吉林大学学报（医学版）Issue(6)：1201-1205,5.DOI:10.13481/j.1671-587x.20140616
环孢素引起肾小管上皮细胞培养液中肾损伤分子-1水平升高的机制
Up-regulation effect of cyclosporine A on level of kidney inj ury molecule-1 in culture supernatant of human kidney cells and its mechanism
摘要
Abstract
Objective To investigate the mechanism of increasing of the level of kidney injury molecule-1(KIM-1)in culture supernatant of human kidney cells(HKC)induced by cyclosporine A(CsA),and to clarify the relationships between the expression levels of KIM-1 and p38 MAPK pathway and ERK1/2MAPK pathway in HKC. Methods The HKC at logarithmic growth phase were randomly divided into control group, CsA control group, CsA + p38 kinase inhibitor group, p38 kinase inhibitor group, CsA + ERK1/2 inhibitor group and ERK1/2 kinase inhibitor group.The inhibitory rates of proliferation of HKC in various groups were detected by MTT assay, and the expression levels of KIM-1 in HKC supernatant in various groups were detected by ELISA;the survival rates,apopototic rates and necrotic rates of the HKC in various groups were detected by flow cytometry. Results Compared with control group,the expression level of KIM-1 protein in the supernatant of HKC in CsA control group was significantly increased (P<0.05),and the survival rate was significantly decreased (P<0.05), while the apoptotic rate and the necrotic rate were significantly increased (P<0.05 ). Compared with control group,the survival rates, the apoptotic rates and the necrosis rates of cells in p38 kinase inhibitor group and ERK1/2 kinase inhibitor group had no significant differences(P>0.05).Compared with CsA control group,the expression levels of KIM-1 protein in CsA+ p38 kinase inhibitor group and CsA+ ERK1/2 kinase inhibitor group were significantly decreased (P<0.05),and the survival rate was significantly increased (P<0.05),while the apoptotic rate and the necrotic rate were significantly decreased (P<0.05).Conclusion p38 MAPK pathway and ERK1/2MAPK pathway are involved in the process of up-regulation of the KIM-1 level in HKC culture supernatant induced by CsA,and the expression of KIM-1 may become the biochemical marker of clinical monitoring of CsA nephrotoxicity.关键词
环孢素A/肾损伤分子-1/人肾小管上皮细胞/p38MAPK通路/ERK1/2MAPK通路Key words
cyclosporine A/kidney injury molecule-1/human kidney cells/p38 MAPK pathway/ERK1/2 MAPK pathway分类
医药卫生引用本文复制引用
宋莲莲,赵军,于金宇,张文岚,薛丽娟,傅耀文..环孢素引起肾小管上皮细胞培养液中肾损伤分子-1水平升高的机制[J].吉林大学学报（医学版）,2014,(6):1201-1205,5.基金项目
吉林省科技厅自然科学基金资助课题 （）
