摘要
目的研究依达拉奉对大鼠脑外伤(TBI)后细胞凋亡率及Bcl-2/Bax表达的影响,探讨其对脑外伤后脑组织损害的保护作用。方法成年SD大鼠36只随机分为假手术组、脑外伤组、依达拉奉组。Allen's改良法制作脑外伤的模型;流式细胞仪检测伤侧海马细胞凋亡率的变化,免疫组化法检测海马细胞Bcl-2和Bax蛋白的表达,图象分析仪进行灰度定量分析。结果假手术组没检测到明显的细胞凋亡;脑外伤组检测到较高的细胞凋亡率;依达拉奉组细胞凋亡率较外伤组明显下降。外伤组脑细胞Bcl-2、Bax蛋白表达水平均明显高于假手术组;与外伤组相比,依达拉奉组Bcl-2蛋白表达水平显著增高,Bax蛋白表达水平明显下降。结论依达拉奉可有效抑制大鼠外伤后神经细胞凋亡,此作用可能与其有效清除氧自由基、上调Bcl-2和下调Bax蛋白表达水平有关。
Objective To investigate the effect of edaravone on the cell apoptosis and the expression of Bcl-2 and Bax protein following traumatic brain-injury in aged rat. Methods 36 SD rats were randomly divided into 3 groups： edaravone-treated group, traumatic brain-injury （TBI） group and control group. The rat model of TBI was established by Allen＇s model. Flow cytometer was used to detect apoptosis, immuno- histochemical staining to detect expression of Bcl-2 and Bax, and Leica Qwin processing and analysis system to observe the gray level of the immuno-positive cells. Results Apoptosis was detected in 3 groups,compared with the control group,the apoptosis in TBI group was higher significantly, but it was reduced significantly after treatment of edaravone. The expression of Bcl-2 and Bax protein were significantly increased in the TBI group compared with the control group. Treatment of edaravone markedly reduced the expression of Bax protein in comparison to the TBI group, while the expression of Bcl-2 was obviously higher in the edaravone-treated group than in the TBI group. Conclusion Edaravone inhibits cell apoptosis following traumatic brain injury, which might be relation with the alleviated oxidative stress, up-regulated Bcl-2 protein and down-regulated expression of Bax protein.
出处
《临床神经外科杂志》
CAS
2009年第2期76-78,共3页
Journal of Clinical Neurosurgery
