title: [Tripotolide ameliorates inflammation and apoptosis induced by focal cerebral ischemia/reperfusion in rats].
abstract: Objective:To investigate the effects of triptolide on inflammation and apoptosis induced by focal cerebral ischemia/reperfusion in rats.Methods:The rat model of focal cerebral ischemia/reperfusion injury was established according to Longa's method. A total of 80 SD rats were randomly divided into 5 groups:normal control, sham group, DMSO group, middle cerebral artery occlusion (MCAO) group, and MCAO with tripolide treatment group. TTC staining was used to examine the site and volume of cerebral infarction, and Longa score was employed for neurological disorders measurement. Number of astrocytes was measured by fluorescence staining, and neuronal apoptosis was determined by TUNEL staining. The expressions of inducible nitric oxide synthase(iNOS), cyclooxygenase 2(COX-2) and NF-κB proteins were detected by immunohistochemistry, and the expression of iNOS, COX-2 mRNA was detected by real-time PCR.Results:Compared with DMSO group and MCAO group, brain edema was improved (80.03±0.46)% (P<0.05), infarct volume was reduced (8.3±1.4)% (P<0.01), Longa score was decreased (1.38±0.20,P<0.05) in triptolide treatment group. Meanwhile triptolide also dramatically reduced the number of GFAP-positive astrocytes (P<0.05), alleviated protein expression of COX-2 (91.67±1.31), iNOS (95.24±5.07) and NF-κB (75.03±2.06) triggered by MCAO (allP<0.05), and induced a down-regulation of cell apoptosis as showed by TUNEL assay (64.15±3.52,P<0.05).Conclusion:Triptolide can reduce the cerebral infarction volume, attenuate brain edema and ameliorate the neurological deficits induced by cerebral ischemia-reperfusion injury rats, indicating that it might be used as a potential anti-inflammatory agent.
authors.affiliation: School of Medicine, Taizhou University, Taizhou 318000, China; Institute of Neuroscience, Zhejiang University School of Medicine, Hangzhou 310058, China.
authors.forename: Shi
authors.initials: S
authors.lastname: Bai
authors.affiliation: Institute of Neuroscience, Zhejiang University School of Medicine, Hangzhou 310058, China.
authors.forename: Yayi
authors.initials: Y
authors.lastname: Sun
authors.affiliation: School of Medicine, Taizhou University, Taizhou 318000, China.
authors.forename: Lijuan
authors.initials: L
authors.lastname: Wu
authors.affiliation: School of Medicine, Taizhou University, Taizhou 318000, China.
authors.forename: Zhongmin
authors.initials: Z
authors.lastname: Wu
authors.affiliation: Institute of Neuroscience, Zhejiang University School of Medicine, Hangzhou 310058, China. fangmaro@zju.edu.cn.
authors.forename: Marong
authors.initials: M
authors.lastname: Fang
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000187:drug effects*; D001253:Astrocytes; D001929:Brain Edema / Q000188:drug therapy; D001930:Brain Injuries / Q000139:chemically induced / Q000188:drug therapy; D002545:Brain Ischemia / Q000139:chemically induced; D051546:Cyclooxygenase 2 / Q000187:drug effects; D004224:Diterpenes / Q000494:pharmacology*; D015536:Down-Regulation / Q000187:drug effects; D004852:Epoxy Compounds / Q000494:pharmacology; D020244:Infarction, Middle Cerebral Artery / Q000139:chemically induced / Q000188:drug therapy*; D007249:Inflammation / Q000188:drug therapy*; D008297:Male; D016328:NF-kappa B / Q000187:drug effects; D052247:Nitric Oxide Synthase Type II / Q000187:drug effects; D010616:Phenanthrenes / Q000494:pharmacology*; D051381:Rats; D017207:Rats, Sprague-Dawley; D015427:Reperfusion Injury / Q000139:chemically induced / Q000188:drug therapy
chemical_list: D004224:Diterpenes; D004852:Epoxy Compounds; D016328:NF-kappa B; D010616:Phenanthrenes; C001899:triptolide; C496319:NOS2 protein, human; D052247:Nitric Oxide Synthase Type II; D051546:Cyclooxygenase 2