Triptriolide antagonizes triptolide-induced nephrocyte apoptosis via inhibiting oxidative stress in vitro and in vivo
2019-10
发表期刊BIOMEDICINE & PHARMACOTHERAPY
ISSN0753-3322
卷号118
发表状态已发表
DOI10.1016/j.biopha.2019.109232
摘要Triptolide(T9) is a predominant bioactive component extracted from Chinese herb Tripterygium wilfordii Hook F. (TwHF), and has multiple pharmacological activities, such as immunosuppressive and anti-inflammatory activities, et al. However, severe adverse effects and toxicity, particularly nephrotoxicity, limit its clinical application. It has been demonstrated that the activation of nuclear factor erythroid 2-related factor 2 (Nrf2) signaling pathway could alleviate T9-induced nephrocyte damage. The aim of this study was to investigate the potential protective role of triptriolide (T11) against T9-induced nephrocyte apoptosis in vitro and in vivo. Renal injury models were established in human kidney 2 (HK2) cells and BALB/c mice using T9, and the protective effects of T11 were probed in vitro and in vivo, respectively. T9 induced nephrocyte damage in HK2 cells and BALB/c mice by induction of reactive oxygen species (ROS), lactate dehydrogenase (LDH), malondialdehyde (MDA) and glutathione (GSH) and reduction of superoxide dismutase (SOD), which resulted in the apoptosis of nephrocyte and injury of renal function. While, pretreatment of T11 effectively reversed these changes, resulting in the obvious decrease of oxidative stress and renal function parameters, ameliorated nephrocyte apoptosis, improved cell morphology, and higher increase of Nrf2, NAD(P)H: quinine oxidoreductase 1 (NQO1) and heme oxygenase 1 (HO-1) protein levels in vitro and in vivo. Altogether, T11 protected against T9-induced nephrocyte apoptosis possibly via suppressing oxidative stress.
关键词Triptriolide Triptolide Oxidative stress Apoptosis Nrf2 pathway
URL查看原文
收录类别SCI ; SCIE
语种英语
资助项目Key Project of First-class University Construction of Guangzhou University of Chinese Medicine[XK2018019] ; Key Project of First-class University Construction of Guangzhou University of Chinese Medicine[XK2019023]
WOS研究方向Research & Experimental Medicine ; Pharmacology & Pharmacy
WOS类目Medicine, Research & Experimental ; Pharmacology & Pharmacy
WOS记录号WOS:000486395000034
出版者ELSEVIER FRANCE-EDITIONS SCIENTIFIQUES MEDICALES ELSEVIER
WOS关键词KIDNEY INJURY ; NRF2 ; ANTIOXIDANT ; PROTECTION ; FIBROSIS ; PATHWAY ; SYSTEM ; TARGET
原始文献类型Article
引用统计
文献类型期刊论文
条目标识符https://kms.shanghaitech.edu.cn/handle/2MSLDSTB/80221
专题免疫化学研究所_特聘教授组_抗体设计学实验室
通讯作者Xu, Peng; Xu, Hong-tao; Liu, Bo
作者单位
1.Guangzhou Univ Chinese Med, Clin Med Coll 2, Guangzhou 510006, Guangdong, Peoples R China
2.Guangzhou Univ Chinese Med, Guangdong Prov Key Lab Clin Res Tradit Chinese Me, Guangzhou 510006, Guangdong, Peoples R China
3.Guangdong Prov Acad Chinese Med Sci, Guangzhou 510006, Guangdong, Peoples R China
4.Guangzhou Univ Chinese Med, Guangdong Prov Key Lab Chinese Med Prevent & Trea, Guangzhou 510006, Guangdong, Peoples R China
5.ShanghaiTech Univ, Shanghai Inst Adv Immunochem Studies, Shanghai 201210, Peoples R China
通讯作者单位免疫化学研究所
推荐引用方式
GB/T 7714
Wang, Xiao-wan,Tian, Rui-min,Yang, Yi-qi,et al. Triptriolide antagonizes triptolide-induced nephrocyte apoptosis via inhibiting oxidative stress in vitro and in vivo[J]. BIOMEDICINE & PHARMACOTHERAPY,2019,118.
APA Wang, Xiao-wan.,Tian, Rui-min.,Yang, Yi-qi.,Lu, Zhao-Yu.,Han, Xiao-dong.,...&Liu, Bo.(2019).Triptriolide antagonizes triptolide-induced nephrocyte apoptosis via inhibiting oxidative stress in vitro and in vivo.BIOMEDICINE & PHARMACOTHERAPY,118.
MLA Wang, Xiao-wan,et al."Triptriolide antagonizes triptolide-induced nephrocyte apoptosis via inhibiting oxidative stress in vitro and in vivo".BIOMEDICINE & PHARMACOTHERAPY 118(2019).
条目包含的文件 下载所有文件
文件名称/大小 文献类型 版本类型 开放类型 使用许可
个性服务
查看访问统计
谷歌学术
谷歌学术中相似的文章
[Wang, Xiao-wan]的文章
[Tian, Rui-min]的文章
[Yang, Yi-qi]的文章
百度学术
百度学术中相似的文章
[Wang, Xiao-wan]的文章
[Tian, Rui-min]的文章
[Yang, Yi-qi]的文章
必应学术
必应学术中相似的文章
[Wang, Xiao-wan]的文章
[Tian, Rui-min]的文章
[Yang, Yi-qi]的文章
相关权益政策
暂无数据
收藏/分享
文件名: 10.1016@j.biopha.2019.109232.pdf
格式: Adobe PDF
所有评论 (0)
暂无评论
 

除非特别说明,本系统中所有内容都受版权保护,并保留所有权利。