中国科学院机构知识库网格
Chinese Academy of Sciences Institutional Repositories Grid
Notoginsenoside R1 attenuates sevoflurane-induced neurotoxicity

文献类型:期刊论文

作者Zhang, Yibing1; Zhao, Yong2; Ran, Yongwang3; Guo, Jianyou5; Cui, Haifeng2; Liu, Sha4
刊名TRANSLATIONAL NEUROSCIENCE
出版日期2020
卷号11期号:1页码:215-226
关键词5 '-AMP-activated protein kinase neurotoxicity notoginsenoside R1 sevoflurane sestrin-2 reactive oxygen species
ISSN号2081-3856
DOI10.1515/tnsci-2020-0118
通讯作者Liu, Sha(JulietteHaydengsx@yahoo.com)
英文摘要Background - Sevoflurane, a volatile anesthetic, is known to induce widespread neuronal degeneration and apoptosis. Recently, the stress-inducible protein sestrin 2 and adenosine monophosphate-activated protein kinase (AMPK) have been found to regulate the levels of intracellular reactive oxygen species (ROS) and suppress oxidative stress. Notoginsenoside R1 (NGR1), a saponin isolated from Panax notoginseng, has been shown to exert neuroprotective effects. The effects of NGR1 against neurotoxicity induced by sevoflurane were assessed. Methods - Sprague-Dawley rat pups on postnatal day 7 (PD7) were exposed to sevoflurane (3%) anesthesia for 6 h. NGR1 at doses of 12.5, 25, or 50 mg/kg body weight was orally administered to pups from PD2 to PD7. Results - Pretreatment with NGR1 attenuated sevoflurane-induced generation of ROS and reduced apoptotic cell counts. Western blotting revealed decreased cleaved caspase 3 and Bad and Box pro-apoptotic protein expression. NGR1 substantially upregulated nuclear factor erythroid 2-related factor 2 (Nrf2) expression along with increased heme oxygenase-1 (HO-1) and NAD(P)H quinone oxidoreductase1 levels, suggesting Nrf2 signaling activation. Enhanced sestrin-2 and phosphorylated AMPK expression were noticed following NGR1 pretreatment. Conclusion - This study revealed the neuroprotective effects of NGR1 through effective suppression of apoptosis and ROS via regulation of apoptotic proteins and activation of Nrf2/HO-1 and sestrin 2/AMPK signaling cascades.
WOS关键词INDUCED OXIDATIVE STRESS ; PANAX-NOTOGINSENG ; INDUCED NEUROAPOPTOSIS ; SIGNALING PATHWAY ; ANTIOXIDANT ; ACTIVATION ; ISOFLURANE ; EXPOSURE ; SESTRINS ; BRAIN
WOS研究方向Neurosciences & Neurology
语种英语
WOS记录号WOS:000543768900001
出版者SCIENDO
源URL[http://ir.psych.ac.cn/handle/311026/32135]  
专题心理研究所_健康与遗传心理学研究室
通讯作者Liu, Sha
作者单位1.Chongqing Med Univ, Sch Tradit Chinese Med, Comprehens Teaching & Res Off Tradit Chinese Med, Chongqing 401331, Peoples R China
2.China Acad Tradit Chinese Med, Inst Chinese Mat Med, GLP Lab, Beijing 100700, Peoples R China
3.Qianjiang Cent Hosp Chongqing, Dept Radiol, Chongqing 409099, Peoples R China
4.Chongqing Med Univ, Sch Tradit Chinese Med, Chongqing 401331, Peoples R China
5.Chinese Acad Sci, Inst Psychol, Beijing 100101, Peoples R China
推荐引用方式
GB/T 7714
Zhang, Yibing,Zhao, Yong,Ran, Yongwang,et al. Notoginsenoside R1 attenuates sevoflurane-induced neurotoxicity[J]. TRANSLATIONAL NEUROSCIENCE,2020,11(1):215-226.
APA Zhang, Yibing,Zhao, Yong,Ran, Yongwang,Guo, Jianyou,Cui, Haifeng,&Liu, Sha.(2020).Notoginsenoside R1 attenuates sevoflurane-induced neurotoxicity.TRANSLATIONAL NEUROSCIENCE,11(1),215-226.
MLA Zhang, Yibing,et al."Notoginsenoside R1 attenuates sevoflurane-induced neurotoxicity".TRANSLATIONAL NEUROSCIENCE 11.1(2020):215-226.

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来源:心理研究所

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