CAJ | 학술논문

目的观察龙血素A对急性脑缺血再灌注引起脑水肿的保护作用,初步阐明其作用机制.方法采用线栓法建立右侧大脑中动脉栓塞(MCAO)再灌注模型,分为假手术组、缺血灌注组、龙血素A(30 mg·k~(-1)、60 mg·kg~(-1)、120 mg·kg~(-1))组和依达拉奉(3 mg·kg~(-1))组.大鼠再灌注24 h后,对其进行神经功能行为学评分,然后断头取脑进行TTC染色计算脑梗死面积,采用干湿重法计算脑含水量,并对脑组织内脂质过氧化产物和抗氧化酶活性进行测定.采用Westem blotting对大鼠脑内水通道蛋白-4的表达进行检测,结果与假手术比较,大鼠MCAO2 h再灌注24 h后,所有动物都出现了神经功能缺损,主要表现为提尾悬空时对侧肩内旋,前肢内收,围绕手术对侧转圈等,模型组最为严重,龙血素A可显著缓解这些神经症状,降低行为学评分.模型组脑组织出现明显的梗塞灶及水肿,MDA含量明显增高,SOD、CAT和GSH-Px活性降低,龙血素A组则具有显著的降低脂质过氧化物、提高抗氧化酶活力,可显著减少梗死面积和脑水肿程度.水通道蛋白-4的表达在模型组缺血侧脑组织出现高表达的现象,龙血素A可显著降低其在缺血侧大脑的表达.结论龙血素A对局灶性脑缺血再灌注引起的损伤具有一定的保护作用,对自由基的清除作用和对水通道蛋白一4表达的抑制作用可能是其作用机制之一.
목적 관찰룡혈소A대급성뇌결혈재관주인기뇌수종적보호작용,초보천명기작용궤제.방법 채용선전법건립우측대뇌중동맥전새(MCAO)재관주모형,분위가수술조、결혈관주조、룡혈소A(30 mg·k~(-1)、60 mg·kg~(-1)、120 mg·kg~(-1))조화의체랍봉(3 mg·kg~(-1))조.대서재관주24 h후,대기진행신경공능행위학평분,연후단두취뇌진행TTC염색계산뇌경사면적,채용간습중법계산뇌함수량,병대뇌조직내지질과양화산물화항양화매활성진행측정.채용Westem blotting대대서뇌내수통도단백-4적표체진행검측,결과 여가수술비교,대서MCAO2 h재관주24 h후,소유동물도출현료신경공능결손,주요표현위제미현공시대측견내선,전지내수,위요수술대측전권등,모형조최위엄중,룡혈소A가현저완해저사신경증상,강저행위학평분.모형조뇌조직출현명현적경새조급수종,MDA함량명현증고,SOD、CAT화GSH-Px활성강저,룡혈소A조칙구유현저적강저지질과양화물、제고항양화매활력,가현저감소경사면적화뇌수종정도.수통도단백-4적표체재모형조결혈측뇌조직출현고표체적현상,룡혈소A가현저강저기재결혈측대뇌적표체.결론 룡혈소A대국조성뇌결혈재관주인기적손상구유일정적보호작용,대자유기적청제작용화대수통도단백일4표체적억제작용가능시기작용궤제지일.
Objective Present study is to investigate the effect of luoreirin A (LA )on brains ischemia-reperfusion in rats and to elucidate its mechanism. Methods Two-hour middle cerebral artery occlusion (MCAO)and 24-hour reperfusion surgery was used to establish the cerebral ischemia-reperfusion model. The modeled rats were randomized into sham-operation group, ischemia-reperfusion group, LA groups (in the dose of 30 mg·kg~(-1), 60 mg·kg~(-1) and 120 mg·kg~(-1), respectively), and edaravone (3 mg·kg~(-1))positive control group. After reperfusion for 24 hours, neurobehavioral scores, infracted cerebral area and the percent of water content in the brain were detected for the evaluation of the protection of LA. Lipid peroxidation level, antioxidase activity and the expression of aquaporin protein 4 (AQP4) were also analyzed for the mechanism investigation. Results Ischemia -reperfusion induced the occurrence of neurologic impairment, manifesting as inward rotation of the opposite shoulder, adduction of anterior limbs, circling around the opposite side of the operated part when the rat tail was lifted. LA can relieve the above manifestations and decrease the neurobehavioral scores. Obvious cerebral infarction and edema occurred, MDA content increased, and the activities of SOD, CAT and GSH-Px were decreased, and AQP4 was presented as high expression in the ischemic brain of the modeled rats, and LA counteracted the above changes. Conclusion Luoreirin A exerts certain protection on the injury induced by cerebral ischemia-reperfusion. The scavenge of free radicals and the inhibition of the expression of AQP4 may be one of its mechanisms.