Objective To investigate the effects of silencing angiotensin Ⅱtype 1 receptor ( AT1R) in apoptosis induced by STZ in mice islet cells NIT -1.Methods Three pairs of siRNA targeting AT1R were designed and synthe-sized.They were transfected into NIT -1 by liposome transfection .Fluorescence microscopy was used to examine the effect of different siRNA concentration on the transfection efficiency .AT1R mRNA expression was detected with real -time PCR to compare silencing effects among the three siRNA sequence and different durations of interference .NIT-1 cells were al-located into 4 groups.The control group did not receive intervention .The STZ group was treated with 5 mmol/L STZ for 30 min.The si-AT1R group was transfected with 40 nmol/L si-AT1R and detected 24 h later.The si-AT1R+STZ group was transfected with 40 nmol/L si-AT1R and 24 h later treated with 5 mmol/L STZ for 30 min.Caspase-3 mR-NA expression was detected by Real -time PCR.Apoptosis rate was measured by Hoechst 33342 staining microscopy and Annexin V-FITC/PI-labeled flow cytomety .Results Transfection with 40 nmol/L siRNA had the greatest fluores-cence.The maximum inhibitory effects of AT1R siRNA transfection on AT1R expression was 40 nmol/L at 24 h with si-AT1R-2.The expression of AT1R mRNA was markedly down regulated by 92.20% compared with that in the control group (P<0.05).The expression of caspase -3 mRNA in the STZ group increased by 2.37 times compared with the control group (P<0.05).The expression of caspase -3 mRNA in the si-AT1R+STZ group decreased by 11.28%compared with the STZ group , but the difference was not statistically significant .Apoptosis rate in the STZ group increased by 3.27 times compared with the control group ( P<0.05) .The cells treated with both si -AT1R and STZ had a signifi-cantly decreased apoptosis rate ( by 26.82%) compared with the STZ group ( P<0.05 ) .Conclusion This study suc-cessfully silenced AT1R in NIT-1 cells and obtained the best efficiency of silence with 40 nmol/L si-AT1R-2 for 24 h.RNA interference of AT1R gene can reduce the expression of Caspase -3 gene and apoptosis induced by STZ , sugges-ting that AT1R mediates the process of apoptosis induced by STZ in NIT -1 cells.%目的：用siRNA干扰技术沉默小鼠胰岛素瘤NIT－1细胞血管紧张素Ⅱ1型受体（ AT1R）基因，探讨其对链脲佐菌素（STZ）诱导的胰岛素瘤细胞凋亡的影响。方法针对小鼠AT1R基因，设计并合成3对siRNA序列，脂质体法转染至NIT－1细胞，荧光显微镜观察荧光强度检测转染效率，Real－time PCR检测AT1R mRNA表达量判断不同干扰序列及干扰时间的基因沉默效果；分4组：空白组不予任何干预，STZ组予5 mmoL／L STZ干预30 min，si－AT1R组予40 nmol／L si－AT1R转染24 h，si－AT1R＋STZ组予40 nmoL／L si－AT1R转染24 h后5 mmoL／L STZ干预30 min；Real－time PCR检测Caspase－3 mRNA表达量，Hoechst33342染色荧光显微镜和Annex-in V－FITC／PI流式细胞术检测细胞凋亡率。结果40 nmol／L siRNA转染的荧光强度最强，转染后AT1R mRNA表达量明显下降，si－AT1R－2转染24 h的沉默效果最佳（92.20％）；Caspase－3 mRNA表达量：STZ组与空白组比增加了2.37倍（P＜0.05），si－AT1R＋STZ组与STZ组比减少了11.28％，但差异无统计学意义；细胞凋亡率：STZ组与空白组比增加了3.27倍（P＜0.05），si－AT1R＋STZ组与STZ组比减少了26.82％（P＜0.05）。结论本研究建立了稳定的胰岛细胞AT1R基因沉默模型；RNA干扰沉默胰岛细胞AT1R基因可通过下调Caspase－3 mRNA表达量降低STZ诱导的细胞凋亡率，提示AT1R介导了STZ诱导的胰岛细胞凋亡过程。
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