Effects of acute carbon monoxide poisoning on the differentiation of oligodendrocyte precursors in the brain of rats

Abstract

Objective To explore the effects of acute carbon monoxide poisoning (ACOP) on the differentiation of oligodendrocyte precursors in the brain of rats. Methods ACOP rat model was developed by intraperitoneal injection of CO to 45 SD rats from the samples of 60 rats and selected 15 rats from the survival rats as the ACOP group, and the remaining 15 rats were designated as the control group, which were injected air according to the same treatment scheme. Following development of the model, brain tissue samples of the rats were collected at day 1, 3, 7, 14 and 30. Immunofluorescence histochemistry was used to detect the number of NG2 and CC1 positive cells in the cortex and hippocampus. Results (1) As compared with the control group, the NG2 positive cells in the ACOP group displayed irregular shape, with shrinkage and a decreased number. (2) Following treatment at day 1 and 3, the number of NG2 positive cells in cerebral cortex of the ACOP group was significantly increased(P<0.05). However, it began to decrease at day 7(P<0.05), and the decreasing trend became more prominent at day 14 and 30(P<0.01). The number of CC1 positive cells began to decrease at day 3(P<0.05), and the decreasing trend became more prominent at day 7(P<0.01). And at day 14 and 30, the number of CC1 positive cells was smaller as compared with that of the control group(P<0.05). However, the number of CC1 positive cells in the cerebral cortex of the ACOP group at day 30 was increased by about 50%, when compared with that at day 14.(3)As compared with the control group, the number of NG2 positive cells in the hippocampus of the ACOP group was obviously increased at day 1 after treatment(P<0.01). However, the decreasing trend became less prominent at day 7, 14 and 30(P<0.01). The number of CC1 positive cells in the hippocampus of the ACOP group was decreased as compared with that of the control group at day 1, 3, 7, 14, 30(P<0.05). Conclusions Following ACOP, oligodendrocyte precursors (OPCs) and oligodendrocytes (OLs) in the brain of rats were damaged to a certain extent, the mechanism might be the mobilization of self-repair, the induction of OPCs proliferation and differentiation of mature OLs, and as a consequence, the repair of damaged myelin was achieved. Key words: Carbon monoxide poisoning; Oligodendrocyte precursor cell; Olidgodendrocyte; Myelin