甲醛炎性痛诱导大鼠海马神经元凋亡

FORMALIN INFLAMMATORY PAIN INDUCED HIPPOCAMPAL NEURONAL APOPTOSIS OF RATS

目的:观察甲醛炎性痛是否可诱导大鼠海马神经元凋亡。方法:采用行为学方法观察大鼠自发痛反应,流式细胞术检测海马神经元凋亡率,免疫组织化学法检测海马神经元p53蛋白的表达。结果:与正常对照组相比,大鼠足底皮下注射甲醛后海马神经元凋亡率显著增高,海马各区p53蛋白表达明显增加,二者均于注射甲醛后3 d达高峰;足底两次注射甲醛和一次注射甲醛组比较,大鼠自发痛反应增强,并且海马神经元凋亡率进一步增加。结论:甲醛炎性痛可诱导大鼠海马神经元凋亡,这种改变具有一定的时程特征;海马神经元凋亡率与疼痛强度有关;p53蛋白的表达增加可能参与了伤害性信息传入对神经元凋亡的诱导。

Aim： To investigate whether formalin inflammatory pain can induce hippocampal neuronal apoptosis of rats or not. Methods： Rats were subcutaneously injected with 0.2 ml 0.5 % formalin into the ventral surface of right hind paw to induce periphery inflammatory pain. The flinches of rats were counted to observe their painful reaction. Flow cytometry was used to assay the ratio of apoptosis of hippocampal neurons. The immunohistochemistry was used to observe the expression of p53 protein in hippocampal subregions. Results： Compared with control group, the apoptotic ratio of hippocampal neurons was significantly increased in rats with inflammatory pain, and formalin inflammatory pain induced up-regulation of p53 protein expression in all hippocampal subregions. Both the apoptotic ratio and the p53 protein expression peaked on the third day after the formalin injection. The twice injection of formalin into the hind paws of rats resulted in an enhancement of painful reaction and increase in apoptotic ratio of hippocampal neurons compared with the rats of injection formalin once group. Condusioil： Formalin inflammatory pain can induce the hippocampal neuronal apoptosis in rats with a certain time course. Neuronal apoptosis is relevant to the intensity of pain. The up-regulation of p53 protein expression may implicate in the induction of hippocampal neuronal apoptosis in rats with inflammatory pain.