title: Neuroprotective effect of sophocarpine against transient focal cerebral ischemia via down-regulation of the acid-sensing ion channel 1 in rats.
abstract: Sophocarpine, one of the major alkaloid compounds isolated from Sophora pachycarpa, is highly valued and important in traditional Chinese medicine. In the present study, we aimed to explore the possible mechanisms underlying sophocarpine-mediated neuroprotection against transient focal cerebral ischemia. Sophocarpine (5, 10, or 20mg/kg) was given 30min before focal ischemia was induced in rats by occlusion of the middle cerebral artery. After sophocarpine treatment, the total infarct volume was significantly decreased in comparison to the ischemia-reperfusion values. The results of a neurological evaluation were significantly improved in the sophocarpine treated group when compared to controls. The number of TUNEL-positive cells was significantly reduced compared to the untreated ischemic group. Results of Western blotting and immunohistochemical staining indicated that pretreatment with sophocarpine down-regulated the expression of acid-sensing ion channel 1 (ASIC1) in the ischemic cortex. These results suggest that sophocarpine ameliorated the ischemic injury induced by transient focal cerebral ischemia in rats and that this neuroprotective effect might be related to the anti-ASIC1 channel and anti-apoptotic action of sophocarpine.
authors.affiliation: Neuroscience Center, Nanjing Medical University, Affiliated Wuxi No. 2 Hospital, Wuxi 214002, China.
authors.forename: Miao
authors.initials: M
authors.lastname: Yifeng
authors.forename: Wu
authors.initials: W
authors.lastname: Bin
authors.forename: Zhang
authors.initials: Z
authors.lastname: Weiqiao
authors.forename: Qiu
authors.initials: Q
authors.lastname: Yongming
authors.forename: Li
authors.initials: L
authors.lastname: Bing
authors.forename: Lu
authors.initials: L
authors.lastname: Xiaojie
mesh_terms: D062565:Acid Sensing Ion Channels; D000470:Alkaloids / Q000494:pharmacology* / Q000627:therapeutic use; D000818:Animals; D017209:Apoptosis / Q000187:drug effects / Q000502:physiology; D020520:Brain Infarction / Q000188:drug therapy* / Q000378:metabolism / Q000473:pathology; D002545:Brain Ischemia / Q000188:drug therapy* / Q000378:metabolism / Q000473:pathology; D004195:Disease Models, Animal; D015536:Down-Regulation / Q000187:drug effects* / Q000502:physiology; D020244:Infarction, Middle Cerebral Artery / Q000188:drug therapy / Q000378:metabolism / Q000473:pathology; D008297:Male; D009419:Nerve Tissue Proteins / Q000037:antagonists & inhibitors* / Q000096:biosynthesis; D018696:Neuroprotective Agents / Q000494:pharmacology* / Q000627:therapeutic use; D051381:Rats; D017207:Rats, Sprague-Dawley; D015222:Sodium Channels / Q000096:biosynthesis; D016896:Treatment Outcome; D000093842:Matrines
chemical_list: D062565:Acid Sensing Ion Channels; D000470:Alkaloids; D009419:Nerve Tissue Proteins; D018696:Neuroprotective Agents; D015222:Sodium Channels; C568268:Asic1 protein, rat; C035933:sophocarpine; D000093842:Matrines