Objective To explore the involvement of AQP0/1 and Ca2+ influx in streptozotoxin (STZ)-in-duced diabetic cataract. Methods Forty male SD rats were divided into diabetic model group (n=20) and calcium channel blocker (nifedipine) group (n=20), while 20 normal rats were taken as control group. The diabetic model group was replicated by injection of streptozotoxin (STZ), and calcium channel blocker group was given 60 mg/kg nifedipine from the fifth week to the eighth week. The concentration of serum blood glucose and cholesterol was ana-lyzed. The expression of AQP0/1 and IL-6 were detected by Western blot. Results Compared with the control group, the expression of AQP0/1 were down-regulated and the expression of IL-6 was up-regulated in diabetic model group (P<0.01). Compared with diabetic model group, the abnormal expression of AQP0/1 and IL-6 was significantly alleviated in calcium channel blocker group (P<0.05). Conclusion High concentration of glycemia upregulated the expression of IL-6 which enhanced the downregulated expression of AQP0/1.%目的：分析钙内流及水通道蛋白AQP0/1在链脲佐菌素(STZ)诱导的糖尿病大鼠白内障发病中的参与机制，为相关研究与临床治疗提供参考。方法40只糖尿病大鼠随机分为糖尿病模型组(n=20)和药物干预组(钙通道阻滞剂硝苯地平组，n=20)，20只同批次相同饲养条件的大鼠作为正常对照组。药物干预组大鼠第5周到8周持续给予钙通道阻滞剂硝苯地平灌胃治疗(60 mg/kg)，共持续4周。Western blot分析各组中AQP0/1及炎症因子IL-6的表达。结果与对照组比较，糖尿病模型组大鼠晶状体中AQP0/1表达下调(P<0.01)，IL-6表达上调(P<0.01)；与糖尿病模型组比较，钙通道阻滞剂可以部分恢复AQP0/1的异常作用(P<0.05)，对IL-6也有一定的改善作用(P<0.05)。结论高血糖诱发炎症因子IL-6上调表达，并进一步增强细胞钙内流及AQP0/1下调表达。
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