Xu Jing, Wang Hui-fang, Zhang Wei
Department of Geriatrics, First Affiliated Hospital, Xi'an Jiaotong University College of Medicine, Xi'an 710061, China.
Nan Fang Yi Ke Da Xue Xue Bao. 2010 Jul;30(7):1691-4, 1702.
To investigate the effect of potassium channel opener (diazoxide) on the islet cells apoptosis and bcl-2 and bax gene expressions in diabetic rats.
Islet cell apoptosis was induced by intraperitoneal injection of streptozocin (STZ). The rats were randomly allocated into normal control group (NC group), diabetes mellitus group (DM group), and diazoxide group (DIA group), all treated with diazoxide for 4 weeks. During and after the treatment, the general state, body weight, fasting plasma glucose (FPG), food intake, and oral glucose tolerance of the rats were assessed. The expressions of Bcl-2 and Bax in rat islet cells were measured by immunohistochemistry, and the cell apoptosis was analyzed by TUNEL assay.
Compared with the NC group, the rats in the DM group showed significantly decreased body weight (P<0.05), increased blood glucose at o and 120 min after oral glucose administration, decreased expressions of Bcl-2 (P<0.01), increased expression of Bax (P<0.01), and increased islet cell apoptosis (P<0.05). Diazoxide treatment significantly decreased the body weight (P<0.05), decreased the blood glucose, increased Bcl-2 expression (P<0.01), decreased Bax expression (P<0.05), and reduced the islet cell apoptosis (P>0.05) of the diabetic rats.
By causing potassium channel opening, diazoxide can obviously improve the oral glucose tolerance, reduce the body weight, and up-regulate Bcl-2 and down-regulate Bax expression in diabetic rats. Diazoxide can also reduce the apoptosis of the islet cells in diabetic rats.
探讨钾通道开放剂（二氮嗪）对糖尿病大鼠胰岛细胞凋亡及bcl-2和bax基因表达的影响。
通过腹腔注射链脲佐菌素（STZ）诱导胰岛细胞凋亡。将大鼠随机分为正常对照组（NC组）、糖尿病组（DM组）和二氮嗪组（DIA组），均给予二氮嗪治疗4周。在治疗期间及治疗后，评估大鼠的一般状态、体重、空腹血糖（FPG）、食物摄入量及口服葡萄糖耐量。采用免疫组化法检测大鼠胰岛细胞中Bcl-2和Bax的表达，并用TUNEL法分析细胞凋亡情况。
与NC组相比，DM组大鼠体重显著降低（P<0.05），口服葡萄糖后0和120分钟血糖升高，Bcl-2表达降低（P<0.01），Bax表达升高（P<0.01），胰岛细胞凋亡增加（P<0.05）。二氮嗪治疗显著降低了糖尿病大鼠的体重（P<"0.05），降低了血糖，增加了Bcl-2表达（P<0.01），降低了Bax表达（P<0.05），并减少了胰岛细胞凋亡（P>0.05）。
二氮嗪通过开放钾通道，可明显改善糖尿病大鼠的口服葡萄糖耐量，降低体重，上调Bcl-2表达，下调Bax表达，还可减少糖尿病大鼠胰岛细胞的凋亡。
