黄芩苷对大鼠局灶性脑缺血再灌注损伤的保护作用  

Protective Effect of Baicalin on Focal Cerebral Ischemia-Reperfusion Injury in Rats

作　　者：刘萍[1] 张岫美[1] 王菊英[1] 李倩[2] 王姿颖[1] 许复郁[3] 马剑峰[1] 刘兆平[4] 

机构地区：[1]山东大学医学院药理学研究所,济南250012 [2]山东省地方病防治研究所,济南250014 [3]山东大学医学院病理学与病理生理学研究所,济南250012 [4]山东大学新药评价中心,济南250012

出　　处：《中国药学杂志》2007年第10期743-748,共6页Chinese Pharmaceutical Journal

摘　　要：目的研究黄芩苷对大鼠局灶性脑缺血再灌注损伤的保护作用,并初步探讨其作用机制。方法Wistar大鼠随机分为假手术组、脑缺血再灌注模型组、黄芩苷组(50,100,200mg.kg-1)以及尼莫地平0.4mg.kg-1组。线栓法制备大鼠局灶性脑缺血再灌注损伤模型。脑缺血1h再灌注24h后,观察黄芩苷对大鼠神经功能缺损症状、脑梗死体积、脑组织病理形态学改变、神经细胞内Ca2+含量以及热休克蛋白(HSP)70表达的影响。结果黄芩苷50,100,200mg.kg-1均可明显改善脑缺血再灌注损伤所致的大鼠神经功能缺损症状以及脑组织病理形态学改变,脑梗死体积从模型组的(370.14±60.40)mm3分别降至(283.63±81.37)、(216.29±74.37)及(186.65±47.67)mm3,神经细胞内Ca2+含量也较模型组有明显降低,HSP70mRNA表达水平从模型组的(0.74±0.14)分别上升至(0.79±0.13)、(0.92±0.08)及(0.96±0.08),其蛋白表达水平比模型组分别上升6.82%、37.88%及49.38%。结论黄芩苷对大鼠局灶性脑缺血再灌注损伤具有明显保护作用,其作用机制可能与黄芩苷降低神经细胞内Ca2+含量,促进HSP70的表达有关。OBJECTIVE To study the protective effect and mechanism of baicalin on focal cerebral ischemia-reperfusion injury inrats. METHODS The models of focal brain ischemia-reperfusion injury was prepared by middle cerebral artery occlusion（MCAO） in Wistar rats. At 1 h after ischemia and 24 h after reperfusion, the extent of neurological deficits was evaluated by Longa method, the in- farction volumes were showed with TIC （2,3,5-triphenyltetrazoliumchloride） staining and quantitated by image analysis system. HE staining was used to observe the pathological changes. Flow cytometry （FCM） was used for the determination of intraneuron calcium content. HSP70 protein expression of the neurons was detected with immunohistochemistry staining. Reverse transcription polymerase chain reaction （RT-PCR） was used to detect the expression of the mRNA level of HSP70. RESULTS Baicalin （50,100,200 mg · kg^-1） significantly ameliorated the neurological deficit and improved the pathological changes induced by MCAO. Compared with the ischemia-reperfusion group, baicalin diminished the infarction volume from （ 370.14 ± 60.40 ） mm^3 to （ 283.63 ±81.37 ） , （ 216.29 ±74.37 ） and （ 186. 65 ± 47.67 ） mm^3. Meanwhile, baicalin decreased the content of intraneuron calcium significantly, increased HSP70 mRNA transcription from （0.74±0.14） to （0.79 ±0.13）, （0.92 ±0.08） and （0.96 ±0.08） ,and increased HSP70 protein expression by 6.82% ,37.88% and 49.38% respectively. CONCLUSION Baicalin can protect the brain from ischemia-reperfusion injury in rats. And the neuroprotective mechenism may be related to inhibiting calcium overload in neuron ,and increasing the transcription of HSP70 mRNA and the expression of the protein.

关 键 词：昔芩苷 脑缺血 再灌注损伤 细胞内钙离子 热休克蛋白70 

分 类 号：R965[医药卫生—药理学] R282.71[医药卫生—药学]