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作 者:孟庆民 赵日新 王伟群[1] 张明月[1] 郭思琪 隋洪玉[1]
机构地区:[1]佳木斯大学基础医学院,黑龙江佳木斯154007
出 处:《广东化工》2018年第4期39-40,共2页Guangdong Chemical Industry
基 金:国家自然科学基金项目(编号:31400994);黑龙江大学生创新创业训练计划项目(编号:201610222030)
摘 要:目的:探讨TNF-α对糖尿病肾病形成中髓袢升支粗段管周膜KCNJ10(Kir4.1)的调控。方法:取SD雄性大鼠随机分成4组,正常对照组(NC)、糖尿病模型组(DM)、NC+TNFR:Fc组和DM+TNFR:Fc组,20天后用Western blot方法检测髓袢升支粗段中TNF-α、KCNJ10、PLA2和PTK的蛋白表达情况。结果:DM组TNF-α蛋白表达显著增加;DM组KCNJ10蛋白表达降低,而PLA2和PTK蛋白表达增加;DM+TNFR:Fc组KCNJ10蛋白表达增加,而PLA2和PTK蛋白表达降低。结论:在糖尿病肾病形成中,TNF-α通过激活PLA2和PTK依赖途径抑制髓袢升支粗段管周膜KCNJ10(Kir4.1)的活性。Purpose: To investigate the regulation of TNF-α on basolateral KCNJ 10 (Kir4.1) in the thick ascending limb of diabetic nephropathy. Methods: The male Sprague-Dawley rats were randomly divided into 4 groups: normal control group (NC), diabetic model group (DM), NC + TNFR:Fc group and DM + TNFR:Fc group. The protein expression ofTNF-α, KCNJ10, PLA2 and PTK was detected by Western blot after 20 days. Result: The protein expression of TNF-a, PLA2 and PTK increased while KCNJ10 decreased in DM group. The protein expression of TNF-α, PLA2 and PTK decreased while KCNJ10 increased in DM + TNFR:Fc group. Conclusion: In the formation of diabetic nephropathy, TNF-a inhibits the activity of basolateral KCNJ10 (Kir4.1) in the thick ascending limb by activating PLA2 and PTK-dependent pathways.
关 键 词:TNF—α糖尿病肾病 髓袢升支粗段 管周膜 KCNJ10(KiN.1)
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