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目的:探讨肌苷对化学性缺氧损伤后少突胶质前体细胞(oligodendrocyte precursor cells,OPC)存活的影响。方法:原代培养新生SD大鼠脑皮层OPC,随机分为四个组,即空白对照组、肌苷对照组、鱼藤酮损伤组和肌苷治疗组。肌苷治疗组是在添加肌苷30 min后再用鱼藤酮损伤,24 h后用MTT、PI染色和免疫荧光组织化学染色检测各组细胞吸光值的差异、细胞死亡比率的差异和细胞凋亡比率的差异。结果:与对照组比较,鱼藤酮损伤组的吸光值明显下降(P<0.001)、细胞死亡比率明显增加(P<0.001)但细胞凋亡比率没有差异;与空白对照组比较,10 mmol/L肌苷对照组的的吸光值明显下降(P<0.01);与鱼藤酮损伤组比较不同剂量肌苷治疗组的吸光值、细胞死亡比率和细胞凋亡比率均没有差异。结论:在鱼藤酮介导的化学性缺氧损伤条件下,肌苷对OPC的存活没有明显的保护作用,而且大剂量肌苷还可损伤正常的OPC,提示大剂量肌苷在中枢神经系统损伤后髓鞘的修复过程中可能具有负面作用。
Objective: To investigate the effect of inosine on the survival of oligodendrocyte precursor cells (OPC) after chemical hypoxia injury. Methods: Primary cultured neonatal SD rat cortical OPCs were randomly divided into four groups: blank control group, inosine control group, rotenone injury group and inosine treatment group. Inosine treatment group was treated with rotenone for 30 min after addition of inosine, and 24 h later, the difference of cell absorbance between the groups was detected by MTT, PI staining and immunofluorescence histochemical staining. The difference of cell death rate and apoptosis rate The difference. RESULTS: Compared with the control group, the absorbance of rotenone group was significantly decreased (P <0.001), the cell death rate was significantly increased (P <0.001), but there was no difference in apoptosis rate. Compared with the blank control group, 10 mmol / L muscle (P <0.01). Compared with rotenone-treated group, there was no difference in absorbance, cell death rate and apoptosis rate of different doses of inosine treatment group. CONCLUSION: In the condition of rotenone-mediated chemical hypoxia injury, inosine has no significant protective effect on the survival of OPC, and high dose of inosine can also damage normal OPC, suggesting that high dose of inosine in central nervous system injury Myelin repair process may have a negative effect.