摘要
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 study the change of brain cell mitochondrial membrane potential （△ψm） in hypoxic-ischemic brain damage （HIBD） and the effect of the non-competitive NMDA receptor antagonist MK-801 on the change in vivo. Methods Neonatal SD rat HIBD model was adopted in this study. SD rat pups were randomly divided into normal （n = 6）, HIBD （n= 10） and HIBD＋MK-801 （n= 10） groups （0.3 mg/kg MK-801 was i.p given before the hypoxia）. Animals were decapitated right after HI imult. The △ψm indicated by the fluorescence of Rhodamine 123 was measured by flow cytometry after the preparation of single brain cell suspension. Results After HIBD, △ψm of both hemispheres were significantly decreased（ P 〈 0.05） （mainly in the ipsilateral side）, The ipsi-△ψm= was decreased from normally （18.93 ＋ 0.74）MFL to（7.95 ＋ 0.32）MFL after HIBD. The ipsi-/contra-△ψm= ratio was signiflcantly decreased from normally （1.06 ±0.05） to （0.80±0.06） after HIBD （decreased by 24.5 %, P 〈 0.05）. In HIBD ＋ MK-801 group, the ipsi-△ψm, was （ 10.83 ± 0.41 ） MFL, the ipsi-/contra-△ψm ration was recovered to 1.07±0.06. Comparing to the HIBD group, there was a significant difference （ P 〈 0.05）. Conclusions After HIBD, brain cell △ψm decreases significantly, which indicates that the mitochondrial function is significantly damaged. MK - 801 can reduce this damage it indicates that NMDA receptor antagonist may treat perinatal HIBD by reducing the HI-induced mitochondrial damage.
出处
《新生儿科杂志》
2005年第4期164-166,共3页
The Journal of Neonatology
