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.
出处
《中国药学杂志》
CAS
CSCD
北大核心
2007年第10期743-748,共6页
Chinese Pharmaceutical Journal
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
baicalin
cerebral ischemia
relaerfusion injury
intracellular calcium ： heat-shock orotein 70
作者简介
刘萍，女，硕士研究生
通讯作者：刘兆平，男，教授，硕士生导师 Tel：（0531）88380319 E-mail：liuzhaoping@sda.edu.cn
