茅莓总皂苷对大鼠局灶性脑缺血/再灌注后神经细胞凋亡及相关蛋白Bcl-2、Bax表达的影响

目的探讨茅莓总皂苷对缺血性脑损伤的神经保护机制。方法采用大鼠大脑中动脉阻塞造成局灶性脑缺血2h,再灌注24 h模型,以HE染色,TUNEL标记和免疫组化的方法观察茅莓总皂苷5、10、20 mg.kg-1对凋亡细胞数目及相关蛋白Bc l-2,Bax表达的变化。结果3个剂量的茅莓总皂苷治疗组显示神经元形态病理改变明显减轻,降低残存细胞中TUNEL阳性细胞的百分率。增加Bc l-2阳性细胞的表达,降低Bax阳性细胞的表达,Bc l-2/Bax的表达比例增加。结论茅莓总皂苷有明显的抗凋亡作用,其机制可能与增加Bc l-2阳性细胞的表达,降低Bax阳性细胞的表达,提高Bc l-2/Bax有关。

Effects of total glucosides of Rubus parviflolius L(TGRP) on neuronal apoptosis and expression of apoptosis related protein Bcl-2 andBax in rat after local cerebral ischemic-reperfusion

Aim To explore the mechanism of neuro-protecting effects of TGRP on ischemic cerebral injury.Methods The middle cerebral artery was occluded for 2 h to produce focal ischemic followed by 24 h reperfusion.HE staining,TUNEL labeling and immunohistochemical methods were used to investigate changes of neuronal apoptosis and expression of the apoptosis-related proteins after administration of TGRP.Result TGRP decreased the pathologic changes significantly.The apoptosis of neural cells and the expression of Bax positive cells in the TGRP groups significantly decreased compared with the control group(P<0.05,P<0.01).However,the expression of Bcl-2 positive cells increased significantly compared with the control group(P<0.05,P<0.01).Bcl-2/Bax expression ratio increased significantly compared with the control group(P<0.05,P<0.01).Conclusion TGRP has action of resisting neuronal apoptosis after cerebral ischemic-reperfusion.The mechanism of neuroprotection may be increased Bcl-2 expression,decreased Bax expression and increased Bcl-2/Bax expression ratio.