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目的了解围生期缺氧缺血性脑损伤(HIBD)后脑细胞线粒体膜电势(△Ψm)的变化及NMDA型谷氨酸受体拮抗剂MK-801对这一变化的影响。方法应用7日龄新生SD大鼠HIBD动物模型,将实验动物分为正常对照组(n=6),HIBD组(n=10)和HIBD+MK-801组(n=10)(MK-801于低氧处理前按0.3mg/kg剂量腹腔注射)。于缺氧缺血后立即断头处死动物,制成脑细胞悬液后,以罗丹明123(Rho123)标记、以流式细胞仪测定△Ψm的变化。结果围产期HIBD时双侧脑细胞△Ψm值均显著降低,差异具有显著性(P<0.05),以损伤侧(右侧)为甚,右侧脑细胞△Ψm由正常状态下的(18.93±0.74)MFL降至损伤后的(7.59±0.32)MFL,右:左△Ψm比值由正常状态下的1.06±0.05降至损伤后的0.80±0.06(降低了24.5%),差异具有显著性(P<0.05)。结论HIBD后脑细胞△Ψm明显降低,提示线粒体功能明显受损;MK-801可减轻这一变化,提示NMDA型谷氨酸受体拮抗剂可通过减轻线粒体功能受损程度治疗围产期缺氧缺血性脑损伤。
Objective To investigate the changes of mitochondrial membrane potential (△ Ψm) and the effect of MK-801, an NMDA-type glutamate receptor antagonist, on the changes of brain cells after perinatal hypoxic-ischemic brain damage (HIBD). Methods HIBD animal models of 7-day-old neonatal SD rats were divided into normal control group (n = 6), HIBD group (n = 10) and HIBD + MK-801 group 0.3 mg / kg dose before hypoxia treatment by intraperitoneal injection). The animals were decapitated immediately after hypoxia and ischemia, and the brain cell suspension was prepared and labeled with rhodamine 123 (Rho123). The changes of △ ψm were determined by flow cytometry. Results The △ Ψm of bilateral brain cells in HIBD during perinatal period were significantly decreased (P <0.05), especially in the lesion side (right). The △ Ψm of the right cerebrum was increased from (18.93 ± 0.74) MFL to (7.59 ± 0.32) MFL after injury, the right: left △ Ψm ratio decreased from 1.06 ± 0.05 in normal state to 0.80 ± 0.06 after injury (24.5% reduction), the difference was significant P <0.05). Conclusions The △ Ψm of brain cells in HIBD group decreased obviously, suggesting that the function of mitochondria was significantly impaired. MK-801 could reduce this change, suggesting that NMDA glutamate receptor antagonist could treat perinatal hypoxia by reducing mitochondrial dysfunction Bloody brain injury.