超短波治疗对急性闭合性颅脑损伤大鼠脑NMDAR1及GAP-43表达的影响

目的探讨超短波治疗对急性闭合性颅脑损伤后神经保护及神经可塑性的影响。方法将54只成年大鼠随机分为超短波治疗组、对照组和正常组,治疗组和对照组又分为伤后1、3、7和14d组,每组6只动物。采用自由落体撞击法制作大鼠急性闭合性颅脑损伤模型。以无热量超短波照射大鼠脑部,用免疫组化方法测定各组大鼠脑N-甲基-D-天冬氨酸受体1(NMDAR1)和生长相关蛋白(GAP-43)的表达。结果与对照组比较,超短波治疗组NMDAR1免疫阳性细胞数在伤后1d时明显降低(P0.05),伤后3、7、14d时则明显升高(P0.05);GAP-43免疫阳性细胞数在伤后1d时与对照组无明显差异(P0.05),在伤后3、7、14d时则明显升高(P0.05)。结论本研究提示,颅脑损伤后适时的超短波治疗对损伤的脑组织有保护作用,这种保护可能是通过其调节MMDAR1和GAP-43的表达来实现的。

Effects of ultrashort wave on the expressions of NMDAR 1 and GAP-43 in brain tissues of rats with closed traumatic brain injury

Objective To investigate the effects of ultrashort wave on the expression of N-methyl-D-aspartate receptor 1 （NMDAR1） and growth-associated protein-43 （GAP-43） in the cerebral tissues of the rats with traumatic brain injury （TBI）. Methods Fifty-four rats were randomly divided into 3 groups, i.e. normal, control and treatment groups. The control and treatment groups were redivided into 4 subgroups, i.e. 1, 3, 7, and 14 days groups after TBI. There were 6 rats in the normal group and each subgroup. The closed TBI was made by a free-falling weight device in the rats of control and treatment groups. The rats with TBI were treated immediately after TBI in the treatment group. The behaviors were observed and the expressions of NMDAR1 and GAP-43 in the cerebral tissues were determined by immunohistochemical method in all the rats. Results The expression levels of NMDAR1 and GAP-43 in the control and treatment groups were significantly higher than those in the normal group （P0.05）. The expression levels of NMDAR1 were significantly lower 1 day after TBI and significantly higher 3, 7, and 14 days after TBI in the treatment group than those in the control group （P0.05）. The expression levels of GAP-43 were significantly higher than those in the control group3, 7, and 14 days after the injury （P0.05）. Conclusion It is suggested that timely therapy with ultrashort wave has pretective effect on the injured brain tissues, which may be realized by the regulation of NMDAR1 and GAP-43 expressions in the cerebral tissues in the rats with TBI.