灵芝对大鼠脑缺血再灌注后神经细胞凋亡率及线粒体跨膜电位的影响

目的探讨灵芝对大鼠脑缺血再灌注后神经细胞凋亡率及线粒体跨膜电位的影响。方法采用线栓阻断大脑中动脉闭塞法（MCAO）建立大鼠局灶性脑缺血再灌注损伤模型。动物随机分为假手术组（Sham）、脑缺血再灌注组（IR）、灵芝组（GA）；于再灌注后3h、12h、24h、48h处死动物取材，流式细胞仪检测脑细胞凋亡率和线粒体跨膜电位。结果（1）IR组和GA组与Sham组比较，脑细胞凋亡率明显增高（P〈0．01）；再灌注3hGA组与IR组比较，脑细胞凋亡率没有明显差异（P〉0．05）；再灌注12h、24h、48hGA组与IR组比较，脑细胞凋亡率降低，有明显差异（P〈0．01）。（2）IR组脑细胞线粒体跨膜电位在再灌注3h、12h、48h较Sham组显著下降（P〈0．05），其中3h值最低，其后逐渐升高，至48h又出现后续性降低；GA组细胞线粒体跨膜电位在再灌注3h较Sham显著下降（P〈0．01）；GA组线粒体跨膜电位在再灌注12h、48h较IR组显著升高（P〈0．05）。结论急性局灶性脑缺血再灌注后大鼠脑细胞凋亡率升高，线粒体跨膜电位显著降低，灵芝具有降低凋亡发生率、改善脑组织细胞线粒体跨膜电位水平的作用。

Effects of Ganoderma on the rate of neural apoptosis and mitochondrial transmembrane potential of the nerve cells in rats with cerebral ischemia/reperfusion

Objective: To observe the effects of Ganoderma (GA) on the rate of neural apoptosis and mitochondrial transmembrane potential of nerve cells in rats with cerebral ischemia/reperfusion. Methods: Adult male SD rats were sub-jected to MCAO/Reperfusion (MCAO/R). They were evenly randomized into sham operation control (sham), IR and IR +GA groups. After cerebral ischemia for 15 minutes and reperfusion for 3 hours, 12 hours, 24 hours and 48 hours, the rats were killed and the mitochondrial membrane potential and the rate of neuronal apoptosis were detected by flow cytometer (FCM). Results:(1)Compared with the sham group, the rate of neuronal apoptosis was significantly increased (P< 0.01) in IR group and GA group . There was no significant difference between GA group and IR group at 3 hours after is-chemia/reperfusion(P>0.05). Compared with IR group, the rate of neuronal apoptosis in GA group was significantly de-creased at 12 hours, 24 hours and 48 hours after iscbemia/reperfusion (P<0.01). (2)Compared with the sham group, the mitochondrial membrane potential of IR group was significantly decreased at 3 hours, 12 hours and 48 hours after ische-mia and reperfusion (P<0.05), it reached the lowest point at 3 hours, then it increased and decreased again at 48 hours. GA decreased the mitochondrial membrane potential obviously (P<0.01) in comparison with the sham group and in-creased the mitochondrial membrane potential at 12 hours and 48 hours after iscbemia and reperfusion compared with IR group(P<0.05). Conclusion: The rate of neural apoptosis in rats increases after acute cerebral ischemia and reperfusion, and the mitochondrial membrane potential decreases significantly. Ganoderma can alleviate cerebral isehemia/repeffusion injury partly by regulating the mitochondrial membrane potential and decreasing the rate of neural apoptosis.