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4-甲基邻苯二酚诱导TM4支持细胞的细胞损伤。

4-Methylcatechol-induced cell damage in TM4 Sertoli cells.

作者信息

Li Chunjin, Li Wanhong, Chen Shuxiong, Kang Zhichen, Sun Lina, Li Hongjiao, Chen Lu, Rao Jiahui, Zhao Yun, Yu Jiaxin, Zhou Xu

机构信息

College of Animal Sciences, Jilin University, 5333 Xi'an Avenue, Changchun, Jilin Province, 130062, P.R. China.

Department of Rehabilitation, The second hospital of Jilin University, Changchun, 130041, P. R. China.

出版信息

Cell Biol Int. 2015 Jun;39(6):770-4. doi: 10.1002/cbin.10420. Epub 2015 Mar 15.

DOI:10.1002/cbin.10420
PMID:25639863
Abstract

4-Methylcatechol (4-MC) is one of the metabolites of quercetin, which is a potential drug for neuroprotection and tumorigenesis inhibition. This study was performed to investigate the cytotoxic effect of 4-MC in mouse TM4 Sertoli cells. TM4 Sertoli cell viability was significantly inhibited by 4-MC in a time- and dose-dependent manner. The number of apoptotic and dead cells was significantly increased after 4-MC treatment. Caspase 3 activity increased by prolonged exposure of TM4 Sertoli cells to 200 μM 4-MC. The 4-MC significantly upregulated the mRNA level of Bax gene and considerably downregulated the Bcl-2 gene expression in a concentration-dependent manner. Results showed that 4-MC could induce TM4 Sertoli cell apoptosis, and the cytotoxic effect of 4-MC on TM4 Sertoli cells may be associated with upregulated Bax gene expression, which induced caspase cascade activation.

摘要

4-甲基儿茶酚(4-MC)是槲皮素的代谢产物之一,槲皮素是一种具有神经保护和抑制肿瘤发生潜力的药物。本研究旨在探讨4-MC对小鼠睾丸支持细胞(TM4)的细胞毒性作用。4-MC以时间和剂量依赖性方式显著抑制TM4支持细胞的活力。4-MC处理后,凋亡细胞和死亡细胞的数量显著增加。将TM4支持细胞长时间暴露于200μM 4-MC后,半胱天冬酶3活性增加。4-MC以浓度依赖性方式显著上调Bax基因的mRNA水平,并显著下调Bcl-2基因的表达。结果表明,4-MC可诱导TM4支持细胞凋亡,其对TM4支持细胞的细胞毒性作用可能与Bax基因表达上调有关,Bax基因表达上调诱导了半胱天冬酶级联激活。

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