Delta阿片受体激活对体外培养大鼠软骨细胞凋亡的影响

Effect of activation of delta opioid receptor on the apoptosis of cultured chondrocytes in rat

目的：研究delta阿片受体激活对体外培养新生大鼠软骨细胞凋亡的影响并探讨其机制。方法：体外分离培养新生大鼠软骨细胞，用delta阿片受体进行干预，MTT法测定细胞活力；AnnexinV-FITC／PI双标记法测定细胞凋亡；免疫印迹分析caspase-3和细胞外信号调节激酶（ERK）蛋白表达水平。结果：delta阿片受体激动剂DADLE（1 μmol／L）可增强软骨细胞ERK蛋白的磷酸化，抑制软骨细胞凋亡，但这种现象可被delta阿片受体阻断剂Naltrindole（10μmol／L）所逆转，并且给予ERK特异性抑制剂U0126（10μmol／L）亦可逆转DADLE抑制细胞凋亡的作用。结论：Delta阿片受体激活可抑制大鼠软骨细胞凋亡，其机制可能与激活ERK途径相关。

Objective： To study the impact of activation of delta opioid receptor on apoptosis of chondrocytes in in vitro cul tured neonatal rats and its mechanism. Methods： In vitro isolated neonatal rat chondrocytes were treated with delta opioid receptor agonist; Annexin V-FITC/PI double staining was used to detect the apoptosis rate of cells; Western blotting analysis was used to detect the expression of caspase-3 and ERK. Results： Delta opioid receptor agonist DADLE （1 μmol/L） enhanced ERK phosphorylation in chondrocytes and inhibited the apoptosis of chondrocytes, while this phenomenon could be reversed by delta opioid receptor antagonist naltrindole （10 μmol/L）, and the ERK inhibitor U0126 （10 μmol/L） was also reversed anti-apoptotic effect of DADLE. Conclusion： Activation of delta opioid receptor can inhibit the apoptosis of rat chondrocytes, and its mechanism may he related to the activation of ERK pathway.