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机构地区:[1]中国医科大学、药学院 [2]中国医科大学、附属第一医院药学部,辽宁沈阳110001
出 处:《细胞与分子免疫学杂志》2012年第10期1013-1015,共3页Chinese Journal of Cellular and Molecular Immunology
基 金:沈阳市科学技术计划(1091142-9-00)
摘 要:目的:探讨过表达大鼠醛酮还原酶AKR7A1蛋白对巴豆醛致畸作用的影响。方法:使用Western blot法和醛酮还原酶(AKR)酶活性技术检测并鉴定外源性AKR7A1在V79-4细胞中的表达水平和催化活性,使用HGPRT基因突变实验检测在V79-4细胞中过表达AKR7A1对巴豆醛致畸作用的影响。结果:Western blot检测显示V79-4细胞中表达高水平的AKR7A1蛋白;AKR酶活性实验结果显示过表达的AKR7A1蛋白具有催化活性;HGPRT基因突变实验结果显示过表达AKR7A1的V79-4细胞对巴豆醛致畸作用的抵抗力明显高于对照细胞。结论:过表达大鼠AKR7A1能显著提高V79-4细胞对巴豆醛致畸作用的抵抗力。AIM: To investigate the effect of overex- pressing rat aldo-keto reductases (AKRTA1) in V79-4 ceils on crotonaldehyde-induced mutagenicity. METHODS: The expression level and enzyme activity of AKR7A1 protein expressed in V79-4 cells were measured by Western blotting and AKR enzyme assay, respectively. HGPRT assay was applied to evaluate the effect of AKR7A1 overexpression on crotonaldehyde-induced mutagenicity in V79-4 cells. RE- SULTS: Western blotting confirmed a high expression level of AKR7A1 protein in V79-4 cells. AKR enzyme assay showed that the overexpressed AKR7A1 protein was func- tionally active. HGPRT assay demonstrated that cells overexpressing AKR7AI exhibited a significant increase in resistance to crotonaldehyde-induced mutagenicity compared to control cells. CONCLUSION: Overexpression of AKFr/A1 can protect V79-4 cells against crotonaldehyde-induced mutagenicity.
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