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香砂六君子汤对萎缩性胃炎大鼠IL-6、IL-17及ERK1/2基因蛋白表达的影响     被引量:3

Influence of Xiangsha Liujunzi Decoction on the Expressions of IL-6,IL-17 and ERK1/2 Gene Protein in CAG Rats

文献类型:期刊文献

中文题名:香砂六君子汤对萎缩性胃炎大鼠IL-6、IL-17及ERK1/2基因蛋白表达的影响

英文题名:Influence of Xiangsha Liujunzi Decoction on the Expressions of IL-6,IL-17 and ERK1/2 Gene Protein in CAG Rats

作者:王强[1];张晓鹏[1];周语平[1];成映霞[2,3];杨亚楠[4];王庆胜[1];鲁鹏程[1];段云燕[3];段永强[2,3];杜娟[3]

第一作者:王强

机构:[1]甘肃中医药大学,甘肃兰州730000;[2]甘肃省中药药理与毒理学重点实验室;[3]甘肃省中医方药挖掘与创新转化重点实验室;[4]西安交通大学医学部

第一机构:甘肃中医药大学

年份:2020

卷号:33

期号:7

起止页码:16

中文期刊名:西部中医药

外文期刊名:Western Journal of Traditional Chinese Medicine

收录:CSTPCD

基金:国家自然科学基金(81260519);甘肃省中医药管理局基金项目(GZK-2014-73);甘肃省中医方药挖掘与创新转化重点实验室开放基金项目(2016-GZY-04)。

语种:中文

中文关键词:慢性萎缩性胃炎;白细胞介素6;白细胞介素17;细胞外调节蛋白激酶1/2;香砂六君子汤;大鼠

外文关键词:CAG;IL-6;IL-17;ERK1/2;Xiangsha Liujunzi decoction;rats

摘要:目的:观察香砂六君子汤对脾胃虚弱型慢性萎缩性胃炎(chronic atrophic gastritis,CAG)大鼠血清白细胞介素6(interleukin-6,IL-6)、白细胞介素17(interleukin-17,IL-17)及胃组织细胞外调节蛋白激酶1/2(extracellular regulated protein kinases,ERK1/2)基因和蛋白表达的影响。方法:按随机数字表法将受试大鼠分为空白组和造模组,通过综合法成功复制CAG模型大鼠后,把造模成功大鼠随机分为5组,即:模型组、阳性对照组和香砂六君子汤高、中、低剂量组。香砂六君子汤高、中、低剂量组分别灌胃24、12、6 g/(kg·d)剂量香砂六君子汤,模型组和空白组灌胃10 mL/kg蒸馏水,阳性对照组灌胃0.30 g/(kg·d)维酶素,连续造模120天后,采用ELISA法检测大鼠血清IL-6、IL-17含量;采取实时荧光定量PCR检测胃窦黏膜组织IL-6、IL-17基因表达水平;Western Blot技术检测ERK1/2蛋白及其磷酸化表达。结果:与空白组比较,模型组大鼠一般生存状况较差,且大鼠血清IL-6含量及胃窦黏膜组织IL-6 mRNA表达升高(P<0.05);血清IL-17含量及胃窦黏膜组织IL-17 mRNA表达升高(P<0.01),胃黏膜组织ERK1/2蛋白表达降低(P<0.01),p-ERK1/2蛋白表达升高(P<0.05);与模型组比较,香砂六君子汤各剂量组大鼠一般生存状况改善,大鼠血清IL-6、IL-17含量及胃窦黏膜组织IL-6 mRNA及IL-17 mRNA表达降低(P<0.05),ERK1/2蛋白表达升高(P<0.05);p-ERK1/2蛋白表达降低(P<0.05);与阳性对照组比较,香砂六君子汤高、中剂量组大鼠血清IL-6、IL-17含量及胃窦黏膜组织IL-6 mRNA及IL-17 mRNA表达降低(P<0.05),ERK1/2蛋白表达升高(P<0.05);p-ERK1/2蛋白表达降低(P<0.05)。结论:香砂六君子汤通过下调IL-6、IL-17表达,激活ERK1/2,抑制p-ERK1/2水平,对脾胃虚弱型CAG胃窦黏膜起保护作用。
Objective: To observe the effects of Xiangsha Liujunzi decoction(XSLJZ) on the expressions of IL-6, IL-7 and ERK1/2 gene and protein in the rats with chronic atrophic gastritis(CAG). Methods: All the rats were divided into the blank group and the modelling group by random number table method, after replicating CAG rat models successfully with comprehensive method, the rat models were randomized into five groups: the model group,high, moderate and low dose groups of XSLJZ and positive control group. High, moderate and low dose groups were drenched with 24, 12 and 6 g/(kg·d) of XSLJZ respectively, the model group and the blank group with 10 mL/kg of distilled water, positive control group with 0.30 g/(kg·d) of vatacoenayme, after modeling for 120 days consecutively,ELISA method was adopted to detect the contents of IL-6 and IL-17 in the serum of the rats;real-time fluorescent quantitative PCR to detect the expressions of IL-6 and IL-17 in antral gastric mucosa;Western blot technique to detect the expression of ERK1/2 protein and its phosphorylation. Results: Compared with the blank group, general living conditions of the rats in the model group were poorer, the contents of IL-6 and the expressions of IL-6 mRNA in antral gastric mucosa of the rats rose(P<0.05);the contents of IL-17 and the expressions of IL-17 mRNA in antral gastric mucosa of the rats rose(P<0.01), the expressions of ERK1/2 protein in gastric mucosa tissue reduced(P<0.01),the expressions of p-ERK1/2 protein rose(P<0.05);compared with the model group, general living conditions of rats in different dose groups of XSLJZ improved, the contents of IL-6 and IL-17, the expressions of IL-6 mRNA and IL-17 mRNA in gastric mucosa tissue reduced(P <0.05), the expressions of ERK1/2 protein rose(P <0.05),p-ERK1/2 protein expressions reduced(P<0.05). Compared with positive control group, the contents of IL-6 and IL-17 in the serum, the expressions of IL-6 mRNA and IL-17 mRNA in gastric mucosa tissue reduced(P<0.05), the expressions of ERK1/2 protein rose(P <0.05), p-ERK1/2 protein expressions reduced(P <0.05) in high and moderate doses groups of XSLJZ(P <0.05). Conclusion: XSLJZ could protect gastric antrum mucosa in CAG of spleen and stomach weakness pattern through downregulating the expressions of IL-6 and IL-17, activating ERK1/2 and inhibiting the levels of p-ERK1/2.

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