β，β-Dimethylacrylshikonin induces mitochondria- dependent apoptosis of human lung adenocarcinoma cells in vitro via p38 pathway activation

• Published in: Acta pharmacologica Sinica Vol. 36; no. 1; pp. 131 - 138
• Main Authors: Wang, Hai-bing, Ma, Xiao-qiong
• Format: Journal Article
• Language: English
• Published: London Nature Publishing Group UK 01.01.2015; Nature Publishing Group
• Subjects: adenocarcinoma; Adenocarcinoma - drug therapy; Adenocarcinoma - metabolism; Adenocarcinoma of Lung; agent; anti-cancer; apoptosis; Apoptosis - drug effects; Biomedical and Life Sciences; Biomedicine; Cell Line, Tumor; Humans; Immunology; Internal Medicine; lung; Lung Neoplasms - drug therapy; Lung Neoplasms - metabolism; MAP Kinase Signaling System - drug effects; Medical Microbiology; mitochondria; Mitochondria - drug effects; Mitochondria - metabolism; Naphthoquinones - pharmacology; Original; original-article; p38; Pharmacology/Toxicology; shikonin; Signal Transduction - drug effects; Vaccine; Z-VAD-FMK;SB203580; β-dimethylacrylshikonin; p38; anti-cancer agent; mitochondria; lung adenocarcinoma; Z-VAD-FMK; apoptosis; β, β-dimethylacrylshikonin; SB203580; shikonin
• ISSN: 1671-4083; 1745-7254
• DOI: 10.1038/aps.2014.108

Aim： β, β-Dimethylacrylshikonin （DMAS） is an anticancer compound extracted from the roots of Lithospermum erythrorhizon. In the present study, we investigated the effects of DMAS on human lung adenocarcinoma cells in vitro and explored the mechanisms of its anti-cancer action. Methods： Human lung adenocarcinoma A549 cells were tested. Cell viability was assessed using an MTT assay, and cell apoptosis was evaluated with flow cytometry and DAPI staining. The expression of the related proteins was detected using Western blotting. The mitochondrial membrane potential was measured using a JC-1 kit, and subcellular distribution of cytochrome c was analyzed using immunofluorescence staining.