title: Osthole attenuates focal inflammatory reaction following permanent middle cerebral artery occlusion in rats.
abstract: Osthole, a main active constituent from Cnidium monnieri (L.) CUSSON, has been considered therapeutic agent in the treatment of ischemic stroke. This study was designed to investigate the effect of osthole on permanent middle cerebral artery occlusion (MCAO) in rats. Osthole was administrated by gavage to the normal and the MCAO rats. Rats were assessed for neurological deficit after 24 h following MCAO, then their brains were evaluated to determine the infarct area, and the mRNA and protein levels of some inflammatory factors were detected. It was found that MCAO animals pre-treated with osthole for 7 d showed significant improvement in all neurological tests compared with vehicle-treated MCAO groups. In addition, there was a significant decrease in infarct volume 24 h after occlusion in animals pre-treated with osthole versus the vehicle-treated MCAO group. MCAO also dramatically caused some inflammatory factors increase. However, pretreatment with osthole restored the mRNA and protein levels of these factors, including tumor necrosis factor-alpha (TNF-α), interleukin-1 beta (IL-1β), cyclooxygenase-2 (COX-2), inducible nitric oxide synthase (iNOS) of ischemic penumbra cortices, suggesting that osthole possessed the function of preventing brain against ischemic damage, while no significant difference was found in any of normal groups with or without osthole. The present study demonstrated that osthole may be a novel neuroprotective therapy in the treatment of focal ischemic stroke.
authors.affiliation: School of Chinese Materia Medica, Shanghai University of Traditional Chinese Medicine, Shanghai 201203, China.
authors.forename: Fei
authors.initials: F
authors.lastname: Li
authors.forename: Qihai
authors.initials: Q
authors.lastname: Gong
authors.forename: Lina
authors.initials: L
authors.lastname: Wang
authors.forename: Jingshan
authors.initials: J
authors.lastname: Shi
mesh_terms: D000818:Animals; D000893:Anti-Inflammatory Agents / Q000494:pharmacology*; D002540:Cerebral Cortex / Q000187:drug effects / Q000378:metabolism; D003374:Coumarins / Q000494:pharmacology*; D051546:Cyclooxygenase 2 / Q000235:genetics; D020244:Infarction, Middle Cerebral Artery / Q000378:metabolism* / Q000473:pathology; D053583:Interleukin-1beta / Q000235:genetics; D008297:Male; D018696:Neuroprotective Agents / Q000494:pharmacology*; D052247:Nitric Oxide Synthase Type II / Q000235:genetics; D012333:RNA, Messenger / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D014409:Tumor Necrosis Factor-alpha / Q000235:genetics
chemical_list: D000893:Anti-Inflammatory Agents; D003374:Coumarins; D053583:Interleukin-1beta; D018696:Neuroprotective Agents; D012333:RNA, Messenger; D014409:Tumor Necrosis Factor-alpha; D052247:Nitric Oxide Synthase Type II; C496318:Nos2 protein, rat; D051546:Cyclooxygenase 2; C489691:Ptgs2 protein, rat; C046627:osthol