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高糖对HK-2细胞缺氧复氧损伤的影响及TLR7-MyD88-NF-κB信号通路的作用
作者:黄亚医  赵博  汪华新  刘康  周芳  肖业达 
单位:武汉大学人民医院 麻醉科, 湖北 武汉 430060
关键词:高糖 缺氧复氧 TLR7-MyD88-NF-κB 
分类号:R692.5
出版年·卷·期(页码):2018·46·第一期(11-14)
摘要:

目的:探讨高糖对HK-2细胞缺氧复氧损伤的影响及TLR7-MyD88-NF-κB信号通路的作用。方法:随机将人肾小管上皮细胞(HK-2)分为低糖组(LG组)、低糖缺氧复氧组(LH/R组)、高糖组(HG组)及高糖缺氧复氧组(HH/R组)4组,每组n=6。采用高糖刺激72 h建立高糖模型,缺氧4 h复氧2 h建立缺氧复氧模型。采用CCK-8和LDH释放实验检测细胞活性,ELISA法检测细胞IL-6和TNF-α水平,免疫荧光法检测肾脏细胞TLR7、MyD88和NF-κB蛋白的表达。结果:与LG组相比,LH/R组、HG组、HH/R组的CCK-8活性下降,LDH、IL-6、TNF-α、TLR7、MyD88及NF-κB蛋白表达增加(均P<0.05);与LH/R组相比,HG组LDH、IL-6、TLR7、MyD88及NF-κB蛋白表达增加(均P<0.05),HH/R组CCK-8活性下降,LDH、IL-6、TNF-α、TLR7、MyD88及NF-κB蛋白表达增加(均P<0.05);与HG组相比,HH/R组CCK-8活性下降,LDH、IL-6、TNF-α、TLR7、MyD88及NF-κB蛋白表达增加(均P<0.05)。与HG组相比,HH/R组MyD88及NF-κB蛋白表达增加(均P<0.05)。结论:TLR7-MyD88-NF-κB信号通路激活参与了HK-2细胞的缺氧复氧损伤,高糖导致该损伤进一步加重。

Objective:To evaluate the effects of high glucose on hypoxia/reoxygenation-induced injury to the HK-2 cells and the TLR7-MyD88-NF-κB signaling pathway. Methods:The HK-2 cell were randomly divided into 4 groups (n=6):low glucose group (group LG), low glucose and hypoxia/reoxygenation group (group LH/R), high glucose group (group HG), high glucose and hypoxia/reoxygenation group (group HH/R). High glucose and hypoxia/reoxygenation model were established by high glucose stimulation of 72 h, and hypoxia 4 h,reoxygenation 2 h. Cell viability was detected by CCK-8 and LDH release assay. The levels of IL-6 and TNF-α were detected by ELISA, and the expression of TLR7, MyD88 and NF-κB protein in renal cells were detected by immunofluorescence. Results:Compared with the group LG, the activity of CCK-8 was decreased, the expression of LDH, IL-6, TNF-α, TLR7, MyD88 and NF-κB protein were increased in the group NH/R, the group HG and the group HH/R (all P<0.05). Compared with the group LH/R, the expression LDH, IL-6, TLR7, MyD88 and NF-κB protein were increased in the group HG and group HH/R(all P<0.05), the activity of CCK-8 was decreased, the expression of LDH, IL-6, TNF-α, TLR7, MyD88 and NF-κB protein were increased in the group HH/R (all P<0.05). Compared with the group HG, the activity of CCK-8 was decreased in group HG and group HH/R, the expression of LDH, IL-6, TNF-α, TLR7, MyD88 and NF-κB were increased in the group HH/R (all P<0.05). Compared with the HG group, the expression of MyD88 and NF-κB protein were increased in group HH/R (all P<0.05). Conclusion:High glucose is involved in the hypoxia/reoxygenation-induced injury of HK-2 cells through the TLR7/MyD88/NF-κB signaling pathway.

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