Role of p38 MAPK activation and mitochondrial cytochrome-c release in allicin-induced apoptosis in SK-N-SH cellsZhuang, Jianhui; Li, Yu; Chi, YufenAnti-Cancer Drugs: April 2016 - Volume 27 - Issue 4 - p 312–317 doi: 10.1097/CAD.0000000000000340 PRECLINICAL REPORTS Buy Abstract Author InformationAuthors Article MetricsMetrics Here, we investigate the apoptotic effect of allicin, the predominant component of freshly crushed garlic, on neuroblastoma cells. In this paper, the authors have first assessed the effect of allicin on human neuroblastoma SK-N-SH cells and then investigated the underlying mechanism. The results indicate that allicin suppresses SK-N-SH cell growth in a dose-dependent and time-dependent manner and that 5 μmol/l of allicin leads to a significant increase in apoptotic rate with annexin-V/PI double staining. Western blot analysis shows that treatment with allicin-induced apoptosis through activation of caspases-3 and 9. Phosphorylation of p38 MAPK contributes to allicin-induced apoptosis upstream of caspase activation. Using p38 MAPK inhibitor, the authors discovered that p38 MAPK activation subsequently induces the release of cytochrome-c from mitochondria into the cytosol. Taken together, the results demonstrate that allicin can activate the p38 MAPK pathway, which leads to mitochondrial release of cytochrome-c, thus inducing SK-N-SH cell apoptosis. Overall, this study suggests that allicin may be used as one of the novel pharmacological treatment strategies in neuroblastoma. Departments of aUrinary Surgery bGynaecology and Obstetrics cPaediatrics, People’s Hospital of Rizhao, Rizhao, Shandong, China Correspondence to Yufen Chi, BSc, Department of Paediatrics, People’s Hospital of Rizhao, Rizhao 276826, Shandong Province, China Tel/fax: +86 633 338 8258; e-mail: email@example.com Received May 27, 2015 Accepted December 21, 2015 Copyright © 2016 Wolters Kluwer Health, Inc. All rights reserved.