Ginsenoside Rg1 ameliorates reproductive function injury in C57BL/6J mice induced by di‐N‐butyl‐phthalate

精子发生 免疫印迹 下调和上调 男科 人参 促黄体激素 内分泌学 PI3K/AKT/mTOR通路 睾酮(贴片) 精子 激素 内科学 化学 促卵泡激素 药理学 生物 医学 信号转导 生物化学 基因 病理 替代医学
作者
Xiaolei Xu,Zhenting Qu,Honghao Qian,Zhongming Li,Xiuling Sun,Xinrui Zhao,Huan Li
出处
期刊:Environmental Toxicology [Wiley]
卷期号:36 (5): 789-799 被引量:23
标识
DOI:10.1002/tox.23081
摘要

Abstract With the aggravation of environmental pollution, the incidence of infertility is increasing. Ginsenoside Rg1 is a monomer component extracted from Panax ginseng . It has been found that Ginsenoside Rg1 is able to prevent premature ovarian failure and delay testicular senescence. Therefore, we speculate Ginsenoside Rg1 may have great potential to prevent and treat infertility. The aim of this work is to explore whether Ginsenoside Rg1 plays a protective role in the dinbutyl phthalate (DBP)‐induced reproductive function injury mice, and to elucidate the potential mechanism. C57BL/6J male mice were administered by DBP with or without Ginsenoside Rg1 treatment and serum, testis and epididymis were collected for further analysis. Sperm analysis, hematoxylin and eosin staining, and serum hormone detection indicated that Ginsenoside Rg1 treatment improved the sperm density and sperm motility, reduced the testicular tissue damage, increased the serum testosterone and luteinizing hormone levels, and decreased the serum follicle‐stimulating hormone level in DBP‐induced mice. Furthermore, Ginsenoside Rg1 treatment upregulated expression levels of spermatogenesis‐related protein, Cx43, E‐cadherin, p‐PI3K, p‐Akt, and mTOR in the mice treated by DBP, observed by using a immunohistochemistry assay, a real‐time quantitative PCR assay, and a western blot analysis. The present study reveals that Ginsenoside Rg1 may exert anti‐DBP‐induced reproductive function injury in C57BL/6J mice. In addition, the protect role of Ginsenoside Rg1 in spermatogenesis may be associated with the regulation of reproductive hormones, upregulation of spermatogenic associated proteins expression, restoration of the gap junctions, and the activation of PI3K/Akt/mTOR signaling pathways.
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