Jiang Ling, Tian Cai-Bo, Ye Rui-Han, Shi Nian, He Xing-Chao, Zhao Yun-Li, Luo Xiao-Dong
Yunnan Characteristic Plant Extraction Laboratory, Key Laboratory of Medicinal Chemistry for Natural Resource, Ministry of Education, Yunnan Key Laboratory of Research and Development for Natural Products, School of Pharmacy, School of Chemical Science and Technology, Yunnan University, Kunming 650091, PR China.
Yunnan Characteristic Plant Extraction Laboratory, Key Laboratory of Medicinal Chemistry for Natural Resource, Ministry of Education, Yunnan Key Laboratory of Research and Development for Natural Products, School of Pharmacy, School of Chemical Science and Technology, Yunnan University, Kunming 650091, PR China.
Fitoterapia. 2025 Jan;180:106297. doi: 10.1016/j.fitote.2024.106297. Epub 2024 Nov 17.
Drug-induced liver injury caused acute hepatic failure and hepatitis frequently. In this investigation, kakuol and asarinin reduced the levels of serum alanine transaminase (ALT), aspartate transaminase (AST) and malondialdehyde (MDA) dramatically, and ameliorated the pathological damage of liver tissues in APAP-induced mice. Furthermore, both compounds increased the viabilities of APAP-induced L-O2 cells and extracellular glutathione (GSH) levels accompanied significantly by reducing the level of intracellular ROS in vitro. In addition, HSP90AA1/CDK2/mTOR signaling pathway and five target proteins (CDK2, HSP90AA1, HRAS, MMP1, mTOR) were proposed from network pharmacology and molecular docking prediction, and then the up-regulation of protein expression of CDK2, mTOR and down-regulation of HSP90AA1, HRAS, MMP1 by kakuol and asarinin in western blotting supported their mechanism.
药物性肝损伤常导致急性肝衰竭和肝炎。在本研究中,细辛脑和细辛脂素显著降低了对乙酰氨基酚(APAP)诱导的小鼠血清丙氨酸转氨酶(ALT)、天冬氨酸转氨酶(AST)和丙二醛(MDA)水平,并改善了肝组织的病理损伤。此外,在体外,这两种化合物均提高了APAP诱导的L-O2细胞的活力以及细胞外谷胱甘肽(GSH)水平,同时显著降低了细胞内活性氧(ROS)水平。另外,通过网络药理学和分子对接预测提出了热休克蛋白90α家族成员1(HSP90AA1)/细胞周期蛋白依赖性激酶2(CDK2)/雷帕霉素靶蛋白(mTOR)信号通路及五个靶蛋白(CDK2、HSP90AA1、哈-柔二氏肉瘤病毒癌基因同源物(HRAS)、基质金属蛋白酶1(MMP1)、mTOR),随后蛋白质印迹法显示细辛脑和细辛脂素上调CDK2、mTOR蛋白表达,下调HSP90AA1、HRAS、MMP1蛋白表达,这支持了它们的作用机制。