Regulatory Effect of Prdx V on Streptozotocin-Induced Apoptosis in MIN6 Cells

Abstract: Peroxiredoxin V (Prdx V) is a thioredoxin peroxidase involved in peroxiredoxins family， which can effectively protect cells against oxidative damage caused by oxidative stress. This study is aimed to explore the molecular mechanism of STZ-induced apoptosis in MIN6 cells and the regulatory function of Prdx V during the process. We used the MTT assay， fluorescence microscopy， flow cytometry and Western blot assay for analyzing the cell viability， the cellular ROS levels， nitric oxide production and apoptosis-related-proteinslevels in STZ-treated MIN6 cells， respectively. The results showed that the STZ-induced MIN6 cell apoptosis was mainly resulted in NO production regulated by p38 signaling pathway， and the Prdx V protein levels were also increased during the process. Furthermore， knockdown the Prdx V gene expressions with Lenti-virus， resulted in decrease of the cell viability and increasing the cell apoptosis in STZ-treated MIN6 cells. Our findings provide a theoretical basis for the study of the mechanism of oxidative stress caused islet cell damage and death. Keywords

CSTR: 32200.14.cjcb.2018.02.0006