title: Antioxidant effect of salvianolic acid B on hippocampal CA1 neurons in mice with cerebral ischemia and reperfusion injury.
abstract: OBJECTIVE
  To investigate the neuroprotective effects and underlying mechanisms of salvianolic acid B (Sal B) extracted from Salvia miltiorrhiza on hippocampal CA1 neurons in mice with cerebral ischemia reperfusion injury.
  
  
  METHODS
  Forty male National Institute of Health (NIH) mice were randomly divided into 4 groups with 10 animals each, including the sham group, the model group, the SalB group (SalB 22.5 mg/kg) and the nimodipine (Nim) group (Nim 1 mg/kg). A mouse model of cerebral ischemia and reperfusion injury was established by bilateral carotid artery occlusion for 30 min followed by 24-h reperfusion. The malondialdehyde (MDA) content, the nitric oxide synthase (NOS) activity, the superoxide dismutase (SOD) activity and total antioxidant capability (T-AOC) of the pallium were determined by biochemistry methods. The morphologic changes and Bcl-2 and Bax protein expression in hippocampal CA1 neurons were observed by using hematoxylineosin staining and immunohistochemistry staining, respectively.
  
  
  RESULTS
  In the SalB group, the MDA content and the NOS activity of the pallium in cerebral ischemia-reperfusion mice significantly decreased and the SOD activity and the T-AOC significantly increased, as compared with the model group (P<0.05 or P<0.01). The SalB treatment also rescued neuronal loss (P<0.01) in the hippocampal CA1 region, strongly promoted Bcl-2 protein expression (P<0.01) and inhibited Bax protein expression (P<0.05).
  
  
  CONCLUSIONS
  SalB increases the level of antioxidant substances and decreases free radicals production. Moreover, it also improves Bcl-2 expression and reduces Bax expression. SalB may exert the neuroprotective effect through mitochondria-dependent pathway on hippocampal CA1 neurons in mice with cerebral ischemia and reperfusion injury and suggested that SalB represents a promising candidate for the prevention and treatment of ischemic cerebrovascular disease.
authors.affiliation: Department of Pathology, Beijing University of Chinese Medicine, Beijing, 100029, China, jiangyf66@aliyun.com.
authors.forename: Yu-feng
authors.initials: YF
authors.lastname: Jiang
authors.forename: Zhi-qin
authors.initials: ZQ
authors.lastname: Liu
authors.forename: Wei
authors.initials: W
authors.lastname: Cui
authors.forename: Wen-tong
authors.initials: WT
authors.lastname: Zhang
authors.forename: Jia-pei
authors.initials: JP
authors.lastname: Gong
authors.forename: Xi-mei
authors.initials: XM
authors.lastname: Wang
authors.forename: Ying
authors.initials: Y
authors.lastname: Zhang
authors.forename: Mei-juan
authors.initials: MJ
authors.lastname: Yang
mesh_terms: D000818:Animals; D000975:Antioxidants / Q000494:pharmacology / Q000627:therapeutic use*; D001572:Benzofurans / Q000737:chemistry / Q000494:pharmacology / Q000627:therapeutic use*; D002545:Brain Ischemia / Q000150:complications / Q000188:drug therapy*; D056547:CA1 Region, Hippocampal / Q000473:pathology*; D002452:Cell Count; D007150:Immunohistochemistry; D008297:Male; D008315:Malondialdehyde / Q000378:metabolism; D051379:Mice; D009474:Neurons / Q000187:drug effects / Q000473:pathology*; D019001:Nitric Oxide Synthase / Q000378:metabolism; D015427:Reperfusion Injury / Q000150:complications / Q000188:drug therapy*; D013482:Superoxide Dismutase / Q000378:metabolism; D051028:bcl-2-Associated X Protein / Q000378:metabolism; D053630:Depsides
chemical_list: D000975:Antioxidants; D001572:Benzofurans; D008315:Malondialdehyde; D019001:Nitric Oxide Synthase; D013482:Superoxide Dismutase; D051028:bcl-2-Associated X Protein; C076944:salvianolic acid B; D053630:Depsides
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