CAJ | 학술논문

目的研究A20基因在创伤性颅脑损伤(traumatic brain injury,TBI))中的抗凋亡脑保护作用.方法实验组与对照组各35只SD大鼠,制作重度TBI模型后,实验组与对照组分别在伤后30 min,在立体定向仪下向损伤灶周边皮质及损伤灶内多点注射脂质体-pcDNA3.1-A20和脂质体-pcDNA3.1空质粒.两组分别于术后12,24,48,72,168 h各取5只大鼠取脑制作切片,免疫组化法检测A20基因的表达和损伤后细胞凋亡的情况;每组剩余的另10只大鼠于TBI后第1,2,3,4周,进行斜板试验测试其神经功能.结果 (1)实验组损伤灶周边A20表达显著高于对照组(P<0.01).(2)TBI后可见损伤侧皮质、海马分布有不同数量的凋亡细胞,以损伤灶周围皮质最为集中;两组的细胞凋亡均在TBI后72 h达到高峰.实验组TBI后12,24,48及72 h神经凋亡数量较对照组明显降低(P<0.01或0.05).(3)伤后第4周,实验组临界角度大于对照组(P<0.05).结论脂质体介导的A20基因治疗能够起到抗损伤后细胞凋亡的神经保护作用.
목적 연구A20기인재창상성로뇌손상(traumatic brain injury,TBI))중적항조망뇌보호작용.방법 실험조여대조조각35지SD대서,제작중도TBI모형후,실험조여대조조분별재상후30 min,재입체정향의하향손상조주변피질급손상조내다점주사지질체-pcDNA3.1-A20화지질체-pcDNA3.1공질립.량조분별우술후12,24,48,72,168 h각취5지대서취뇌제작절편,면역조화법검측A20기인적표체화손상후세포조망적정황;매조잉여적령10지대서우TBI후제1,2,3,4주,진행사판시험측시기신경공능.결과 (1)실험조손상조주변A20표체현저고우대조조(P<0.01).(2)TBI후가견손상측피질、해마분포유불동수량적조망세포,이손상조주위피질최위집중;량조적세포조망균재TBI후72 h체도고봉.실험조TBI후12,24,48급72 h신경조망수량교대조조명현강저(P<0.01혹0.05).(3)상후제4주,실험조림계각도대우대조조(P<0.05).결론지질체개도적A20기인치료능구기도항손상후세포조망적신경보호작용.
Objective To investigate the anti-apoptotic effect of gene A20 in treatment of trau-matic brain injury (TBI). Methods Thirty-five Sprague-Dawley rats were made severe TBI models and assigned randomly to experimental group and control group (35 rats in each group). After severe TBI, the rats in experimental group were injected with liposome-pcDNA3.1-A20 and those in control group injected with liposome pcDNA3.1-A20 at 30 minutes after severe TBI. The animals in both groups were sacrificed to remove the brain of five rats from each group at 12, 24, 48, 72 and 168 hours for sec-tioning. The expression of A20 and neurocyte apoptosis were defined by immunohistological method and TUNEL accordingly. The other ten rats were testified for neurological function at 1,2, 3 and 4 weeks af-ter TBI. Results The expression of A20 in experimental group was higher than that in control group, with statistical differences (P < 0. 01). The peak neurocyte apoptosis was found at 72 hours after TBI. The number of apoptosis cells in experimental group was lower than that in control group at 12, 24, 48 and 72 hours afte TBI (P < 0.01 or 0.05). At the 4th week after TBI, the neurological function in exper-imental group was better than that in control group (P < 0.05). Conclusion Gene therapy with A20 may have anti-apoptosis effect and exert neuroprotective effect on severe TBI.