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Effect of hyperbaric oxygen therapy on delayed neuronal damage after acute carbon monoxide poisoning in rats
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- Author:
- No author available
- Journal Title:
- CHINESE JOURNAL OF NAUTICAL MEDICINE AND HYPERBARIC MEDICINE
- Issue:
- 2
- DOI:
- 10.3760/cma.j.issn.1009-6906.2007.02.002
- Key Word:
- 急性一氧化碳中毒;迟发性脑损伤;神经元损伤;组织病理学;免疫组织化学;细胞凋亡;高压氧;大鼠
Abstract： 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s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.
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