Ginsenoside Rg1 protects against transient focal cerebral ischemic injury and suppresses its systemic metabolic changes in cerabral injury rats

Ginsenoside Rg1 (GR), a major bioactive compound of traditional Chinese medicine, such as Panax ginseng or Radix Notoginseng, has been shown to exert neuroprotective effects against ischemic stroke. However, pharmacokinetic studies have suggested that GR could not be efficiently transported through...

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Main Authors: Mingbao Lin, Wei Sun, Wan Gong, Yasi Ding, Yuanyan Zhuang, Qi Hou
Format: Article
Language:English
Published: Elsevier 2015-05-01
Series:Acta Pharmaceutica Sinica B
Subjects:
Online Access:http://www.sciencedirect.com/science/article/pii/S221138351500026X
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author Mingbao Lin
Wei Sun
Wan Gong
Yasi Ding
Yuanyan Zhuang
Qi Hou
author_facet Mingbao Lin
Wei Sun
Wan Gong
Yasi Ding
Yuanyan Zhuang
Qi Hou
author_sort Mingbao Lin
collection DOAJ
description Ginsenoside Rg1 (GR), a major bioactive compound of traditional Chinese medicine, such as Panax ginseng or Radix Notoginseng, has been shown to exert neuroprotective effects against ischemic stroke. However, pharmacokinetic studies have suggested that GR could not be efficiently transported through the blood–brain barrier. The mechanism by which GR attenuates cerebral ischemic injury in vivo remains largely unknown. Therefore, this study explored potential neuro-protective effects of GR through its systemic metabolic regulating mechanism by using mass spectrometry–based metabolomic profiling. Rats with middle cerebral artery occlusion (MCAO) were treated with GR intravenously. Their metabolic profiles in serum were measured by gas chromatography coupled with mass spectrometry on 1 and 3 days after MCAO. GR exhibited a potent neuro-protective effect by significantly decreasing the neurological scores and infarct volume in the MCAO rats. Moreover, 18 differential metabolites were tentatively identified, all of which appeared to correlate well with these disease indices. Our findings suggested that GR carries a therapeutic potential in stroke possibly through a feed-back mechanism by regulating systematic metabolic mediation.
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spelling doaj.art-ac4f49eb61ce43eea676efa3ff959bfc2022-12-22T03:06:57ZengElsevierActa Pharmaceutica Sinica B2211-38352211-38432015-05-015327728410.1016/j.apsb.2015.02.001Ginsenoside Rg1 protects against transient focal cerebral ischemic injury and suppresses its systemic metabolic changes in cerabral injury ratsMingbao Lin0Wei Sun1Wan Gong2Yasi Ding3Yuanyan Zhuang4Qi Hou5State Key Laboratory of Bioactive Substance and Function of Natural Medicines, Institute of Materia Medica, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing 100050, ChinaClinical Laboratory Center, Beijing Friendship Hospital, Capital Medical University, Beijing 100050, ChinaCollege of Basic Medical Science, Zhejiang Chinese Medical University, Hangzhou 310053, ChinaState Key Laboratory of Bioactive Substance and Function of Natural Medicines, Institute of Materia Medica, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing 100050, ChinaState Key Laboratory of Bioactive Substance and Function of Natural Medicines, Institute of Materia Medica, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing 100050, ChinaState Key Laboratory of Bioactive Substance and Function of Natural Medicines, Institute of Materia Medica, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing 100050, ChinaGinsenoside Rg1 (GR), a major bioactive compound of traditional Chinese medicine, such as Panax ginseng or Radix Notoginseng, has been shown to exert neuroprotective effects against ischemic stroke. However, pharmacokinetic studies have suggested that GR could not be efficiently transported through the blood–brain barrier. The mechanism by which GR attenuates cerebral ischemic injury in vivo remains largely unknown. Therefore, this study explored potential neuro-protective effects of GR through its systemic metabolic regulating mechanism by using mass spectrometry–based metabolomic profiling. Rats with middle cerebral artery occlusion (MCAO) were treated with GR intravenously. Their metabolic profiles in serum were measured by gas chromatography coupled with mass spectrometry on 1 and 3 days after MCAO. GR exhibited a potent neuro-protective effect by significantly decreasing the neurological scores and infarct volume in the MCAO rats. Moreover, 18 differential metabolites were tentatively identified, all of which appeared to correlate well with these disease indices. Our findings suggested that GR carries a therapeutic potential in stroke possibly through a feed-back mechanism by regulating systematic metabolic mediation.http://www.sciencedirect.com/science/article/pii/S221138351500026XGinsenoside Rg1MCAOMetabolitesBiomarkers
spellingShingle Mingbao Lin
Wei Sun
Wan Gong
Yasi Ding
Yuanyan Zhuang
Qi Hou
Ginsenoside Rg1 protects against transient focal cerebral ischemic injury and suppresses its systemic metabolic changes in cerabral injury rats
Acta Pharmaceutica Sinica B
Ginsenoside Rg1
MCAO
Metabolites
Biomarkers
title Ginsenoside Rg1 protects against transient focal cerebral ischemic injury and suppresses its systemic metabolic changes in cerabral injury rats
title_full Ginsenoside Rg1 protects against transient focal cerebral ischemic injury and suppresses its systemic metabolic changes in cerabral injury rats
title_fullStr Ginsenoside Rg1 protects against transient focal cerebral ischemic injury and suppresses its systemic metabolic changes in cerabral injury rats
title_full_unstemmed Ginsenoside Rg1 protects against transient focal cerebral ischemic injury and suppresses its systemic metabolic changes in cerabral injury rats
title_short Ginsenoside Rg1 protects against transient focal cerebral ischemic injury and suppresses its systemic metabolic changes in cerabral injury rats
title_sort ginsenoside rg1 protects against transient focal cerebral ischemic injury and suppresses its systemic metabolic changes in cerabral injury rats
topic Ginsenoside Rg1
MCAO
Metabolites
Biomarkers
url http://www.sciencedirect.com/science/article/pii/S221138351500026X
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