文献类型：期刊文献

中文题名：平胃胶囊调节M2巨噬细胞改善慢性萎缩性胃炎的机制研究

英文题名：Study on the mechanism of Pingwei Capsule(平胃胶囊)in ameliorating chronic atrophic gastritis by regulating M2 macrophages

作者：刘克成[1];王小英[1];刘坦[1];张晶[1,2];毛兰芳[2]

第一作者：刘克成

机构：[1]甘肃中医药大学,甘肃兰州730000;[2]甘肃中医药大学附属医院,甘肃兰州730000

第一机构：甘肃中医药大学

年份：2026

卷号：37

期号：1

起止页码：70

中文期刊名：时珍国医国药

外文期刊名：JOURNAL OF LI-SHIZHEN TRADITIONAL CHINESE MEDICINE

收录：;北大核心:【北大核心2023】；

基金：兰州市科技计划项目(2023-ZD-200,2023-ZD-222);甘肃中医药大学附属医院国家中医脾胃病优势专科2023年专项经费开放基金项目(2023PW-06)。

语种：中文

中文关键词：平胃胶囊;慢性萎缩性胃炎;M2型巨噬细胞;JAK1/STAT6;STAT抑制剂(AS1517499)

外文关键词：Pingwei Capsule(平胃胶囊);Chronic atrophic gastritis;M2 macrophage;JAK1/STAT6;AS1517499

摘要：目的基于Janus激酶1/信号转导与转录激活蛋白6(JAK1/STAT6)信号通路,研究平胃胶囊对M2型巨噬细胞和慢性萎缩性胃炎(CAG)SD大鼠的影响。方法将SD大鼠分为空白组与造模组,造模组通过N-甲基-N`-硝基-N-亚硝酸胍灌胃+饥饱失常建立CAG模型,造模成功后再分为模型组、平胃胶囊组(低、中、高剂量)、平胃胶囊中剂量+AS1517499组,给药4周。HE染色察胃组织病变,ELISA、Western blot、RT-PCR、免疫荧光标记检测相关因子表达水平。结果与空白组相比,模型组大鼠出现胃窦萎缩,固有腺体减少、排列紊乱,固有层炎性细胞浸润;胃组织CD68表达增多,血清白介素4(IL-4)、白介素10(IL-10)含量和胃组织JAK1、STAT6、CD206、Arg-1表达降低。与模型组相比,平胃胶囊各剂量组能不同程度改善胃组织的病理变化,下调胃组织CD68表达水平,升高血清IL-4、IL-10含量,上调胃组织JAK1、STAT6、CD206、Arg-1表达水平。且平胃胶囊中剂量组效果优于联合AS1517499组。结论平胃胶囊可以改善CAG模型大鼠胃组织病理和炎症,机制与激活JAK1/STAT6信号通路诱导巨噬细胞向M2表型转化相关。
Objective To investigate the effects of Pingwei Capsule(平胃胶囊,PWC)on M2 macrophages and SD rats with chronic atrophic gastritis(CAG)based on the Janus kinase 1/signal transducer and activator of transcription 6(JAK1/STAT6)signaling pathway.Methods SD rats were randomly divided into a blank control group and a model group.The CAG model was established in the model establishment group via intragastric administration of N-methyl-N’-nitro-N-nitrosoguanidine(MMNG)combined with irregular feeding(alternating between satiety and hunger).After successful modeling,the model rats were further subdivided into the CAG model subgroup,PWC subgroups(low-/medium-/high-doses),and a medium-dose PWC+AS1517499 subgroup,with continuous drug administration for 4 weeks.Pathological changes in gastric tissues were evaluated using hematoxylin-eosin(HE)staining.Enzymelinked immunosorbent assay(ELISA),Western blot(WB),reverse transcription-polymerase chain reaction(RT-PCR),and immunofluorescence staining were employed to detect the expression levels of related factors.Results Compared with the blank control group,the CAG model subgroup exhibited gastric antral atrophy,reduced and disarranged intrinsic glands,and inflammatory cell infiltration in the lamina propria.CD68 expression in gastric tissues was increased,while serum levels of interleukin-4(IL-4)and interleukin-10(IL-10),and the expression of JAK1,STAT6,CD206,and Arg-1 in gastric tissue were decreased.Compared with the CAG model subgroup,each PWC subgroup showed varying degrees of improvement in gastric tissue,down-regulated CD68 expression in gastric tissues,increased serum IL-4 and IL-10 levels,and up-regulated the expression of JAK1,STAT6,CD206,and Arg-1 in gastric tissues.The medium-dose PWC subgroup exhibited superior efficacy to the medium-dose PWC+AS1517499 subgroup.Conclusion PWC can improve gastric histopathology and inflammation in CAG model rats,and its mechanism is related to the activation of the JAK1/STAT6 signaling pathway and the induction of macrophage polarization towards the M2 phenotype.