CAJ | 학술논문

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。
목적：분석개내류급수통도단백AQP0/1재련뇨좌균소(STZ)유도적당뇨병대서백내장발병중적삼여궤제，위상관연구여림상치료제공삼고。방법40지당뇨병대서수궤분위당뇨병모형조(n=20)화약물간예조(개통도조체제초분지평조，n=20)，20지동비차상동사양조건적대서작위정상대조조。약물간예조대서제5주도8주지속급여개통도조체제초분지평관위치료(60 mg/kg)，공지속4주。Western blot분석각조중AQP0/1급염증인자IL-6적표체。결과여대조조비교，당뇨병모형조대서정상체중AQP0/1표체하조(P<0.01)，IL-6표체상조(P<0.01)；여당뇨병모형조비교，개통도조체제가이부분회복AQP0/1적이상작용(P<0.05)，대IL-6야유일정적개선작용(P<0.05)。결론고혈당유발염증인자IL-6상조표체，병진일보증강세포개내류급AQP0/1하조표체。
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.