Oxymatrine protects rat brains against permanent focal ischemia and downregulates NF-kappaB expression.
BACKGROUND
Oxymatrine is proven to protect ischemic and reperfusion injury in liver, intestine and heart, this effect is via anti-inflammation and anti-apoptosis. Whether this protective effect applies to ischemic injury in brain, we therefore investigate the potential neuroprotective role of oxymatrine and the underlying mechanisms.


METHODS
Male, Sprague-Dawley rats were randomly assigned to four groups: permanent middle cerebral artery occlusion (pMCAO), high dose (pMCAO+oxymatrine 120 mg/kg), low dose (pMCAO+oxymatrine 60 mg/kg) and sham operated group. We used a permanent middle cerebral artery occlusion model and administered oxymatrine intraperitoneally immediately after cerebral ischemia and once daily on the following days. At 24 h after MCAO, neurological deficit was evaluated using a modified six point scale; brain water content was measured; NF-kappaB expression was measured by immunohistochemistry, Western blotting and RT-PCR. Infarct volume was analyzed with 2, 3, 5-triphenyltetrazolium chloride (TTC) staining at 72 h.


RESULTS
Compared with pMCAO group, neurological deficit in high dose group was improved (P<0.05), infarct volume was decreased (P<0.001) and cerebral edema was alleviated (P<0.05). Consistent with these indices, immunohistochemistry, Western blot and RT-PCR analysis indicated that NF-kappaB expression was significantly decreased in high dose group. Low dose of oxymatrine did not affect NF-kappaB expression in pMCAO rats.


CONCLUSIONS
Oxymatrine reduced infarct volume induced by pMCAO, this effect may be through the decreasing of NF-kappaB expression.
Liu
Ying
Y
Department of Neurology, Second Hospital of Hebei Medical University. Shijiazhuang 050000, China.
Zhang
Xiang-Jian
XJ
Department of Neurology, Second Hospital of Hebei Medical University. Shijiazhuang 050000, China. Electronic address: zhang6xj@heinfo.net.
Yang
Chen-Hui
CH
Department of Neurology, Second Hospital of Hebei Medical University. Shijiazhuang 050000, China.
Fan
Hong-Guang
HG
Department of Neurology, Second Hospital of Hebei Medical University. Shijiazhuang 050000, China.
D000470:Alkaloids / Q000008:administration & dosage* / Q000737:chemistry / Q000494:pharmacology; D000818:Animals; D001834:Body Water / Q000378:metabolism; D001921:Brain / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology; D001929:Brain Edema / Q000188:drug therapy; D002467:Cell Nucleus / Q000187:drug effects / Q000378:metabolism; D003593:Cytoplasm / Q000187:drug effects / Q000378:metabolism; D015536:Down-Regulation / Q000187:drug effects; D020244:Infarction, Middle Cerebral Artery / Q000188:drug therapy* / Q000378:metabolism / Q000473:pathology; D008297:Male; D016328:NF-kappa B / Q000378:metabolism*; D018696:Neuroprotective Agents / Q000008:administration & dosage* / Q000494:pharmacology; D011807:Quinolizines / Q000008:administration & dosage* / Q000737:chemistry / Q000494:pharmacology; D012333:RNA, Messenger / Q000378:metabolism; D011897:Random Allocation; D051381:Rats; D017207:Rats, Sprague-Dawley; D051996:Transcription Factor RelA / Q000378:metabolism; D000093842:Matrines
D000470:Alkaloids; D016328:NF-kappa B; D018696:Neuroprotective Agents; D011807:Quinolizines; D012333:RNA, Messenger; D051996:Transcription Factor RelA; C037573:oxymatrine; D000093842:Matrines