首页分享杨桃根DMDD调控JNK/P38MAPK通路抑制2型糖尿病合并非酒精性脂肪肝小鼠肝脏内质网应激

杨桃根DMDD调控JNK/P38MAPK通路抑制2型糖尿病合并非酒精性脂肪肝小鼠肝脏内质网应激

来源：花匠小妙招时间：2026-02-15 08:39

谢静晓, 王誉湘, 张晓萍, 陈秋燕, 王璐, 庞川皓, 李吉星, 陈林倩, 黄仁彬, 韦晓洁. 杨桃根DMDD调控JNK/P38MAPK通路抑制2型糖尿病合并非酒精性脂肪肝小鼠肝脏内质网应激[J]. 广西医科大学学报, 2023, 40(5): 786-791. DOI: 10.16190/j.cnki.45-1211/r.2023.05.011

引用本文: 谢静晓, 王誉湘, 张晓萍, 陈秋燕, 王璐, 庞川皓, 李吉星, 陈林倩, 黄仁彬, 韦晓洁. 杨桃根DMDD调控JNK/P38MAPK通路抑制2型糖尿病合并非酒精性脂肪肝小鼠肝脏内质网应激[J]. 广西医科大学学报, 2023, 40(5): 786-791. DOI: 10.16190/j.cnki.45-1211/r.2023.05.011

Xie Jingxiao, Wang Yuxiang, Zhang Xiaoping, Cheng Qiuyan, Wang lu, Pang Chuanhao, Li Jixing, Chen Lin-qian, Huang Renbin, Wei Xiaojie. DMDD isolated from the root of Averrhoa carambola L.regulating the JNK/P38MAPK path⁃way to inhibit hepatic endoplasmic reticulum stress in mice with type 2 diabetes mellitus com⁃bined with non-alcoholic fatty liver disease[J]. Journal of Guangxi Medical University, 2023, 40(5): 786-791. DOI: 10.16190/j.cnki.45-1211/r.2023.05.011

Citation: Xie Jingxiao, Wang Yuxiang, Zhang Xiaoping, Cheng Qiuyan, Wang lu, Pang Chuanhao, Li Jixing, Chen Lin-qian, Huang Renbin, Wei Xiaojie. DMDD isolated from the root of Averrhoa carambola L.regulating the JNK/P38MAPK path⁃way to inhibit hepatic endoplasmic reticulum stress in mice with type 2 diabetes mellitus com⁃bined with non-alcoholic fatty liver disease[J]. Journal of Guangxi Medical University, 2023, 40(5): 786-791. DOI: 10.16190/j.cnki.45-1211/r.2023.05.011

谢静晓1, 王誉湘1, 张晓萍1, 陈秋燕1, 王璐1, 庞川皓1, 李吉星1, 陈林倩1, 黄仁彬1, , , 韦晓洁2, ,

1. 广西医科大学药学院, 南宁 530021;

2. 广西中医药大学基础医学院, 南宁 530200

详细信息

通讯作者:

黄仁彬,E-mail:huangrenbin518@163.com

韦晓洁,E-mail:116190888@qq.com

中图分类号: R285.5

计量文章访问数: 0 HTML全文浏览量: 0 PDF下载量: 0 出版历程收稿日期: 2023-03-08 网络出版日期: 2024-01-31 刊出日期: 2023-05-01

DMDD isolated from the root of Averrhoa carambola L.regulating the JNK/P38MAPK path⁃way to inhibit hepatic endoplasmic reticulum stress in mice with type 2 diabetes mellitus com⁃bined with non-alcoholic fatty liver disease

Xie Jingxiao1, Wang Yuxiang1, Zhang Xiaoping1, Cheng Qiuyan1, Wang lu1, Pang Chuanhao1, Li Jixing1, Chen Lin-qian1, Huang Renbin1, , , Wei Xiaojie2, ,

1. Pharmaceutical College, Guangxi Medical University, Nanning 530021, China;

2. School of Basic Medicine, Guangxi University of Chinese Medicine, Nanning 530200, China

摘要

摘要目的：探讨杨桃根2-十二烷基-6-甲氧基-2, 5-二烯-1, 4-环己二酮（DMDD）通过调控JNK/P38MAPK 抑制2 型糖尿病（T2DM）合并非酒精性脂肪肝（NAFLD）小鼠内质网应激的机制。方法：将C57BL/6J小鼠分为正常组、模型组、4-苯基丁酸（4-PBA）组、衣霉素（TM）组及DMDD高、中、低剂量组（DMDDH组、DMDDM组、DMDDL组）。连续予高脂饲料喂养4周后，再一次性腹腔注射链脲佐菌素（STZ）建立T2DM 合并NAFLD 小鼠模型。连续给药8周后检测小鼠空腹血糖水平及肝组织丙氨酸氨基转移酶（ALT）、谷草转氨酶（AST）和血脂水平。采用苏木精—伊红（HE）染色、油红O 染色观察肝组织病理学改变，western blotting 法检测肝组织grp78、Chop、JNK、磷酸化（P）-JNK、P38MAPK、P-P38MAPK、Bcl-2 和Bax 蛋白表达。结果：与模型组相比，DMDD 各剂量组空腹血糖、ALT、AST、总胆固醇（TC）、甘油三酯（TG）、低密度脂蛋白胆固醇（LDL-C）水平降低，高密度脂蛋白胆固醇（HDL-C）水平增高（P< 0.05），肝组织病理损伤减轻，grp78、Chop、P-JNK、Bax 和P-P38MAPK 蛋白表达水平降低，Bcl-2 蛋白表达水平升高（均P< 0.05）。结论：杨桃根DMDD 可能通过抑制JNK/P38MAPK 通路减轻T2DM 合并NAFLD 小鼠肝脏内质网应激及肝细胞损伤和凋亡。

Abstract Objective:To explore the mechanism of 2-dodecyl-6-methoxy-2, 5-diene-1, 4-cyclohexanedione(DMDD) isolated from the root of Averrhoa carambola L.on the inhibition of endoplasmic reticulum stress(ERS) in mice with type 2 diabetes mellitus (T2DM) combined with non-alcoholic fatty liver disease (NAFLD)by regulating the JNK/P38MAPK pathway.Methods:The C57BL/6J mice were divided into normal group, mod-el group, 4-phenyl butyric acid (4-PBA) group, tunicamycin (TM) group, and high-, medium-, and low-dose DMDD groups (DMDDH, DMDDM, DMDDL).Streptozotocin (STZ) was injected intritoneally after 4 weeks of a continuous high-fat diet to establish a T2DM combined with the NAFLD mouse model.The fasting blood glu-cose (FBG) levels, alanine aminotransferase (ALT), aspartate aminotransferase (AST) and blood lipid levels in liver tissue of mice were detected after continuous administration for 8 weeks.The pathological state of the liver was observed by Hematoxylin-eosin (HE) staining and Oil Red O staining, and the expressions of grp78, Chop, JNK, phosphorylated (P)-JNK, P38MAPK, P-P38MAPK, Bcl-2 and Bax proteins in liver tissues were detected by western blotting.Results: Compared with the model group, the levels of FBG, ALT, AST, TC, TG and LDL-C in DMDD groups were reduced, the level of HDL-C increased(P< 0.05), the pathological injury of liver tissue was alleviated, the protein expression levels of grp78, Chop, PJNK, Bax and P-P38MAPK decreased and the expression level of Bcl-2 protein increased(all P< 0.05).Conclusion: DMDD may ameliorate endoplasmic reticulum stress, hepatocyte injury and apoptosis in mice with T2DM combined with NAFLD by inhibiting JNK/P38MAPK pathway.

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