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桑色素通过刺激小鼠睾丸分泌睾酮和促进生殖细胞增殖减轻镉诱导的睾丸损伤。

Morin mitigates cadmium-induced testicular impairment by stimulating testosterone secretion and germ cell proliferation in mice.

作者信息

Annie Lalrawngbawli, Nicy Vanrohlu, Rempuia Vanlal, Marak Chuckles Ch, Gurusubramanian Guruswami, Roy Vikas K

机构信息

Department of Zoology, Mizoram University, Aizawl, Mizoram, India.

出版信息

J Biochem Mol Toxicol. 2023 Sep;37(9):e23400. doi: 10.1002/jbt.23400. Epub 2023 Jun 19.

Abstract

Cadmium (Cd) is one of the heavy metal pollutants present in the environment due to human intervention. It is well known that Cd causes toxicological effects on various organs, including the testes. Morin hydrate is a plant-derived bioflavonoid with antioxidant, anti-inflammatory, and anti-stress properties. Thus, the question can be raised as to whether Morin has an effect on Cd-intoxication-induced testicular impairment. Therefore, the aim of this study was to investigate the role of Morin on Cd-mediated disruption of testicular activity. Mice were divided into three groups: group 1 served as the control group, group 2 was given Cd (10 mg/kg) orally for 35 days, and group 3 was given Cd and Morin hydrate (100 mg/kg) for 35 days. To validate the in vivo findings, an in vitro study on testicular explants was also performed. The results of the in vivo study showed that Cd-intoxicated mice had testicular disorganization, reduced circulating testosterone levels, decreased sperm density, and elevated oxidative stress and sperm abnormality. The expression of the germ cell proliferation marker, germ cell nuclear acidic protein (GCNA), and adipocytokine visfatin were also downregulated. It was observed that Morin hydrate upregulated testicular visfatin and GCNA expression in Cd-intoxicated mice, along with improvement in circulating testosterone, testicular histology, and sperm parameters. Furthermore, the in vitro study showed that Cd-mediated downregulation of testicular visfatin and GCNA expression, along with the suppressed secretion of testosterone from testicular explants, was normalized by Morin treatment, whereas visfatin expression was not. Overall, these data indicate that environmental cadmium exposure impairs testicular activity through downregulation of visfatin and GCNA expression, and Morin might play a protective role against Cd-induced testicular toxicity.

摘要

镉(Cd)是由于人类干预而存在于环境中的重金属污染物之一。众所周知,镉会对包括睾丸在内的各种器官产生毒理学影响。水合桑色素是一种植物来源的生物类黄酮,具有抗氧化、抗炎和抗应激特性。因此,可以提出水合桑色素是否对镉中毒诱导的睾丸损伤有影响这一问题。因此,本研究的目的是探讨水合桑色素在镉介导的睾丸活动破坏中的作用。将小鼠分为三组:第1组作为对照组,第2组口服镉(10毫克/千克)35天,第3组口服镉和水合桑色素(100毫克/千克)35天。为了验证体内研究结果,还进行了睾丸外植体的体外研究。体内研究结果表明,镉中毒小鼠出现睾丸组织紊乱、循环睾酮水平降低、精子密度下降、氧化应激增加和精子异常。生殖细胞增殖标志物、生殖细胞核酸性蛋白(GCNA)和脂肪细胞因子内脂素的表达也下调。观察到水合桑色素上调了镉中毒小鼠睾丸内脂素和GCNA的表达,同时循环睾酮、睾丸组织学和精子参数得到改善。此外,体外研究表明,镉介导的睾丸内脂素和GCNA表达下调以及睾丸外植体睾酮分泌受抑制,通过水合桑色素处理得以恢复正常,但内脂素表达除外。总体而言,这些数据表明环境镉暴露通过下调内脂素和GCNA表达损害睾丸活动,而水合桑色素可能对镉诱导的睾丸毒性起到保护作用。

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