空军医学杂志
空軍醫學雜誌
공군의학잡지
MEDICAL JOURNAL OF AIR FORCE
2013年
2期
93-95,101
,共4页
赵安东%李玉亮%辛益妹%葛华%詹皓
趙安東%李玉亮%辛益妹%葛華%詹皓
조안동%리옥량%신익매%갈화%첨호
银杏叶提取物%脑%自由基%抗氧化功能
銀杏葉提取物%腦%自由基%抗氧化功能
은행협제취물%뇌%자유기%항양화공능
Extracts of Ginkgo biloba leaf(EGB)%Brain%Free radical%Antioxidative function
目的观察银杏叶提取物(extracts of Ginkgo biloba leaf, EGB)对大鼠脑缺血再灌注氧化损伤的保护作用,为进一步开展复方候选新药筛选研究提供参考依据。方法雄性Wistar大鼠60只,随机等分为①对照组,②模型组,③假手术组,④EGB低剂量组,⑤EGB中剂量组,⑥EGB高剂量组。第①~③组灌胃给予蒸馏水l0 ml/kg,第④~⑥组分别灌胃给予含EGB 25、50、100 mg/kg的蒸馏水混悬液l0 ml/kg,连续14 d。最后一次灌胃后1h,②、④、⑤、⑥组大鼠均结扎双颈总动脉造成不完全性脑缺血1 h,复灌30 min;①组不做处理,③组仅做手术处理不结扎颈总动脉。取各组大鼠大脑皮层制备组织匀浆,检测超氧化物歧化酶(SOD)和一氧化氮合酶(NOS)活性,谷胱甘肽(GSH)和丙二醛(MDA)含量以及总抗氧化能力(T-AOC)等指标的变化。结果与对照组相比,模型组脑组织中的SOD活性、GSH含量和T-AOC显著下降,而NOS活性和MDA含量明显升高;与模型组相比,给于EGB使脑组织中SOD活性、GSH含量和T-AOC明显升高,NOS活性和MDA含量明显降低,中剂量的效果较好。结论 EGB对大鼠脑缺血再灌注氧化损伤具有明显保护作用,且呈一定的剂量相关特性。
目的觀察銀杏葉提取物(extracts of Ginkgo biloba leaf, EGB)對大鼠腦缺血再灌註氧化損傷的保護作用,為進一步開展複方候選新藥篩選研究提供參攷依據。方法雄性Wistar大鼠60隻,隨機等分為①對照組,②模型組,③假手術組,④EGB低劑量組,⑤EGB中劑量組,⑥EGB高劑量組。第①~③組灌胃給予蒸餾水l0 ml/kg,第④~⑥組分彆灌胃給予含EGB 25、50、100 mg/kg的蒸餾水混懸液l0 ml/kg,連續14 d。最後一次灌胃後1h,②、④、⑤、⑥組大鼠均結扎雙頸總動脈造成不完全性腦缺血1 h,複灌30 min;①組不做處理,③組僅做手術處理不結扎頸總動脈。取各組大鼠大腦皮層製備組織勻漿,檢測超氧化物歧化酶(SOD)和一氧化氮閤酶(NOS)活性,穀胱甘肽(GSH)和丙二醛(MDA)含量以及總抗氧化能力(T-AOC)等指標的變化。結果與對照組相比,模型組腦組織中的SOD活性、GSH含量和T-AOC顯著下降,而NOS活性和MDA含量明顯升高;與模型組相比,給于EGB使腦組織中SOD活性、GSH含量和T-AOC明顯升高,NOS活性和MDA含量明顯降低,中劑量的效果較好。結論 EGB對大鼠腦缺血再灌註氧化損傷具有明顯保護作用,且呈一定的劑量相關特性。
목적관찰은행협제취물(extracts of Ginkgo biloba leaf, EGB)대대서뇌결혈재관주양화손상적보호작용,위진일보개전복방후선신약사선연구제공삼고의거。방법웅성Wistar대서60지,수궤등분위①대조조,②모형조,③가수술조,④EGB저제량조,⑤EGB중제량조,⑥EGB고제량조。제①~③조관위급여증류수l0 ml/kg,제④~⑥조분별관위급여함EGB 25、50、100 mg/kg적증류수혼현액l0 ml/kg,련속14 d。최후일차관위후1h,②、④、⑤、⑥조대서균결찰쌍경총동맥조성불완전성뇌결혈1 h,복관30 min;①조불주처리,③조부주수술처리불결찰경총동맥。취각조대서대뇌피층제비조직균장,검측초양화물기화매(SOD)화일양화담합매(NOS)활성,곡광감태(GSH)화병이철(MDA)함량이급총항양화능력(T-AOC)등지표적변화。결과여대조조상비,모형조뇌조직중적SOD활성、GSH함량화T-AOC현저하강,이NOS활성화MDA함량명현승고;여모형조상비,급우EGB사뇌조직중SOD활성、GSH함량화T-AOC명현승고,NOS활성화MDA함량명현강저,중제량적효과교호。결론 EGB대대서뇌결혈재관주양화손상구유명현보호작용,차정일정적제량상관특성。
Objective We tried to observe the protective effects of extracts of Ginkgo biloba leaf(EGB) on cerebral ischemia/reperfusion induced oxidative injury in rats. Methods Sixty male Wistar rats were randomly divided into following six groups(n=10for each): (a)normal control,(b) injury model,(c)sham operation,(d)low dose of EGB,(e)middle dose of EGB,(f) high dose of EGB. EGB dissolved in distilled in water at dosages of 25,50 and 100mg/kg was given to group d,e,f by gastric tube, continued for 14d; but group a,b,c was only given the equal volume of distilled water at dose of 10ml/kg. At 1 h after the last drug administration, the rats in group b,d,e,f were submitted to incomplete cerebral ischemia(1h)/reperfusion(30min) injury;but group c was only operated and not submitted to cerebral ischemia/reperfusion injury. The cerebral cortex tissue was taken and homogenized for following index assays:SOD and NOS activities, GSH,MDA content and total antioxidative catacity(T-AOC). Results Compared with the normal control, the SOD activity, GSH content and T-AOC in rat brain significantly decreased, but NOS activity and MDA content significantly increased in injury model group. Compared with the injury model, SOD activity, GSH content and T-AOC in rat brain significantly increased, but NOS activity and MDA content were significantly decreased after administration of EGB,especially at dosage of 50 mg/kg. Conclusions EGB has protective effects on cerebral ischemia/reperfusion induced oxidative injury in rats and shared the characteristic of dose-related effect.