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目的:探讨缺血再灌注损伤早期肾脏皮质内大电导钙依赖性钾通道(BK)通道的表达及意义。方法:建立成年SD大鼠肾脏急性缺血再灌注损伤模型,快速收集24小时缺血大鼠与对照大鼠血和损伤侧肾脏皮质标本,使用ELISA方法检测血肌酐和尿素氮含量,实时荧光定量RT-PCR和蛋白免疫印迹方法检测肾脏组织中BK通道α亚基的m RNA表达水平和蛋白表达水平。结果:(1)急性缺血再灌注大鼠损伤侧肾脏皮质BK通道α亚基m RNA水平较对照大鼠同侧肾脏皮质的表达明显降低(P<0.01)。(2)急性缺血再灌注大鼠损伤侧肾脏皮质BK通道α亚基蛋白水平较对照大鼠同侧肾脏皮质的表达也明显降低(P<0.05)。(3)NS1619预处理缺血再灌注大鼠血尿素氮和血肌酐含量显著降低(P<0.05)。结论:BK通道表达和功能的改变是参与大鼠肾脏缺血再灌注损伤的重要机制。
Objective: To investigate the expression and significance of large conductance calcium-dependent potassium channel (BK) in early renal cortex of ischemia-reperfusion injury. Methods: Acute ischemia-reperfusion injury model of adult SD rats was established. The blood and injured renal cortex samples of 24-hour ischemic and control rats were collected rapidly. The levels of serum creatinine and urea nitrogen were measured by ELISA. Real-time fluorescence quantitative RT-PCR and Western blotting were used to detect the m RNA expression and protein expression of BK channel α subunit in kidney. Results: (1) The expression of α-subunit m RNA of BK channel in the injured cortex of rats with acute ischemia-reperfusion injury was significantly lower than that of the control rat (P <0.01). (2) The expression of B-subunit α-subunit of renal ischemic cortex in acute ischemic reperfusion injury rats was also significantly lower than that in control rats (P <0.05). (3) The levels of blood urea nitrogen and serum creatinine in NS1619 preconditioning rats were significantly decreased (P <0.05). Conclusion: The change of BK channel expression and function is an important mechanism involved in renal ischemia-reperfusion injury in rats.