锌通过半胱天冬酶-3介导的途径减轻乙醇诱导的支持细胞毒性和凋亡。
Zinc attenuates ethanol-induced Sertoli cell toxicity and apoptosis through caspase-3 mediated pathways.
作者信息
Pourhassanali Nazila, Roshan-Milani Shiva, Kheradmand Fatemeh, Motazakker Morteza, Bagheri Morteza, Saboory Ehsan
机构信息
Student Research Committee, Urmia University of Medical Sciences, Urmia, Iran; Department of Physiology, Neurophysiology Research Center, Faculty of Medicine, Urmia University of Medical Sciences, Urmia, Iran; Cellular and Molecular Research Center, Urmia University of Medical Sciences, Urmia, Iran.
Department of Physiology, Neurophysiology Research Center, Faculty of Medicine, Urmia University of Medical Sciences, Urmia, Iran; Cellular and Molecular Research Center, Urmia University of Medical Sciences, Urmia, Iran.
出版信息
Reprod Toxicol. 2016 Jun;61:97-103. doi: 10.1016/j.reprotox.2016.03.041. Epub 2016 Mar 23.
Ethanol enhances apoptosis in testicular germ cells. Zinc reduces ethanol-induced apoptosis of somatic cells through inhibition of caspase-mediated pathways. Little is known about the effects of ethanol on Sertoli cells and the effects of Zinc on ethanol-induced testicular injury. The hypothesis tested was that ethanol enhances apoptosis of Sertoli cells through up-regulation of caspase-3 and Zinc inhibits ethanol-induced effects. Cultured Sertoli cells (TM4) were exposed to ethanol (160mM), Zinc (8μM) and Zinc prior to ethanol for duration of 24 or 48h and their effects on TM4 cell viability was then investigated by MTT assay. Caspase-3 mRNA expression was also investigated using real-time RT-PCR. Cell viability decreased and caspase-3 mRNA expresstion increased in cells exposed to ethanol, while exposure to Zinc showed opposite effects. Pretreatment with Zinc recovered ethanol-induced anti-proliferative effects and over-expression of caspase-3. Zinc reduced ethanol-induced Sertoli cell toxicity and apoptosis via caspase-3 mediated pathways.
乙醇可增强睾丸生殖细胞的凋亡。锌通过抑制半胱天冬酶介导的途径减少乙醇诱导的体细胞凋亡。关于乙醇对支持细胞的影响以及锌对乙醇诱导的睾丸损伤的影响，人们了解甚少。所检验的假设是，乙醇通过上调半胱天冬酶-3增强支持细胞的凋亡，而锌可抑制乙醇诱导的效应。将培养的支持细胞（TM4）分别暴露于乙醇（160mM）、锌（8μM）以及乙醇处理前先加入锌的环境中，持续24或48小时，然后通过MTT法研究它们对TM4细胞活力的影响。还使用实时逆转录聚合酶链反应研究了半胱天冬酶-3 mRNA的表达。暴露于乙醇的细胞活力下降，半胱天冬酶-3 mRNA表达增加，而暴露于锌则显示出相反的效果。锌预处理可恢复乙醇诱导的抗增殖效应和半胱天冬酶-3的过表达。锌通过半胱天冬酶-3介导的途径降低乙醇诱导的支持细胞毒性和凋亡。
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