摘要
目的观察奥美拉唑对酒精性脑损伤的保护作用。方法观察奥美拉唑(20 mg·kg-1)对酒精中毒半数致死量和乙醛脱氢酶2(ALDH2)活力的影响,测定ALDH2激动剂和奥美拉唑对正常大鼠及酒精中毒大鼠大脑中动脉阻塞(MCAO)后的梗死面积。结果长期酒精摄入,会加重缺血性脑损伤[(59.1±6.2)%vs(43.7±5.3)%,P<0.01)],奥美拉唑能提高酒精的半数致死量,使肝脏ALDH2活性提高达266%;奥美拉唑对正常大鼠MCAO后梗死面积无明显作用,但能减轻酒精中毒大鼠MCAO后梗死面积[(48.3±5.1)%vs(59.1±6.2)%,P<0.05)]。结论奥美拉唑能减轻酒精中毒后的缺血性脑损伤,机制可能与提高ALDH2活性有关。
Objective To investigate the protect effects of omeprazole on alcoholic cerebral injure in rats. Methods The effect of omeprazole ( 20 mg ·kg^-1) on lethal median dose ( LD50 ) of alcohol and the activity of aldehyde dehydrogenase 2 ( ALDH2 ) were determined. And the effect of ALDH2 agonist on infract area in middl cerebral artery (MCAO) rats was obsereved. Also the effect of omeprazole on infract area was obsereved in normal rats and alcoholism rats with MCAO. Results Long - term alcohol intaking can aggravate ischemic brain damage [ (59. 1 ±6.2)% vs (43.7 ±5.3)%, P 〈0.01)]. Omeprazole can increase LD50 of alcohol in mice. The activity of ALDH2 in liver was elevated by omeprazole. The infarct size didn't decrease in normal rats, but it decreased from (59. 1 ±6. 2) % to (48. 3 ±5. 1 ) % in alcoholism rats ( P 〈 0. 05) by omeprazole. Conclusion Omeprazole can decrease cerebral injure induced by alcoholism. It is most likely through activation ALDH2.
出处
《中国临床药理学杂志》
CAS
CSCD
北大核心
2013年第11期837-839,共3页
The Chinese Journal of Clinical Pharmacology
基金
无锡市科技局科技支撑指导性与支撑指令性基金资助项目(CSZ00N1233
CSE01N1236)
关键词
奥美拉唑
酒精性脑损伤
乙醛脱氢酶2
omeprazole
alcoholic cerebral injure
aldehyde dehydrogenase 2