从JAK1/STAT3信号通路探讨复方胃炎合剂抑制慢性萎缩性胃炎进展的分子机制  

Discussion on Molecular Mechanism of Compound Gastritis Mixture Inhibiting Progress of Chronic Atrophic Gastritis from JAK1/STAT3 Signaling Pathway

作　　者：田琳 黄铭涵[1,2] 李思汉 林平[1,2] 郑榕 施婧瑶[4] TIAN Lin;HUANG Minghan;LI Sihan;LIN Ping;ZHENG Rong;SHI Jingyao(The Second People's Hospital Affiliated to Fujian University of Traditional Chinese Medicine,Fuzhou 350003,Fujian,China;Dominant Subject of Spleen-Stomach Characteristics Fujian University of Traditional Chinese Medicine,Fuzhou 350003,Fujian,China;School of Basic Medicine,Guangzhou University of Traditional Chinese Medicine,Guangzhou 510006,Guangdong,China;Peopled Hospital Affiliated to Fujian University of Traditional Chinese Medicine,Fuzhou 350004,Fujian,China)

机构地区：[1]福建中医药大学附属第二人民医院,福建福州350003 [2]福建中医药大学,福建福州350100 [3]广州中医药大学基础医学院,广东广州510006 [4]福建中医药大学附属人民医院,福建福州350004

出　　处：《实用中医内科杂志》2021年第9期37-40,I0011,共5页Journal of Practical Traditional Chinese Internal Medicine

基　　金：福建省创新项目(2018-CX-47);福建省卫健委中青年骨干人才培养项目(2019-ZQN-79);福建省卫健委青年项目(2018-1-79);福建中医药大学中医脾胃学科开放项目(X2019014-学科)。

摘　　要：目的探讨复方胃炎合剂对慢性萎缩性胃炎(CAG)模型大鼠JAK1/STAT3信号通路及炎性因子释放水平的影响。方法随机将SPF级Wistar大鼠分为空白组、空白+中药组、模型组、维酶素组及复方胃炎合剂低、中、高剂量组,采用"饥饱失常+潮湿环境+高脂高糖饮食"造模方法构建病证结合CAG大鼠模型,采用HE染色观察大鼠胃黏膜病变情况,并运用Real-time PCR、ELISA法检测胃组织中JAK1、STAT3 mRNA及血清中TNF-α、IL-6、IL-8、IL-10的表达量。结果 HE染色提示,与空白组比较,模型组大鼠胃黏膜萎缩、减少,可见肠上皮化生及上皮内瘤变。大鼠胃黏膜组织JAK1、STAT3表达水平明显升高(P<0.01);与模型组比较,中药各治疗组胃黏膜固有腺体萎缩及炎症程度均有明显改善,组织中JAK1、STAT3 mRNA与促炎因子TNF-α、IL-6、IL-8表达水平均有所下降,抗炎因子IL-10表达水平均有所上升(P<0.05或P<0.01)。结论复方胃炎合剂可能通过抑制JAK1/STAT3信号通路,调控炎性细胞TNF-α、IL-6、IL-8、IL-10的转录及释放,从而抑制CAG的进展。Objective To study the effect of compound gastritis mixture on JAK1/STAT3 signaling pathway and inflammatory factor release level in rats with chronic atrophic gastritis. Methods The clean-grade Wistar rats were randomly divided into blank group, blank+traditional Chinese medicine group, model group, vitacoenzyme tablet group and low, medium and high dose groups of Compound Gastritis Mixture. The CAG rats with spleen deficiency and damp-heat syndrome was established by using the method of "hunger and satiety disorder+wet environment+high fat and high sugar diet". HE staining was used to observe the gastric mucosal lesions of rats, and Real-time PCR and ELISA were used to detect gastric tissues. Results HE staining showed that compared with the blank group, the gastric mucosa of the model group was atrophied and decreased, intestinal metaplasia and intraepithelial neoplasia were visible, and the expression levels of JAK1 and STAT3 in gastric mucosa of rats were significantly increased(P<0.01). Compared with those of the model group, the atrophy and inflammation degree of the inherent glands of gastric mucosa in each treatment group were significantly improved, and the expressions of JAK1, STAT3, TNF-α, IL-6 and IL-8 were decreased, while the expressions of IL-10 increased(P<0.05 or P<0.01). Conclusion Compound Gastritis Mixture may regulate the transcription and release of TNF-α, IL-6, IL-8 and IL-10 in inflammatory cells by inhibiting JAK1/STAT3 signaling pathway, and thus inhibiting the progress of CAG.

关 键 词：复方胃炎合剂 慢性萎缩性胃炎 JAK1 STAT3 

分 类 号：R289.1[医药卫生—方剂学]