摘要
目的探讨组蛋白乙酰化酶6(histonedeacetylases 6,HDAC6)选择性抑制剂23BB通过抑制人肾小管上皮细胞(HK-2)凋亡的肾脏保护机制。方法使用亚铁肌红蛋白诱导HK-2模拟横纹肌溶解致急性肾损伤的体外模型,将HK-2细胞分5组:空白对照组、亚铁肌红蛋白(myoglobin)组(200μM)、23BB治疗组(1.25nM)、4-PBA治疗组(2.0mM)及Tunicamycin刺激组(25ng/mL),采用逆转录-聚合酶链反应和蛋白质印迹法检测凋亡相关基因和蛋白情况。结果 Myoglobin诱导HK-2细胞模型中,23BB调控凋亡相关基因和蛋白表达。结论 HDAC6抑制剂23BB通过抑制肌红蛋白诱导HK-2细胞凋亡。
Objective To investigate the protective effects and mechanism of selective HDAC6 inhibitor 23 BB in myoglobin-induced proximal tubular cell lines(HK-2).Methods HK-2 cells were divided into control group,myoglobin(200μM)group,myoglobin+23 BB(1.25 nM)group,myoglobin+4-PBA(2 mM)group and myoglobin+23 BB+TM(25 ng/ml)group.Cells were collected at 24 hafter treatment.The apoptosis related gene mRNA level and marker protein expression were evaluated by RT-PCR and Western blotting.Results The apoptosis-related mRNA and marker protein expression were found to increase in response to myoglobin treatment.Conclusion The protective effect of HDAC6 inhibitor 23 BB was through the inhibition of myoglobin-induced apoptosis in HK-2 cells.
作者
杜晓艳
林琳
马良
郭帆
付平
DU Xiaoyan;LIN Lin;MA Liang;GUO Fan;FU Ping(Department of Pharmacy,West China Hospital,Sichuan University,Chengdu 610041,China;West-district,Outpatient Department of West China Hospital of Stomatology,Sichuan University,Chengdu 610041,China;Kidney Research Lab,Divisimi of Nephrology,West China Hospital,Sichuan University,Chengdu 610041,China)
出处
《西部医学》
2019年第2期180-184,共5页
Medical Journal of West China
基金
国家自然科学基金(81402782)