氧化应激
KEAP1型
化学
泛素
细胞生物学
谷胱甘肽
活性氧
信号转导
药理学
丙二醛
氧化磷酸化
超氧化物歧化酶
抗氧化剂
内分泌学
生物
生物化学
转录因子
基因
作者
Lei Zhang,Xian Gao,Zhiqiang Qin,Xiaokai Shi,Kai Xu,Shangqian Wang,Min Tang,Wei Wang,Shenglin Gao,Li Zuo,Lifeng Zhang,Wei Zhang
标识
DOI:10.1016/j.scitotenv.2021.146898
摘要
Di-n-butylphthalate (DBP) has been listed as an environmental priority pollutant in China due to its distinct biotoxicity. Epidemiological studies have shown that exposure to DBP is closely related to a series of congenital and acquired defects in the male reproductive system. The oxidative stress injury caused by DBP plays an important role in these defects. Previous studies have demonstrated that the Keap1/Nrf2 antioxidative pathway plays a protective role in DBP-induced oxidative stress injury. However, the further molecular regulation mechanism of the activation of Nrf2 pathway remains unclear. Here, we demonstrate that DBP caused testicular oxidative stress injury and Nrf2 pathway was activated in response to the injury in vivo and in vitro. Moreover, we validated that reduced level of USP15 attenuates DBP-induced oxidative stress injury through restraining the ubiquitylation and degradation of Nrf2. Notably, USP15 is confirmed as a target of miR-135b-5p and miR-135b-5p mediated inhibition of USP15 is involved in the DBP-induced oxidative stress injury. Collectively, these findings indicated that decreased level of USP15 functions a significant protective effect on the oxidative stress injury of testis caused by DBP via regulating the Keap1/Nrf2 signaling pathway.
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