中文摘要：

目的：以不同浓度血管紧张素Ⅱ（AngⅡ）及AngⅡ1型受体（AT1受体）拮抗剂氯沙坦作用于RIN-m细胞（来源于射线诱导的褐鼠胰岛素细胞瘤）,观察RIN-m合成及分泌胰岛素功能及细胞凋亡的情况。为进一步在临床中研究血管紧张素受体拮抗剂对糖代谢的改善作用提供实验证据。方法：细胞的培养及干预：RIN-m细胞（40～50代）接种于3mL含5.6mmol/L葡萄糖的RPMI1640培养液中。A组加入10μL生理盐水,B、C、D、E组加入终浓度分别为0.1、1、10及100nmol/L的AngⅡ,F组在加入100nmol/L的血管紧张素Ⅱ醋酸盐前10mim给予氯沙坦1μmol/L。各组处理后继续置于37℃、5%CO2的恒温培养箱中48h。RIN-m细胞行流式细胞仪（AnnexinV/FITC）及TUNEL检测凋亡。结果：两种凋亡检测结果大致相似,TUNNEL检测各组凋亡率分别为（7.50±1.18）%,（8.15±0.97）%,（12.67±1.35）%,（15.88±1.75）%,（20.66±0.80）%,（7.74±0.84）%;流式细胞仪检测各组凋亡率分别为（7.62±0.87）%,（8.74±1.31）%,（14.64±1.48）%,（16.47±0.88）%,（20.51±1.03）%,（7.63±0.79）%。AngⅡ干预组凋亡率高于空白对照组,并呈剂量-效应依赖关系,氯沙坦预处理＋AngⅡ组与空白对照组比较差异无统计学意义（P=0.98）。结论：AngⅡ可能通过与胰岛β细胞表面AT1受体结合而诱导RIN-m细胞凋亡,氯沙坦可抑制AngⅡ的促凋亡作用。

英文摘要：

Objective To investigate the effect of Angiotensin Ⅱ （Ang Ⅱ） on inducing RIN-m cells apoptosis. Methods RIN-m cells （40 ～ 50th） were culture in RPMI 1640 medium with 10% fetal bovine serum. Six groups of RIN-m cells were transferred to 24-well culture plate. Ang Ⅱ at dose of 0.1, 1, 10 and 100 nmol / L was used to treat RIN-m cells for 48 hours, Losartan were added 10 minutes prior to treatement.RIN-m cells apoptosis was detected using flow cytometry （Annexin V/FITC） and TUNNEL assays. Results RIN-m cells apoptosis of Ang Ⅱ-treated group was higher than that of control group （P 0.001）. No significant difference was observed between losartan-pretreated and Ang Ⅱ-treated group and the control group （P = 0.98）. Conclusions Ang Ⅱ can induce RIN-m cells apoptosis, Losartan can inhibit Ang Ⅱ-induced apoptosis.