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目的观察脂联素对胰岛β细胞胰岛素分泌、UCP-2、PPARγmRNA表达和凋亡的影响。方法大鼠胰岛细胞株RIN-m5F分别用5.6mmol/L和16.7 mmol/L葡萄糖,并加入不同浓度的球形脂联素(0～2500μg/L)培养48 h。放免法测定胰岛素含量,RT-PCR检测UCP-2、PPARγmRNA的表达。流式细胞仪检测细胞凋亡率,Western Blot检测激活型Caspase3的表达。结果高糖培养下脂联素同时干预后基础胰岛素分泌显著降低,高糖刺激的胰岛素分泌显著增加。和高糖组比较,脂联素组UCP-2、PPARγmRNA的表达显著降低(P<0.05),细胞凋亡率和激活型Caspase-3的表达显著降低(P<0.05)。结论脂联素能改善高糖所致的β细胞胰岛素分泌异常,其机制可能与通过下调PPARγ降低UCP-2的表达有关。脂联素可拮抗高糖所致的β细胞凋亡。
Objective To observe the effects of adiponectin on insulin secretion, UCP-2, PPARγ mRNA expression and apoptosis in pancreatic β cells. Methods Rat islet cell line RIN-m5F was cultured with glucose (5.6 mmol / L and 16.7 mmol / L) for 48 h with different concentrations of globulin (0-2500 μg / L). Insulin content was determined by radioimmunoassay. The expression of UCP-2 and PPARγmRNA was detected by RT-PCR. Flow cytometry was used to detect the apoptosis rate. Western Blot was used to detect the expression of activated Caspase3. Results The basal insulin secretion was significantly decreased and the insulin secretion stimulated by high glucose significantly increased after adiponectin intervention in high glucose. Compared with high glucose group, the expression of UCP-2 and PPARγmRNA in adiponectin group was significantly decreased (P <0.05), and the apoptosis rate and active Caspase-3 expression were significantly decreased (P <0.05). Conclusion Adiponectin can improve the abnormal insulin secretion induced by high glucose, and its mechanism may be related to down-regulating PPARγ and decreasing the expression of UCP-2. Adiponectin can antagonize β-cell apoptosis induced by high glucose.