中国药理学与毒理学杂志
中國藥理學與毒理學雜誌
중국약이학여독이학잡지
CHINESE JOURNAL OF PHARMACOLOGY AND TOXICOLOGY
2006年
6期
455-460
,共6页
胡赫%汤志宇%陈世忠%王银叶
鬍赫%湯誌宇%陳世忠%王銀葉
호혁%탕지우%진세충%왕은협
和厚朴酚%脑缺血%再灌注损伤%行为动物%过氧化物酶%超氧化物歧化酶
和厚樸酚%腦缺血%再灌註損傷%行為動物%過氧化物酶%超氧化物歧化酶
화후박분%뇌결혈%재관주손상%행위동물%과양화물매%초양화물기화매
honokiol%cerebral ischemia%reperfusion injury%behavior,animal%peroxidase%superoxide dismutase
目的 研究和厚朴酚对局灶性脑缺血的保护作用和缺血再灌注脑组织对活性氧清除能力的影响.方法 用线栓法造成大鼠大脑中动脉阻塞模型,观察大鼠行为学改变和脑梗死体积.用双侧颈动脉结扎30 min, 再灌注30 min造成小鼠脑缺血再灌注损伤,测定脑组织中相关酶的活性,脂质过氧化产物丙二醛的含量和脑组织Na+-K+-ATP酶的活性.结果 和厚朴酚5～50 μg·kg-1在大脑中动脉阻塞后0.25和3 h iv给药, 可显著改善脑缺血大鼠的神经学评分,明显减少脑梗死体积.和厚朴酚7～70 μg·kg-1分别于阻塞前和再灌注前2 min iv给药,可明显升高小鼠脑组织中超氧化物歧化酶、过氧化氢酶、谷胱甘肽过氧化物酶和过氧化物酶的活性; 显著降低丙二醛的含量.同时和厚朴酚也升高脑组织Na+-K+-ATP酶的活性.结论 和厚朴酚可改善局部脑缺血引起的神经行为缺陷和缩小脑梗死体积;并提高缺血再灌注脑组织对活性氧的清除能力和Na+-K+-ATP酶活性,表明它对脑缺血和缺血再灌注损伤均有保护作用.
目的 研究和厚樸酚對跼竈性腦缺血的保護作用和缺血再灌註腦組織對活性氧清除能力的影響.方法 用線栓法造成大鼠大腦中動脈阻塞模型,觀察大鼠行為學改變和腦梗死體積.用雙側頸動脈結扎30 min, 再灌註30 min造成小鼠腦缺血再灌註損傷,測定腦組織中相關酶的活性,脂質過氧化產物丙二醛的含量和腦組織Na+-K+-ATP酶的活性.結果 和厚樸酚5～50 μg·kg-1在大腦中動脈阻塞後0.25和3 h iv給藥, 可顯著改善腦缺血大鼠的神經學評分,明顯減少腦梗死體積.和厚樸酚7～70 μg·kg-1分彆于阻塞前和再灌註前2 min iv給藥,可明顯升高小鼠腦組織中超氧化物歧化酶、過氧化氫酶、穀胱甘肽過氧化物酶和過氧化物酶的活性; 顯著降低丙二醛的含量.同時和厚樸酚也升高腦組織Na+-K+-ATP酶的活性.結論 和厚樸酚可改善跼部腦缺血引起的神經行為缺陷和縮小腦梗死體積;併提高缺血再灌註腦組織對活性氧的清除能力和Na+-K+-ATP酶活性,錶明它對腦缺血和缺血再灌註損傷均有保護作用.
목적 연구화후박분대국조성뇌결혈적보호작용화결혈재관주뇌조직대활성양청제능력적영향.방법 용선전법조성대서대뇌중동맥조새모형,관찰대서행위학개변화뇌경사체적.용쌍측경동맥결찰30 min, 재관주30 min조성소서뇌결혈재관주손상,측정뇌조직중상관매적활성,지질과양화산물병이철적함량화뇌조직Na+-K+-ATP매적활성.결과 화후박분5～50 μg·kg-1재대뇌중동맥조새후0.25화3 h iv급약, 가현저개선뇌결혈대서적신경학평분,명현감소뇌경사체적.화후박분7～70 μg·kg-1분별우조새전화재관주전2 min iv급약,가명현승고소서뇌조직중초양화물기화매、과양화경매、곡광감태과양화물매화과양화물매적활성; 현저강저병이철적함량.동시화후박분야승고뇌조직Na+-K+-ATP매적활성.결론 화후박분가개선국부뇌결혈인기적신경행위결함화축소뇌경사체적;병제고결혈재관주뇌조직대활성양적청제능력화Na+-K+-ATP매활성,표명타대뇌결혈화결혈재관주손상균유보호작용.
AIM To investigate the effects of honokiol on ischemic neurological deficiency and on the scavenging ability of ischemia reperfusion (I-R) brain tissue for reactive oxygen species (ROS). METHODSCerebral ischemia was induced by middle cerebral artery occlusion (MCAO) in rats. I-R in mice were induced by blood stream pause in bilateral common carotid arteries for 30 min and reperfusion for 30 min. The activities of ROS scavenging enzymes were determined with colorimetric methods. RESULTS Intravenous honokiol in 5-50 μg·kg-1 significantly decreased the neurological deficiency score, and diminished cerebral infarction volume in rats. In I-R brain tissue of mice, intravenous honokiol in 7-70 μg·kg-1 evidently enhanced the activities of superoxide dismutase, catalase, glutathione peroxidase and peroxidase, and markedly lowered lipid peroxidative product malondialdehyde content. Moreover honokiol significantly increased Na+-K+-ATPase activity in I-R brain tissue. CONCLUSION Honokiol ameliorates the neurological deficiency behavior and diminishes infarction volume in MCAO rats; and enhances cerebral scavenging ability for ROS and Na+-K+-ATPase activity in cerebral I-R mice. It is indicated that honokiol is a protective agent for cerebral ischemia and I-R.
