摘要
目的:探讨氯沙坦对百草枯诱导HK-2细胞损伤的影响及机制。方法:常规培养HK-2细胞,分为空白对照组:未采用任何药物干预培养24h;模型组:以800μmol/L百草枯培养24h;氯沙坦预治疗组:先以75μmol/L氯沙坦培养1h,再以75μmol/L氯沙坦+800μmol/L百草枯培养24h。观察各组细胞TLR-4、NF-?B、TNF-α、IL-6的表达。结果:与空白对照组相比,模型组TLR-4、NF-?B、TNF-α、IL-6表达升高(P<0.05);与模型组相比,氯沙坦预治疗组TLR-4、NF-?B、TNF-α、IL-6表达水平显著降低(P<0.05)。结论:氯沙坦预处理能够抵抗百草枯诱导的HK-2细胞损伤,其机制可能与抑制TLR-4/NF-?B信号通路活化,减少炎症因子的表达有关。
Objective:To investigate the effect of losartan on HK-2 cell injury induced by paraquat-and its underlying mechanisms.Methods:HK-2 cells were routinely cultured and divided into the blank control group,the model group and the losartan pretreatment group.The blank control group was induced 24h without any drugs,the model group was cultured with 800μmol/L paraquat for 24h,the losartan pretreatment group was induced 1h by 75μmol/L losartan,then,was induced 24h by 75μmol/L losartan +800μmol/L paraquat.The expression of TLR-4,NF-k B,TNF-α and IL-6 in each group were observed.Results:Compared with the blank control group,the expression of TLR-4,NF-k B,TNF-α,and IL-6 were increased in the model group(P<0.05).Compared with the model group,the level of TLR-4,NF-k B,TNF-α,and IL-6 in the losartan pretreatment group were significantly decreased(P<0.05).Conclusions:Losartan pretreatment can reduce the paraquat-induced HK-2 cell injury.The mechanism of it may be related to inhibition of TLR-4/ NF-kB signaling pathway and decreased expression of inflammatory factors.
出处
《大众科技》
2019年第1期38-40,共3页
Popular Science & Technology
基金
广西研究生教育创新计划项目"血管紧张素II参与百草枯肾损伤的作用及机制"(YCSW2018111)
南宁市科学研究与技术开发计划"简明自救互救医疗技术的研究及推广"(03201215107D)