n/a
Article Publish Status: FREE
Abstract Title:

Shikonin attenuates HO-induced oxidative injury in HT29 cells via antioxidant activities and the inhibition of mitochondrial pathway-mediated apoptosis.

Abstract Source:

Exp Ther Med. 2021 Oct ;22(4):1118. Epub 2021 Aug 4. PMID: 34504572

Abstract Author(s):

Yu Zhong, Ao Qi, Lulu Liu, Qionglin Huang, Junjie Zhang, Kangrong Cai, Chun Cai

Article Affiliation:

Yu Zhong

Abstract:

Shikonin, a natural naphthoquinone extracted from the roots of, possesses multiple pharmacological properties, including antioxidant, anti-inflammatory and antitumor effects. It has been hypothesized that the properties of shikonin are associated with its oxygen free radical scavenging abilities. However, the mechanism underlying the antioxidant activity of shikonin is not completely understood. The aim of the present study was to investigate the effect of shikonin against HO-induced oxidative injury in HT29 cells and to explore the underlying molecular mechanism. The concentration and duration of HOtreatment to cause maximal damage, and the effects of shikonin (2.5, 5 or 10µg/ml) on the activity of HO-induced HT29 cells were determined by MTT assay. The apoptotic rate in HT29 cells was determined by annexin V/propidium iodide staining. HT29 cell cycle alteration was also analyzed by propidium iodide staining. Reactive oxygen species (ROS) production was assessed by monitoring 2',7'-dichlorofluorescin in diacetate fluorescence. Mitochondrial membrane potentials were determined by JC-1 staining. The activities of malondialdehyde, superoxide dismutase, caspase-9 and caspase-3 were measured using spectrophotometric assays. The expression levels of Bcl-2, Bax and cytochromewere determined by western blotting. The results suggested that shikonin increased cell viability, reduced cell apoptosis and increased the proliferation index in HO-treated HT29 cells. Shikonin also significantly inhibited increases in intracellular reactive oxygen species (ROS), restored the mitochondrial membrane potential, prevented the release of lactic dehydrogenase and decreased the levels of superoxide dismutase and malondialdehyde in HO-induced HT29 cells. Furthermore, shikonin significantly decreased caspase-9 and caspase-3 activities, increased Bcl-2 expression and decreased Bax and cytochromeexpression levels in HO-induced HT29 cells. The results indicated that shikonin protected against HO-induced oxidative injury by removing ROS, ameliorating mitochondrial dysfunction, attenuating DNA oxidative damage and inhibiting mitochondrial pathway-mediated apoptosis.

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.