目的 探讨柴芍和胃颗粒对大鼠免疫性胃炎的保护作用及其机制。方法 以弗氏完全佐剂制备免疫性胃炎大鼠模型。将模型大鼠随机分为模型组，三九胃泰颗粒阳性对照组，柴芍和胃颗粒（0.8、1.6、3.2 g/kg剂量）组，另设对照组；于开始造模后第28天ig给药，连续给药28 d。在造模不同时间称大鼠体质量，给药结束后检测大鼠血清中NO、白细胞介素-2（IL-2）水平，胃组织匀浆谷胱甘肽过氧化物酶（GSH-Px）活性、丙二醛（MDA）水平，观察胃组织病理学改变。结果 与模型组相比，柴芍和胃颗粒低、中、高剂量组大鼠血清NO水平分别降低20.53%、63.95%、69.85%；使大鼠胃黏膜组织匀浆中GSH-Px的活性分别增加16.11%、16.11%、30.33%，MDA水平分别降低5.37%、25.4%、34.69%；使大鼠血清IL-2水平有增加的趋势，以高剂量组作用明显，但与模型组相比差异不显著。病理组织学观察可见，模型组大鼠胃黏膜的固有层内出现结缔组织增生及淋巴小结增多，黏膜肌层增厚，平滑肌纤维走向紊乱，炎性细胞浸润严重；柴芍和胃颗粒低、中、高剂量组大鼠黏膜层增生及其炎性浸润均有不同程度的减轻和恢复。结论 柴芍和胃颗粒对大鼠胃黏膜损伤具有一定的保护作用，其机制可能与其增强抗氧化酶活性、减轻自由基损伤和抑制脂质过氧化物反应有关。

Objective To investigate the protection and mechanism of Chaishao Hewei Granule (CHG) on autoimmune gastritis in rats. Methods The model of autoimmune gastritis of rats was established by Freund’s complete adjuvant. The rats were randomly divided into control, model, Sanjiu Weitai Granule (positive control), low-, mid-, and high-dose (0.8, 1.6, and 3.2 g/kg) CHG groups. After the day 28 of modeling, the rats were ig administered for continuous 28 d. The body weight of rats was measured at different time points of modeling. After the last administration, the contents of nitric oxide (NO) and interleukin-2 (IL-2) in serum and glutathione peroxidase (GSH-Px) and maleic dialdehyde (MDA) in gastric homogenate were determined, and the changes of gastric histopathology were observed. Results Compared with the model group, the low-, mid-, and high-dose CHG could decrease the contents of NO in rats by 20.53%, 63.95%, and 69.85%, respectively, increase the activities of GSH-Px in gastric homogenate by 16.11%, 16.11%, and 30.33%, respectively, and decrease the levels of MDA in gastric homogenate by 5.37%, 25.4%, and 34.69% obviously. CHG could make the level of IL-2 increase, more obviously in the high-dose CHG group, but there was no significant difference compared with the model group. Gastric mucosal histopathology showed desmoplasia and lymphoid nodules in mucosal lamina propria of rats in the model group; The muscularis mucosa was thicken, the smooth muscle fibers were disordered, and the infiltration of inflammatory cells was severe. In CHG treatment groups in various doses, there were varying degrees of restoration and mitigation in inflammatory infiltration. Conclusion CHG has protective action on gastric mucosal damage and the mechanism may be related to increasing the activity of anti-oxidase, scavenging free radicles, and inhibiting the lipid peroxidation.