摘要
目的观察健脾清化中药复方对慢性萎缩性胃炎(CAG)大鼠TLR4及下游My D88依赖途径相关蛋白表达及炎性因子TNF-α的影响,探讨健脾清化中药复方治疗CAG的分子机制。方法将53只Wistar大鼠随机分为空白组8只和CAG造模组45只,以"氨水+去氧胆酸钠+乙醇"法复制CAG大鼠模型。确认造模成功后,将造模组余下40只CAG大鼠随机分为模型组、维酶素组、中药低、中、高剂量组,各8只。各组给予相应药物灌胃,连续30 d。HE染色观察病理组织学改变,Western blot法检测TLR4、My D88、NF-κB、COX-2的蛋白表达量,ELISA法检测血清中TNF-α含量。结果模型组大鼠TLR4、My D88、NF-κB、COX-2蛋白表达水平明显增高(P<0.01),血清TNF-α含量明显增高(P<0.01)。与模型组比较,健脾清化中药复方低、中、高剂量组胃黏膜病变明显改善,TLR4、My D88、NF-κB、COX-2蛋白表达水平均明显下降(P<0.05或P<0.01),血清TNF-α含量降低(P<0.05或P<0.01)。结论健脾清化中药复方可有效改善CAG大鼠胃黏膜组织病理改变,其治疗机制可能与降低组织中TLR4-My D88依赖途径中相关蛋白表达,以及抑制炎症因子的表达有关。
Aim To investigate Jianpi Qinghua Chinese herbal compound（ JQCC） on the expressions of the relevant proteins of TLR4 and its downstream My D88-dependent pathways, and on the inflammatory factor TNF-α in the animal model of chronic atrophic gastritis（ CAG） in rats,so as to discuss the molecular mechanism of JQCC in the treatment of CAG. Methods 53 Wistar rats were randomly divided into the blank control group（ n = 8） and the CAG model group（ n = 45）,and the animal model of CAG in rats was replicated by the ＂ammonia ＋ sodium deoxycholic acid ＋ ethanol ＂method. After the successful modeling was confirmed,the rest of the 40 CAG rats in the CAG model group were divided into the model group,the vitacoenzymetablet group,the low dose of JQCC group,the medium dose of JQCC group,the high dose of JQCC group（ each group n = 8）. The experimental animals of all the groups were given intragastric administration of medication continuously for 30 days. Then the pathological histological changes were observed by HE staining. The protein expressions of TLR4,My D88,NF-КB and COX-2 were tested by Western-blot assay.And the serum TNF-α level was measured by ELISA.Results The protein expressions of TLR4,My D88,NF-КB and COX-2 and the serum TNF-α level in the rats in the model group were increased evidently（ P 0. 01）. Compared with the model group,the gastric mucosa lesions were improved in the low dose of JQCC group,the medium dose of JQCC group,the high dose of JQCC group,together with significant decreases of the protein expressions of TLR4,My D88,NF-κB and COX-2 and the serum TNF-α level（ P 0. 05 or P 0. 01）. Conclusion JQCC could effectively improve the pathological and histological changes in the gastric mucosa in CAG rats,and the therapeutic mechanism might be related to the expressions of the relevant proteins of TLR4-My D88-dependent pathways and the expressions of anti-inflammatory cytokines.
作者
黄铭涵
黄健
陈琴
李思汉
林建龙
钟国栋
黄恒青
林平
HUANG Ming-han HUANG Jian CHEN Qing LI Si-han LIN Jian-long ZHONG Guo-dong HUANG Heng-qing LIN Ping(The Second People＇s Hospital Affiliated to Fujian University of Traditional Chinese Medicine, Fuzhou 350003, China Dept of Gynaecology and Obstetrics, Fujian Medical University Teaching Hospital, Fujian Maternity and Child Health Hospital,Fuzhou 350001 ,China Xiehe Hospital Affiliated to Fujian Medical University, Fuzhou 350001, China Dept of Postgraduates, Fujian University of Traditional Chinese Medicine, Fuzhou 350108 ,China)
出处
《中国药理学通报》
CAS
CSCD
北大核心
2016年第9期1321-1325,共5页
Chinese Pharmacological Bulletin
基金
福建省科技厅重点项目(No 2015Y0023)
福建省自然科学基金项目(No 2015J01403)
福建省卫计委青年科研项目(No 2013-1-10)
福建省卫计委中医科研项目(No wzpw201305)
福建省中青年教师教育科研项目(No JA15247)
