Next Article in Journal
Antifungal Activity of Denture Soft Lining Material Modified by Silver Nanoparticles—A Pilot Study
Previous Article in Journal
Epigenetics: New Questions on the Response to Hypoxia
Article Menu

Export Article

Open AccessArticle
Int. J. Mol. Sci. 2011, 12(7), 4722-4734;

Microcystin-LR Induces Apoptosis via NF-κB /iNOS Pathway in INS-1 Cells

Department of Cardiothoracic Surgery, The Affiliated Jiangyin people’s Hospital of Southeast university medical college, No.163 Shoushan Road, Jiangyin 214400, Jiangsu, China
Key Laboratory of Human Functional Genomics of Jiangsu Province, Nanjing Medical University, Nanjing 210029, Jiangsu, China
Author to whom correspondence should be addressed.
Received: 15 June 2011 / Revised: 14 July 2011 / Accepted: 18 July 2011 / Published: 22 July 2011
(This article belongs to the Section Biochemistry)
Full-Text   |   PDF [825 KB, uploaded 19 June 2014]


Cyanobacterial toxins, especially the microcystins, are found in eutrophied waters throughout the world, and their potential to impact on human and animal health is a cause for concern. Microcystin-LR (MC-LR) is one of the common toxic microcystin congeners and occurs frequently in diverse water systems. Recent work suggested that apoptosis plays a major role in the toxic effects induced by MC-LR in hepatocytes. However, the roles of MC-LR in pancreatic beta cells have not been fully established. The aim of the present study was to assess possible in vitro effects of MC-LR on cell apoptosis in the rat insulinoma cell line, INS-1. Our results demonstrated that MC-LR promoted selectively activation of NF-κB (increasing nuclear p50/p65 translocation) and increased the mRNA and protein levels of induced nitric oxide synthase (iNOS). The chronic treatment with MC-LR stimulated nitric oxide (NO) production derived from iNOS and induced apoptosis in a dose dependent manner in INS-1 cells. Meanwhile, this effect was inhibited by the NF-κB inhibitor PDTC, which reversed the apoptosis induced by MC-LR. Our observations indicate that MC-LR induced cell apoptosis via an iNOS-dependent pathway. A well-known nuclear transcription factor, NF-κB, is activated and mediates intracellular nitric oxide synthesis. We suggest that the apoptosis induced by chronic MC-LR in vivo presents a possible cause of β-cell dysfunction, as a key environmental factor in the development of diabetes mellitus. View Full-Text
Keywords: INS-1; NF-κB, iNOS; Microcystin-LR; apoptosis INS-1; NF-κB, iNOS; Microcystin-LR; apoptosis
This is an open access article distributed under the Creative Commons Attribution License (CC BY 3.0).

Share & Cite This Article

MDPI and ACS Style

Ji, Y.; Lu, G.; Chen, G.; Huang, B.; Zhang, X.; Shen, K.; Wu, S. Microcystin-LR Induces Apoptosis via NF-κB /iNOS Pathway in INS-1 Cells. Int. J. Mol. Sci. 2011, 12, 4722-4734.

Show more citation formats Show less citations formats

Related Articles

Article Metrics

Article Access Statistics



[Return to top]
Int. J. Mol. Sci. EISSN 1422-0067 Published by MDPI AG, Basel, Switzerland RSS E-Mail Table of Contents Alert
Back to Top