores. TNF-α，IL-6，and IL-10 levels in gastric mucosal supernatants，iNOS and CD86 mRNA expression，and phosphorylated NF- κB inhibitor α （p-IκBα） and phosphorylated NF-κB p65 subunit （p-p65） protein levels were significantly increased， while Arg-1 and CD206 mRNA expression were significantly decreased， the difference being statistically significant （P＜0.05） . Compared with the model group，medium- and high-dose rutaecarpine treatment reduced inflammatory cell infiltration，restored cellular arrangement，increased glandular structures in the lamina propria， and significantly lowered gastric mucosal histopathology scores，TNF-α，IL-6，and IL-10 levels，iNOS and CD86 mRNA expression，and p-p65 and p-IκBα protein expression were significantly reduced，whereas Arg-1 and CD206 mRNA expression were significantly increased，the difference being statistically significant （P＜ 0.05）， with dose-dependent effects. Conclusion Rutaecarpine ameliorates Hp-induced CAG by modulating macrophage polarization and attenuating inflammatory responses，likely through downregulation of p-p65 and p- IκBα expression and subsequent inhibition of NF-κB pathway activation.

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四川省中医药管理局科学技术研究专项课题 （编号：2020JC0077） ；南充市市校科技战略合作专项 （编号：22SXQT0071）