人参总皂苷对大鼠脑外伤后神经细胞凋亡的影响

Effect of ginseng total saponins on neuronal apoptosis in rats with traumatic brain injury

目的 研究人参总皂苷对脑外伤大鼠神经细胞凋亡的影响,探讨其抑制创伤性脑损伤（TBI）后继发性损伤的作用机制.方法 采用改良的Feeney自由落体法建立脑外伤模型,将Sprague-Dawley大鼠54只按照随机数字表法分为假手术组、脑外伤组、人参总皂苷治疗组（治疗组）,每组18只.模型建立后24h处死大鼠,采用干湿重法测量脑水含量,光镜下观察尼氏染色海马细胞形态,凋亡细胞原位末端标记法（TUNEL）和免疫组织化学方法观察大脑皮质、海马神经细胞凋亡及凋亡基因bax、bcl-2、caspase-3的蛋白表达情况.结果 与脑外伤组比较,人参总皂苷治疗后的治疗组脑含水量明显减低,损伤侧海马病理学改变明显减轻,神经细胞凋亡减少,bcl-2的表达增高,bax、caspase-3的表达减少,差异均有统计学意义（P＜0.05）.结论 人参总皂苷可以减轻脑外伤后继发性损伤,其机制可能是升高bcl-2的表达,抑制bax、caspase-3的表达,从而阻滞TBI后神经细胞凋亡.

Objective To observe the effect of ginseng total saponins （GTS） on neuronal apoptosis in rats with traumatic brain injury （TBI）, and explore the underlying mechanisms of GTS in the treatment of secondary brain injury. Methods SD rats were randomly divided into sham-operated group, TBI group and GTS-treatment group （n=18）. TBI models were established with the modified Feeney＇s method. Three h after the success of model making, 20 mg/kg GTS was given to the GTS-treatment group through intraperitoneal injection and the same amount of normal saline was given to the TBI group. Twenty-four hours after the success of model making, the rats were sacrificed; the brain water content was measured by wet-dry weight method; the morphological changes of neurons in the hippocampal area were observed under optical microscope after Nissl staining. The neuronal apoptosis and the protein expressions of bax, bcl-2 and caspase-3 in the cortex and hippocampus were determined by TUNEL and immunohistochemical technique, respectively. Results Compared with TBI group,treatment with GTS decreased the water content of the brain, alleviated the damage of hippocampal area,reduced the number of TUNEL positive cells and the bax and caspase-3 positive cells, and increased the number of bcl-2 positive cells. Conclusion GTS can exert a neuroprotective effect in rats with TBI.The underlying mechanism of this effect is potentially related to the elevation of expression of bcl-2 and reduction of expression ofbax and caspase-3, and thereby, restraining the neuronal apoptosis in the brain tissue.