PMID: 20650758Jul 24, 2010Paper

Glitazones protects beta cell function from cytotoxic cytokines through PPAR gamma-dependent mechanisms

Nan fang yi ke da xue xue bao = Journal of Southern Medical University
Xia LiZhi-guang Zhou

Abstract

To investigate the protective effects of glitazones on islet beta cells and PPAR gamma dependence of such effects. IL-1beta and IFN-gamma were used to treat NIT-1 cells, a beta cell line, to induce beta cell damage. The cells were pretreated with rosiglitazone and pioglitazone at different concentrations to study the protective effects of these drugs. The cell apoptosis rate was determined with Annexin V-FITC by flow cytometry, and the insulin secretion capacity of the cells was assessed with ELISA. GW9662 and PPARgamma-SiRNA were used to specifically inhibit PPAR to investigate the PPAR gamma-dependent mechanisms. Rosiglitazone and pioglitazone at 10 micromol/L could significantly decrease the apoptosis of beta cells induced by the cytokines (apoptotic rates of 13.99% and 16.67% vs 51.33%, P<0.01). Rosiglitazone at 10 micromol/L and pioglitazone at 20 micromol/L were less effective than 10 micromol/L rosiglitazone and pioglitazone. The insulin secretion of the cytokine-treated cells decreased from 8.5-/+0.6 ng/ml of the control group to 3.6-/+0.5 ng/ml, while rosiglitazone and pioglitazone could increase the insulin secretion to 6.8-/+0.7 ng/ml and 5.9-/+0.9 ng/ml, respectively. When PPAR gamma was specifically inhibited by GW...Continue Reading

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Apoptosis

Apoptosis is a specific process that leads to programmed cell death through the activation of an evolutionary conserved intracellular pathway leading to pathognomic cellular changes distinct from cellular necrosis

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