版权说明 操作指南
首页 > 成果 > 详情

Hydrogen sulfide alleviates uranium-induced rat hepatocyte cytotoxicity via inhibiting Nox4/ROS/p38 MAPK pathway

认领
导出
下载 Link by 万方学术期刊
反馈
分享
QQ微信 微博
成果类型:
期刊论文
作者:
Yi, Juan;Yuan, Yan;Zheng, Jifang*;Zhao, Tingting
通讯作者:
Zheng, Jifang
作者机构:
[Zheng, Jifang; Yuan, Yan; Zhao, Tingting; Yi, Juan] Univ South China, Sch Pharmaceut & Biol Sci, Dept & Inst Biol, Changsheng West Rd 28, Hengyang 421001, Hunan, Peoples R China.
通讯机构:
[Zheng, Jifang] U
Univ South China, Sch Pharmaceut & Biol Sci, Dept & Inst Biol, Changsheng West Rd 28, Hengyang 421001, Hunan, Peoples R China.
语种:
英文
关键词:
hepatotoxicity;hydrogen sulfide (H 2 S);oxidative stress;signaling pathway;uranium
期刊:
JOURNAL OF BIOCHEMICAL AND MOLECULAR TOXICOLOGY
ISSN:
1095-6670
年:
2019
卷:
33
期:
3
页码:
e22255
基金类别:
Natural Science Foundation of Hunan ProvinceNatural Science Foundation of Hunan Province [14JJ2087]; National Natural Science Foundation of ChinaNational Natural Science Foundation of China (NSFC) [81071005]
机构署名:
本校为第一且通讯机构
院系归属:
药学与生物科学学院
摘要:
As a gasotransmitter, hydrogen sulfide (H 2 S) plays a crucial role in regulating the signaling pathway mediated by oxidative stress. The purpose of this study was to investigate the protective effects of H 2 S on uranium-induced rat hepatocyte cytotoxicity. Primary hepatocytes were isolated and cultured from Sprague Dawley rat liver tissues. After pretreating with sodium hydrosulfide (an H 2 S donor) for 1 hour (or GKT-136901 for 30 minutes), hepatocytes were treated by uranyl acetate for 24 hours. Cell viability, reactive oxygen species (ROS)...

反馈

验证码:
看不清楚,换一个
确定
取消

成果认领

标题:
用户 作者 通讯作者
请选择
请选择
确定
取消

提示

该栏目需要登录且有访问权限才可以访问

如果您有访问权限,请直接 登录访问

如果您没有访问权限,请联系管理员申请开通

管理员联系邮箱:yun@hnwdkj.com