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红白兰参提取物通过调节AMPK通路减轻CoCl诱导的H9C2细胞凋亡。

Hong-Bai-Lan-Shen Extract Alleviates the CoCl-Induced Apoptosis in H9C2 Cells by Regulating the AMPK Pathway.

作者信息

Ding Jinxue, Meng Jinwu, Wang Wenjia, Gu Bolin, Hu Mengxin, Liu Jiaguo

机构信息

College of Animal Science, Anhui Science and Technology University, Chuzhou 233100, China.

Institute of Traditional Chinese Veterinary Medicine, College of Veterinary Medicine, Nanjing Agricultural University, Nanjing 210095, China.

出版信息

Vet Sci. 2025 Mar 13;12(3):267. doi: 10.3390/vetsci12030267.

Abstract

This study aims to explore the protective effects of Hong-bai-lan-shen (HBLS) extract, a traditional Chinese medicine compound, on myocardial injury based on metabolomics. H9C2 cells were cultured with HBLS extract for 12 h, and then the cells were cultured in a CoCl-containing medium, a model simulating the ischemic-hypoxic damage in myocardial cells, for an additional 12 h. The cell viability, cytotoxicity, intracellular metabolite and reactive oxygen species (ROS), mitochondrial membrane potential, apoptosis, and adenosine monophosphate-activated protein kinase (AMPK) signal pathway were determined. The results showed that HBLS extract significantly increased cell viability, stabilized cell morphology, reduced lactate dehydrogenase (LDH) release and ROS production, blocked cysteine-aspartic acid protease 3 (caspase-3) and bcl-2-associated X protein (Bax) expression and decreased apoptotic cell numbers. Meanwhile, HBLS increased membrane potential and the expression of B-cell lymphoma-2 (Bcl-2). Additionally, HBLS extract upregulated the expression of AMPK, PI3K, and protein kinase B (AKT) ( < 0.05, < 0.01). These findings suggest that HBLS extract has a protective effect on myocardial cells by regulating the AMPK signal pathway and may be a promising therapeutic candidate for ischemic heart disease.

摘要

本研究旨在基于代谢组学探讨中药复方红百兰参(HBLS)提取物对心肌损伤的保护作用。将H9C2细胞用HBLS提取物培养12小时,然后将细胞在含氯化钴的培养基中培养12小时,该培养基模拟心肌细胞的缺血缺氧损伤。测定细胞活力、细胞毒性、细胞内代谢物和活性氧(ROS)、线粒体膜电位、细胞凋亡以及腺苷酸活化蛋白激酶(AMPK)信号通路。结果表明,HBLS提取物显著提高细胞活力,稳定细胞形态,减少乳酸脱氢酶(LDH)释放和ROS产生,阻断半胱氨酸天冬氨酸蛋白酶3(caspase-3)和bcl-2相关X蛋白(Bax)表达并减少凋亡细胞数量。同时,HBLS增加膜电位和B细胞淋巴瘤-2(Bcl-2)的表达。此外,HBLS提取物上调AMPK、磷脂酰肌醇-3激酶(PI3K)和蛋白激酶B(AKT)的表达(<0.05,<0.01)。这些发现表明,HBLS提取物通过调节AMPK信号通路对心肌细胞具有保护作用,可能是缺血性心脏病的一种有前景的治疗候选药物。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/21bb/11946019/5fdb599e0f44/vetsci-12-00267-g001.jpg

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