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Notoginsenoside R1 ameliorates mitochondrial dysfunction to circumvent neuronal energy failure in acute phase of focal cerebral ischemia
Liu, Bowen1; Zhao, Tingting2; Li, Yiyang1; Han, Yan1; Xu, Youhua2; Yang, Hua3; Wang, Shengpeng1; Zhao, Yonghua1; Li, Ping3; Wang, Yitao1
2022-04-13
Source PublicationPhytotherapy Research
ISSN0951-418X
Volume36Issue:5Pages:2223-2235
Abstract

Due to sudden loss of cerebral blood circulation, acute ischemic stroke (IS) causes neuronal energy attenuation or even exhaustion by mitochondrial dysfunction resulting in aggravation of neurological injury. In this study, we investigated if Notoginsenoside R1 ameliorated cerebral energy metabolism by limiting neuronal mitochondrial dysfunction in acute IS. Male Sprague–Dawley rats (260–280 g) were selected and performed by permanent middle cerebral artery occlusion model. In vitro, the oxygen glucose deprivation (OGD) model of Neuro2a (N2a) cells was established. We found Notoginsenoside R1 treatment reduced rats' cerebral infarct volume and neurological deficits, with increased Adenosine triphosphate (ATP) level together with upregulated expression of glucose transporter 1/3, monocarboxylate transporter 1 and citrate synthase in brain peri-ischemic tissue. In vitro, OGD-induced N2a cell death was inhibited, cell mitochondrial morphology was improved. Mitochondrial amount, mitochondrial membrane potential, and mitochondrial DNA copy number were increased by Notoginsenoside R1 administration. Furthermore, mitochondrial energy metabolism-related mRNA array found Atp12a and Atp6v1g3 gene expression were upregulated more than twofold, which were also verified in rat ischemic tissue by quantitative polymerase chain reaction (qPCR) assay. Therefore, Notoginsenoside R1 administration increases cerebral glucose and lactate transportation and ATP levels, ameliorates neuronal mitochondrial function after IS. Notoginsenoside R1 may be a novel protective agent for neuronal mitochondria poststroke.

KeywordEnergy Metabolism Ischemic Stroke Mitochondrial Dysfunction Neuroprotection Notoginsenoside R1
DOI10.1002/ptr.7450
URLView the original
Indexed BySCIE
Language英語English
WOS Research AreaPharmacology & Pharmacy
WOS SubjectChemistry, Medicinal ; Pharmacology & Pharmacy
WOS IDWOS:000782285600001
Scopus ID2-s2.0-85128186672
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Document TypeJournal article
CollectionInstitute of Chinese Medical Sciences
Corresponding AuthorZhao, Yonghua; Wang, Yitao
Affiliation1.Institute of Chinese Medical Sciences, State Key Laboratory of Quality Research in Chinese Medicine, University of Macau, Macao
2.Faculty of Chinese Medicine, Macau University of Science and Technology, Macao
3.State Key Laboratory of Natural Medicines, School of Traditional Chinese Pharmacy, China Pharmaceutical University, Nanjing, China
First Author AffilicationInstitute of Chinese Medical Sciences
Corresponding Author AffilicationInstitute of Chinese Medical Sciences
Recommended Citation
GB/T 7714
Liu, Bowen,Zhao, Tingting,Li, Yiyang,et al. Notoginsenoside R1 ameliorates mitochondrial dysfunction to circumvent neuronal energy failure in acute phase of focal cerebral ischemia[J]. Phytotherapy Research,2022,36(5):2223-2235.
APA Liu, Bowen,Zhao, Tingting,Li, Yiyang,Han, Yan,Xu, Youhua,Yang, Hua,Wang, Shengpeng,Zhao, Yonghua,Li, Ping,&Wang, Yitao.(2022).Notoginsenoside R1 ameliorates mitochondrial dysfunction to circumvent neuronal energy failure in acute phase of focal cerebral ischemia.Phytotherapy Research,36(5),2223-2235.
MLA Liu, Bowen,et al."Notoginsenoside R1 ameliorates mitochondrial dysfunction to circumvent neuronal energy failure in acute phase of focal cerebral ischemia".Phytotherapy Research 36.5(2022):2223-2235.
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