摘要
目的探讨一氧化碳(CO)中毒迟发性脑损伤的病理机制,及高压氧治疗对迟发性脑损伤的作用,为临床治疗提供实验依据。方法参照Ischiropoulos的方法制备急性CO中毒动物模型。采用组织病理学、免疫组织化学等方法检测大鼠染毒后1、3、5、7、14、21d等各时间点脑组织病理改变的特点并与高压氧治疗组比较,以此评价高压氧的治疗作用。通过原位末端转移酶标记(TUNEL)技术方法进行细胞凋亡的检测,观察急性CO中毒及高压氧治疗后神经元凋亡的发生情况。结果急性CO中毒大鼠脑内发生广泛的病理损伤,中毒组大鼠脑皮质、海马和纹状体等部位神经元出现变性坏死,其中大脑皮质、海马等部位损伤较重。TUNEL染色表明,CO中毒大鼠海马神经元发生凋亡,凋亡神经元从染毒后第3天开始显著增加,第7天达到高峰(P<0.01),以后逐渐减少。CO中毒动物,高压氧治疗组与非治疗组比,脑内神经元变性坏死明显较轻,各时间点海马区损伤均较轻;凋亡神经元数目较少,尤以CO中毒后第5天和第7天明显(P<0.01)。高压氧促进CO中毒大鼠海马区Bcl-2蛋白表达,尤以CO暴露后第3、5天明显(P<0.01)。结论急性CO中毒大鼠出现广泛的迟发性神经元损伤,表现为迟发的神经元坏死和凋亡。高压氧治疗可以有效减少神经元变性坏死,促进凋亡抑制基因Bcl-2表达,从而抑制神经元坏死和凋亡。
Objective To investigate the mechanism of delayed neuronal damage induced by acute carbon monoxide poisoning and the effect of hyperbaric oxygen treatment on delayed neurological syndrome （DNS） ,so as to provide experimental basis for clinical research. Methods Acute carbon monoxide poisoning animal models were established according to Ischiropoulos＇s method. The approaches of histopathology （HP） and immunohistochemistry were offered to observe the neurological damage in the brain of rat at different time after CO exposure,including 1,3,5,7, 14,21 d. At the same time, HBO-treated group with CO-exposed group were compared to assess the effect of hyperbaric oxygen on carbon monoxide poisoning. Terminal deoxynucleotidyl transferase mediated UTP end labeling （TUNEL） was used to detect neural apoptosis and assess the effect of HBO on neural apoptosis induced by CO poisoning. Results There were diffused pathology injuries in the brains of rats following acute CO poisoning. Compared with control group, neural necrosis was observed in pallium ,hippocampus and striatum after CO poisoning. Especially, the pathological damage of pallium and hippocampus was more severe. In the hippocampus of CO-exposed rats, neuronal apoptosis was observed by TUNEL stain. The number of neuronal apoptosis increased significantly beginning from the 3rd day,and reached the pinnacle at the 7th day after CO poisoning （P 〈0.01 ）. HBO treatment can alleviate neural necrosis induced by CO poisoning. The number of neural necrosis in HBO-treated group was fewer than that in CO-treated group. Compared with CO-exposed group, the number of neuronal apoptosis of HBO-treated group was decreased,especially significantly at the 5th and 7th day after CO exposure （P 〈 0.01 ）. At the same time, the expression of protein Bcl-2 increased after HBO treatment,especially at the 3rd and 5th day after CO exposure （P 〈 0.01 ）. Conclusions Acute CO poisoning induced pathology injury in the brains of rats diffusely, manifesting delayed neu
出处
《中华航海医学与高气压医学杂志》
CAS
CSCD
2007年第2期69-73,共5页
Chinese Journal of Nautical Medicine and Hyperbaric Medicine
基金
全军"十一五"医药卫生课题(06MA213)
