创伤性脑损伤大鼠RSTN基因表达与人参皂苷的干预作用

来源 :中华中医药学刊 | 被引量 : 0次 | 上传用户:zjyeling
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目的:观察创伤性脑损伤大鼠皮层RSTN基因表达的规律及人参皂苷干预对其的影响作用。方法:选取健康SD大鼠48只,随机分为正常对照组(12只)、假手术组(12只)、损伤组(12只)和人参皂苷干预组(12只),制模后按照Longa评分法于术后12 h,24 h,72 h及1周进行神经功能评分,同时取各组大鼠脑皮层组织,采用Western blot法检测RSTN蛋白的表达并采用RT-PCR分析RSTN mRNA的转录。结果:以对照组评分为基准,损伤组在致伤后即刻评分分值升高,到1周一直呈现持续高分值状态。人参皂苷干预组趋势相同(各P均<0.05)。与损伤组比较,人参皂苷干预组在伤后1周的神经功能评分分值出现明显下降,差异有统计学意义(P<0.05);Resistin基因的表达(mRNA和蛋白)在正常对照组和假手术组之间没有显著差异(P>0.05)。以对照组为基准,损伤组在伤后12 h表达量即升高,到伤后1周一直呈持续升高表达(各P均<0.05)。人参皂苷干预组伤后24 h才开始出现表达量的升高,伤后72 h达到峰值,伤后1周时呈现下降(各P均<0.05),且与损伤组比较,人参皂苷干预组各时点RSTN表达的绝对水平均较低(P<0.05)。结论:创伤性脑损伤存在大脑皮质RSTN基因表达的升高,人参皂苷能抑制RSTN基因的高表达,并可能因此发挥对颅脑创伤后继发性脑损伤的保护作用。 OBJECTIVE: To observe the regularity of RSTN gene expression in cortex of traumatic brain injury and the effect of ginsenoside intervention on it. Methods: Forty-eight healthy SD rats were randomly divided into normal control group (12 rats), sham operation group (12 rats), injury group (12 rats) and ginsenoside intervention group (12 rats) The scores of neurological function were evaluated at 12 h, 24 h, 72 h and 1 week after operation. The expression of RSTN protein was detected by Western blot and the transcription of RSTN mRNA was analyzed by RT-PCR . Results: Based on the score of the control group, the score of the injury group increased immediately after the injury and continued to score high until 1 week. Ginsenoside intervention group the same trend (all P <0.05). Compared with the injury group, the score of neurological score of the ginsenoside intervention group decreased significantly at 1 week after injury (P <0.05). The expression of Resistin mRNA and protein in the normal control group and the sham group There was no significant difference between the operation groups (P> 0.05). On the basis of the control group, the expression of the injury group increased 12 h after injury and continuously increased (all P <0.05) 1 week after injury. Ginsenoside intervention group began to express 24 h after injury, the peak value reached the peak at 72 h after injury, and decreased at 1 week (all P <0.05). Compared with the injury group, Ginsenoside intervention group The absolute level of RSTN expression at the time point was lower (P <0.05). CONCLUSION: There is an increase of RSTN gene expression in cerebral cortex in traumatic brain injury. Ginsenoside can inhibit the high expression of RSTN gene and may play a protective role in secondary brain injury following traumatic brain injury.
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