详细记录  
题名:Testosterone protects against glucotoxicity induced apoptosis of pancreatic beta-cells (INS-1) and male mouse pancreatic islets.
作者:HANCHANG W; SEMPRASERT N; LIMJINDAPORN T; YENCHITSOMANUS PT; KOOPTIWUT S;
来源:Endocrinology. 2013 Aug 22. [ IF= 4.72 ] ]
URL :10.1210/en.2013-1351
日期:20130902
摘要:Male hypogonadism associates with type 2 diabetes (T2D) and testosterone can
protect pancreatic beta-cells from glucotoxicity. However, the protective
mechanism is still unclear. This study thus aims to examine the anti-apoptotic
mechanism of testosterone in pancreatic beta cells cultured in high-glucose
medium. Testosterone (0.0005-2 mug/ml) was added to INS-1 cells cultured in basal
glucose or high-glucose media. Then, cellular apoptosis, oxidative stress, and
cell viability were measured. ER stress markers and sensors and the
anti-apoptotic protein (Bcl2) were investigated by real time PCR and Western blot
analysis. ER stress markers were also measured in male mouse pancreatic islet
cultured in similar conditions. Testosterone (0.05 and 0.5mug/ml) did not have
any effect on apoptosis and viability of INS-1 cells cultured in basal glucose
medium, but it could reduce apoptosis and increase viability of INS-1 cells
cultured in high-glucose medium. The protective effect of testosterone is
diminished by androgen receptor inhibitor. Testosterone (0.05 mug/ml) could
significantly reduce nitrotyrosine levels, mRNA, and protein levels of ER stress
markers and sensors those were induced, when INS-1 cells were cultured in
high-glucose medium. It could also significantly increase the survival proteins,
sarco/endoplasmic reticulum Ca2+ ATPase (SERCA-2) and Bcl2, in INS-1 cells
cultured in the same conditions. Similarly, it could reduce ER stress markers and
increase SERCA protein levels in male mouse pancreatic islets cultured in high
glucose medium. Testosterone can protect against male pancreatic beta-cell
apoptosis from glucotoxicity via reduction of both oxidative stress and ER
stresses.

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