摘要
目的:观察黄芪建中汤对脾胃虚寒型胃溃疡大鼠血清炎症因子、胃黏膜表皮生长因子受体(EGFR)表达的影响,探究黄芪建中汤改善脾胃虚寒型胃溃疡的作用机制。方法:将60只大鼠随机分为正常组、模型组、奥美拉唑组和黄芪建中汤组。除正常组外,其余组大鼠用耗气破气法结合饥饱失常法以及冰醋酸法建立脾胃虚寒证胃溃疡大鼠模型。模型组继续隔日上午给予致虚药并当日禁食,共持续20 d;奥美拉唑组、黄芪建中汤组大鼠在模型组的基础上每日下午使用相应药物治疗;正常组隔日上午及每日下午蒸馏水灌胃。观察各组大鼠形态改变,HE染色观察大鼠胃黏膜病理学改变,评估胃黏膜损伤指数(UI),ELISA法检测大鼠血清炎症因子水平,分别采用PCR、Western blot检测大鼠胃黏膜EGFR mRNA、蛋白表达。结果:黄芪建中汤组与奥美拉唑组大鼠胃黏膜损伤较模型组明显减轻,均可见轻度水肿,有少量炎性细胞浸润,腺体排布大致规整,未见明显溃疡。与正常组比较,模型组UI评分显著增加(P<0.01);与模型组比较,黄芪建中汤组和奥美拉唑组大鼠UI评分明显降低(均P<0.01)。与正常组比较,模型组大鼠胃黏膜组织EGFR mRNA及蛋白表达显著降低(均P<0.05);与模型组比较,奥美拉唑组、黄芪建中汤组大鼠胃黏膜组织EGFR mRNA及蛋白表达明显升高(均P<0.05);与正常组比较,模型组大鼠血清白介素-1β(IL-1β)、肿瘤坏死因子-α(TNF-α)及白介素-6(IL-6)水平显著升高(均P<0.01);与模型组比较,奥美拉唑组、黄芪建中汤组大鼠血清IL-1β、TNF-α及IL-6表达显著降低(均P<0.01)。结论:黄芪建中治疗脾胃虚寒型胃溃疡可显著改善胃黏膜损伤,其作用机制可能与黄芪建中汤上调EGFR mRNA及蛋白表达、降低炎症因子水平有关。
Objective:To observe the effects of Huangqi Jianzhong decoction on the expression of serum inflammatory factors and gastric mucosa epidermal growth factor receptor(EGFR)in rats with gastric ulcer of spleen-stomach deficiency cold syndrome,and explore the mechanism of Huangqi Jianzhong decoction in improving spleen-stomach deficiency cold syndrome gastric ulcer.Methods:60 rats were randomly divided into normal group,model group,omeprazole group and Huangqi Jianzhong decoction group.Except the normal control group,the model of gastric ulcer of spleen-stomach deficiency cold syndrome was established in rats,the rat model of spleen-stomach deficiency cold was established by the method of consuming qi and breaking qi,and glacial acetic acid method.The rats in the model group continued to be given asthenia-inducing drugs in the morning every other day and fasted the same day,then resumed eating the next day for 20 days.Based on the model group,the rats in omeprazole group and Huangqi Jianzhong decoction group were treated with corresponding therapeutic drugs every afternoon.The normal group was intragastric with distilled water every other morning and every afternoon.Morphological changes of rats in each group were observed,pathological changes of gastric mucosa were observed by HE staining,and gastric mucosal damage ulcer index(UI)was evaluated.Serum inflammatory factors of rats were detected by ELISA,EGFR mRNA and protein expressions were detected by PCR and Western blot,respectively.Results:Compared with the model group,the gastric mucosa damage in the Huangqi Jianzhong decoction group and omeprazole group was significantly reduced,with mild edema,a small amount of inflammatory cell infiltration,gland arrangement roughly organized,and no obvious ulcers.Compared with normal group,UI score of model group was significantly increased(P<0.01).Compared with model group,UI scores in Huangqi Jianzhong decoction group and omeprazole group were significantly decreased(all P<0.01).Compared with normal group,EGFR mRNA and protein expressions in gastric mucosa of rats in model group were significantly decreased(all P<0.05).Compared with model group,EGFR mRNA and protein expression in gastric mucosa of omeprazole group and Huangqi Jianzhong decoction group were significantly increased(all P<0.05).Compared with normal group,serum levels of IL-1β,TNF-αand IL-6 in model group were significantly increased(all P<0.01).Compared with model group,serum expressions of IL-1β,TNF-αand IL-6 in omeprazole group and Huangqi Jianzhong decoction group were significantly decreased(all P<0.01).Conclusion:Huangqi Jianzhong decoction in the treatment of spleen-stomach deficiency cold syndrome gastric ulcer can significantly improve the damage of gastric mucosa,the mechanism of which may be related to the increase of EGFR mRNA and protein expression and the decrease of inflammatory factors.
作者
陈思清
周赛男
韩运宗
刘琴
周姝
CHEN Siqing;ZHOU Sainan;HAN Yunzong;LIU Qin;ZHOU Shu(Hunan University of Traditional Chinese Medicine,Changsha 410007,China)
出处
《陕西中医》
CAS
2023年第8期1032-1036,共5页
Shaanxi Journal of Traditional Chinese Medicine
基金
湖南省自然科学基金资助项目(2022JJ70031)
湖南省中医药科研计划重点项目(2021203)
湖南中医药大学中医学国内一流建设学科项目(2018ZYX13,4901-020000200205)。
关键词
胃溃疡
黄芪建中汤
脾胃虚寒证
表皮生长因子受体
炎症因子
大鼠
Gastric ulcer
Huangqi Jianzhong decoction
Spleen-stomach deficiency cold syndrome
Epithelial growth factor receptor
Inflammatory factors
Rats