To examine the role of glycogen synthase kinase 3 （GSK-3） in the apoptosis of pancreatic β-cells to better understand the pathogenesis and to find new approach to the treatment of type 2 diabetes, apoptosis was induced by oleic acid （OA） in INS-1 cells and the activity of GSK-3 was inhibited by LiCl. The PI staining and flow cytometry were employed for the evaluation of apoptosis. The phosphorylation level of GSK-3 was detected by Western blotting. The results showed that OA at 0.4 mmol/L could cause conspicuous apoptosis of INS- 1 cells and the activity of GSK-3 was significantly increased. After the treatment with 24 mmolFL of LiCl, a inhibitor of GSK-3, the OA-induced apoptosis of INS-1 cells was lessened and the phosphorylation of GSK-3 was increased remarkably. It is concluded that GSK-3 activation plays an important role in OA-induced apoptosis in pancreatic β-cells and inhibition of the GSK-3 activity can effectively protect INS-1 cells from the OA-induced apoptosis. Our study provides a new experimental basis and target for the clinical treatment of type-2 diabetes.
目的观察宫内炎性预敏及生后60％氧暴露对肺增殖性细胞核抗原（PCNA）及肺细胞凋亡影响的动态变化规律及Bcl-2家族中Bax、Bcl-2基因的表达对肺细胞凋亡的调控作用；探讨其与新型支气管肺发育不良（BPD）发病机制之间的关系。方法早产大鼠随机分为生理盐水＋高氧组、脂多糖（LPS）＋高氧组、LPS组和正常对照组，于生后第1、7和14天利用简单随机抽样方法取8只，采用免疫组织化学染色方法检测各组肺组织PCNA表达水平及脱氧核糖核酸转移酶介导的细胞凋亡标记技术（TUNEL）和逆转录聚合酶链反应技术（RT—PCR）检测各组肺组织凋亡和Bax、Bcl-2基因表达水平。结果①PCNA的表达：LPS组和生理盐水＋高氧组在生后第1天表达明显低于对照组（LPS组：0．18±0．01；生理盐水＋高氧组：0．53±0．11；对照组：1．16±0．31；P=0．005，0．021）；LPS＋高氧组在生后第14天明显低于其他3组（对照组：0．89±0．22；LPS组：1．03±0．07；生理盐水＋高氧组：0．96±0．16；LPS＋高氧组：0．47±0．08；P=0．048，0．019，0．030）。②凋亡指数（AI）：LPS组在生后第1天明显高于对照组（17．73±2．21VS7．16±0．31，P=0．021）；生理盐水＋高氧组在生后第7天最高；LPS＋高氧组在生后第14天表达明显高于其他3组（对照组：20．53±4．51；LPS组：13．99±1．69；生理盐水＋高氧组：35．08±4．96；LPS＋高氧组：49．92±7．93；P=0．005，0．002，0．048）。③BaxmRNA的表达：LPS组在生后1d明显高于其他3组（LPS组：0．73±0．06；对照组：0．16±0．03；生理盐水＋高氧组：0．23±0．03；LPS＋高氧组：0．24±0．13；P=0．001，0．002，0．002）；生理盐水＋高氧组在生后第7天表达明显高于对照组（0．58±0．06 vs 0．19±0．05，P=0．002）；LPS＋高氧组在出生后第14天明显高于对照组（0．58±0．01 vs 0．29±0．09，P=
