Triptriolide antagonizes triptolide-induced nephrocyte apoptosis via inhibiting oxidative stress in vitro and in vivo

doi:10.1016/j.biopha.2019.109232

KMS > 免疫化学研究所 > 特聘教授组 > Richard A. Lerner组

	Triptriolide antagonizes triptolide-induced nephrocyte apoptosis via inhibiting oxidative stress in vitro and in vivo
	Wang, Xiao-wan 1,2; Tian, Rui-min 1,2,3; Yang, Yi-qi 1,2; Lu, Zhao-Yu 1,2,3; Han, Xiao-dong 1,2,3; Liu, Xu-sheng 1,2,3; Mao, Wei 1,2,3; Xu, Peng 1,3,4; Xu, Hong-tao5 ; Liu, Bo 1,2,3
	2019-10
发表期刊	BIOMEDICINE & PHARMACOTHERAPY
ISSN	0753-3322
卷号	118
发表状态	已发表
DOI	10.1016/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).