Ginsenoside Rg1 protects against transient focal cerebral ischemic injury and suppresses its systemic metabolic changes in cerabral injury rats.
10.1016/j.apsb.2015.02.001
- Author:
Mingbao LIN
1
;
Wei SUN
2
;
Wan GONG
3
;
Yasi DING
1
;
Yuanyan ZHUANG
1
;
Qi HOU
1
Author Information
1. State 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, China.
2. Clinical Laboratory Center, Beijing Friendship Hospital, Capital Medical University, Beijing 100050, China.
3. College of Basic Medical Science, Zhejiang Chinese Medical University, Hangzhou 310053, China.
- Publication Type:Journal Article
- Keywords:
Biomarkers;
Ginsenoside Rg1;
MCAO;
Metabolites
- From:
Acta Pharmaceutica Sinica B
2015;5(3):277-284
- CountryChina
- Language:English
-
Abstract:
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.
