高压氧对急性CO 中毒大鼠脑内源性神经干细胞的影响

目的:探讨高压氧对急性CO中毒大鼠脑内源性神经干细胞的影响,分析HBO治疗急性CO中毒脑损伤的机制。方法:建立急性CO中毒大鼠模型,给予高压氧(HBO)治疗后,H-E染色观察大鼠脑组织病理学变化,免疫组织化学方法检测大鼠脑内神经干细胞(nestin)和星形胶质细胞(GFAP)的表达。结果:H-E染色标本上,对照组脑内神经元形态正常,染毒组脑皮质出现大量变性坏死细胞,海马锥体细胞层稀疏,HBO组坏死细胞明显减少。免疫组化结果显示对照组nestin和GFAP表达数量形态均正常,染毒组nestin表达增加,但无统计学意义,GFAP形态数量发生改变,HBO组nestin表达明显增加,且在大脑皮层可见部分nestin阳性细胞和nestin-GFAP双阳性细胞;GFAP表达趋于正常。结论:急性CO中毒作为脑损伤因素可轻度激活大鼠脑内源性神经干细胞,并使星形胶质细胞增生变形、神经元变性坏死,HBO治疗可减轻星形胶质细胞损伤,明显激活内源性神经干细胞,并促使其增殖、迁移和分化。提示HBO可能通过激活神经干细胞起治疗作用。

Effect of HBO on Neural Stem Cells in Rat Models of Acute CO Poisoning

Objective: To discuss the effect of HBO on neural stem cells(NSCs) in rat models of acute CO poisoning,and to analyze the mechanism of HBO treating brain injury after acute CO poisoning.Methods: After set up models of acute CO poisoning,rats from CO group gave HBO treatment.H-E staining was used to observe the pathological changes of brain tissues and immunohistoc-hemical staining was used to observe the expression of neural stem cells(nestin) and astrocytes(GFAP).Results: The H-E staining showed that the morphology of neurons in control group were normal,and that of CO-poisoned groups were degenerated and necrotic in spot and sheet,and the cortex of CO-poisoned groups were looser as well as the pyramidal layer of hippocampus got thinner,but in HBO group the degenerated and necrotic neurons were less than CO group.The immunohistochemical staining showed that expression of nestin and GFAP was normal in quantity and morphology in control group,but in CO poisoned groups the expression of nestin increased and the expression of GFAP was abnormal in quantity and morphology.In HBO group these nestin positive cells increased significantly and astrocytes became normal.And there were nestin-GFAP double positive cells in cortex.Conclusions: CO poisoning made NSCs increased,but there were no differences between CO group and control group.But HBO makes the increase significant and caused NSCs’ generation,differentiation and immigration.It suggests that HBO may treat the brain injury by activating NSCs.