Interference effect of picroside II on cerebral ischemia reperfusion injury in rats
Interference effect of picroside II on cerebral ischemia reperfusion injury in rats
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DOI：
10.3969/j.issn.0529-1356.2010.01.002
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发表时间：
2010-02-01
期刊：
影响因子：
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通讯作者：
Luan Li-ju
中科院分区：
文献类型：
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作者：
Li Zhen;Li Qin;Luan Li-ju
目的探讨苦毒苷II对大鼠脑缺血再灌注损伤的保护作用。方法采用线栓法建立大鼠大脑中动脉闭塞再灌注模型。治疗组尾静脉注射苦毒苷Ⅱ（10 mg/kg）和丹参素A钠（10 mg/kg）。采用Bederson试验评价神经行为功能。氯化四氮唑（TTC）染色观察脑梗死体积。组织病理学观察细胞结构。用末端脱氧核苷酸转移酶介导的dUTP缺口末端标记法（TUNEL）计数凋亡阳性细胞。结果MCAO/R大鼠均出现神经行为学障碍。脑缺血再灌注损伤后梗死灶位于缺血侧半球。苦味酸Ⅱ和丹参素A钠治疗组与模型对照组相比，凋亡阳性细胞数减少，脑梗死体积缩小，神经行为功能明显改善（P < 0.05）。脑梗死体积小，苦味酸II组明显小于丹参酸A钠组（P < 0.05）。结论Picrodide II可通过抑制脑缺血再灌注损伤诱导的神经细胞凋亡，缩小脑梗死体积，改善神经行为功能。
Objective To investigate the neuroprotective effects of picrodide II on cerebral ischemic reperfusion injury in rats. Methods Intraluminal thread methods were applied to establish the left middle cerebral artery occlusion reperfusion models (MCAO/R) in rats. Picrodide II (10mg/kg) and salvianic acid A sodium (10mg/kg) were injected from tail vein for treatment. The neurological behavioral function was evaluated with Bederson's test. The cerebral infarction volume was observed with tetrazolium chloride (TTC) staining. The structure of cells was observed with histopathology. The apoptosis positive cells were counted by terminal deoxynucleotidyl transferase midiated dUTP nick end labeling (TUNEL). Results The neurological behavioral malfunction appeared in all rats with MCAO/R. The infarction focus showed in the ischemic hemisphere following cerebral ischemia reperfusion injury. In the picrodide II and salvianic acid A sodium treatment groups, the number of apoptosis positive cells decreased and the cerebral infarction volume reduced, while the neurological behavioral function was significantly improved than those in the model control group (P < 0.05). The cerebral infarction volume in the picrodide II group was smaller than that in the salvianic acid A sodium group (P < 0.05). Conclusion Picrodide II might reduce cerebral infarction volume and improve the neurological behavioral function through inhibiting the neuronal apoptosis induced by ischemia reperfusion injury.