n/a
Abstract Title:

Shikonin protects H9C2 cardiomyocytes against hypoxia/reoxygenation injury through activation of PI3K/Akt signaling pathway.

Abstract Source:

Biomed Pharmacother. 2018 May 25 ;104:712-717. Epub 2018 May 25. PMID: 29807220

Abstract Author(s):

Shuang Wang, Yanfang Zhu, Ruixia Qiu

Article Affiliation:

Shuang Wang

Abstract:

Myocardial ischemic/reperfusion (I/R) injury often leads to irreversible myocardial cell death and even heart failure, with limited therapeutic possibilities. In the present study, we evaluated the protective effects of shikonin (SHK) against hypoxia/reoxygenation (H/R)-induced cardiomyocyte damage and explored the underlying mechanisms. H9C2 cardiomyocytes were pretreated with different doses of SHK prior to H/R exposure. We observed that SHK pretreatment significantly increased cell viability, attenuated LDH release, and suppressed cardiomyocyte apoptosis induced by H/R exposure. SHK pretreatment also restored the loss of mitochondrial membrane potential (MMP) and cytochrome c release. In addition, SHK significantly enhanced the phosphorylation of Akt and GSK-3β in H/R-treated H9C2 cells. These protective effects of SHK were partially reversed by LY294002, a specific PI3K/Akt inhibitor. Therefore, our findings suggested that SHK might be a promising agent for myocardial I/R injury, and PI3K/Akt signaling plays a crucial role during this process.

Study Type : In Vitro Study

Print Options


Key Research Topics

This website is for information purposes only. By providing the information contained herein we are not diagnosing, treating, curing, mitigating, or preventing any type of disease or medical condition. Before beginning any type of natural, integrative or conventional treatment regimen, it is advisable to seek the advice of a licensed healthcare professional.

© Copyright 2008-2024 GreenMedInfo.com, Journal Articles copyright of original owners, MeSH copyright NLM.