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目的:研究人参皂苷对重型脑外伤后大鼠神经细胞凋亡的保护作用及其机制。方法:健康雄性W ist-ar大鼠60只,分为正常对照组10只,未治疗组10只,人参皂苷治疗组40只。参照Feeney法制作重型颅脑损伤模型,并于术后6h、24h、48h、72h、5天、7天共6个时相点取大鼠脑组织,用TUNEL法观察凋亡细胞,并计算凋亡指数;透射电镜下观察细胞线粒体形态的改变;应用RT-PCR法检测神经细胞COX-2 mRNA的表达。结果:未治疗组脑外伤后6h出现较多TUNEL染色阳性细胞,72h达到高峰,5天后明显减少;人参皂苷治疗组各个时间点TUNEL染色阳性细胞数明显低于未治疗组。电镜下可见细胞固缩,凋亡小体形成,线粒体肿胀变形。COX-2mRNA的表达与细胞凋亡同步升高并同步下降,治疗组各个时间点COX mRNA的表达明显低于未治疗组。结论:COX-2诱导线粒体途径细胞凋亡作用在重型脑外伤后的损伤中起重要作用。人参皂苷对大鼠重型脑外伤后神经细胞凋亡有保护作用,其作用机制可能与人参皂苷抑制COX-2的表达,从而抑制COX-2诱导的线粒体途径细胞凋亡有关。
Objective: To study the protective effect and mechanism of ginsenoside on neuronal apoptosis after severe traumatic brain injury in rats. METHODS: Sixty Wistar rats were divided into normal control group, 10 untreated groups and 40 ginsenoside-treated groups. The severe brain injury model was made according to Feeney’s method. Rat brain tissue was taken at 6 hours, 24 hours, 48 hours, 72 hours, 5 days and 7 days after operation. The apoptotic cells were observed by TUNEL method and the apoptosis was calculated. The index of death was observed. The changes of mitochondrial morphology were observed under transmission electron microscope. The expression of COX-2 mRNA was detected by RT-PCR. RESULTS: In the untreated group, more TUNEL-positive cells appeared at 6 h after traumatic brain injury, peaked at 72 h, and decreased significantly after 5 days. The number of TUNEL-positive cells in the ginsenoside-treated group was significantly lower than that in the untreated group. Under electron microscope, cells were pyknotic, apoptotic bodies formed, and mitochondria were swollen and deformed. COX-2 mRNA expression and cell apoptosis increased synchronously and decreased simultaneously. The expression of COX mRNA was significantly lower in the treatment group than in the untreated group. CONCLUSION: COX-2 induces apoptosis in the mitochondrial pathway and plays an important role in injury after severe traumatic brain injury. Ginsenosides have protective effects on neuronal apoptosis after severe traumatic brain injury in rats. The mechanism of action may be related to the inhibition of COX-2 expression by ginsenosides, thereby inhibiting COX-2-induced mitochondrial pathway apoptosis.