title: Protective effect of astragaloside on focal cerebral ischemia/reperfusion injury in rats.
abstract: This study was to observe the neurological protective effects of astragalosides (AST) on focal cerebral ischemia-reperfusion (I/R) injury in rats and to explore its possible mechanism. Male SD rats received right middle cerebral artery occlusion for 120 min and AST (40 mg/kg) was orally administered. The rats were decapitated 1, 3, 7, and 14 days after reperfusion. The neurological deficit score, infarct volume and water content of brain were measured; the activity of superoxide dismutase (SOD), lactate dehydrogenase (LDH) and nitric oxide synthase (NOS), and the content of malondialdehyde (MDA), lactate (LD) and nitric oxide (NO) of brain tissue were detected too. The expression of inducible nitric synthase (iNOS), nerve growth factor (NGF) and tropomyosin receptor kinase A (TrkA) mRNA were measured by RT-PCR or real-time PCR. AST could significantly reduce the neurological deficit score; infract volume and water content, increase SOD and LDH activities, decrease NOS activity and MDA, LD and NO content. AST treatment could down-regulate expression of iNOS mRNA, while, NGF and TrkA mRNA were up-regulated. Our data suggest that AST have the protective effects on focal cerebral ischemia in rats at the different reperfusion time points, the mechanism may be related to the antioxidation, regulated the expressions of iNOS, NGF and TrkA mRNA.
authors.affiliation: Department of Pharmacology, Anhui Medical University, HeFei, China. yinyanyan5678@126.com
authors.forename: Yan-Yan
authors.initials: YY
authors.lastname: Yin
authors.forename: Wei-Ping
authors.initials: WP
authors.lastname: Li
authors.forename: Hui-Ling
authors.initials: HL
authors.lastname: Gong
authors.forename: Fen-Fang
authors.initials: FF
authors.lastname: Zhu
authors.forename: Wei-Zu
authors.initials: WZ
authors.lastname: Li
authors.forename: Guo-Cui
authors.initials: GC
authors.lastname: Wu
mesh_terms: D000818:Animals; D001921:Brain / Q000187:drug effects / Q000378:metabolism / Q000473:pathology; D002545:Brain Ischemia / Q000150:complications; D002544:Cerebral Infarction / Q000209:etiology / Q000517:prevention & control; D004365:Drugs, Chinese Herbal / Q000494:pharmacology; D020244:Infarction, Middle Cerebral Artery / Q000150:complications; D007770:L-Lactate Dehydrogenase / Q000378:metabolism; D007773:Lactates / Q000378:metabolism; D008297:Male; D008315:Malondialdehyde / Q000378:metabolism; D020932:Nerve Growth Factor / Q000235:genetics; D018696:Neuroprotective Agents / Q000494:pharmacology*; D009569:Nitric Oxide / Q000378:metabolism; D052247:Nitric Oxide Synthase Type II / Q000235:genetics; D051381:Rats; D017207:Rats, Sprague-Dawley; D020917:Receptor, trkA / Q000235:genetics; D015427:Reperfusion Injury / Q000209:etiology / Q000517:prevention & control*; D020133:Reverse Transcriptase Polymerase Chain Reaction; D012503:Saponins / Q000494:pharmacology*; D013482:Superoxide Dismutase / Q000378:metabolism; D013997:Time Factors; D014315:Triterpenes / Q000494:pharmacology*; D014867:Water / Q000378:metabolism
chemical_list: D004365:Drugs, Chinese Herbal; D007773:Lactates; D018696:Neuroprotective Agents; D012503:Saponins; D014315:Triterpenes; D014867:Water; D009569:Nitric Oxide; C052064:astragaloside A; D008315:Malondialdehyde; D020932:Nerve Growth Factor; D007770:L-Lactate Dehydrogenase; D052247:Nitric Oxide Synthase Type II; D013482:Superoxide Dismutase; D020917:Receptor, trkA