CAJ | 학술논문

目的探讨重组人促红细胞生成素(rhEPO)对大鼠创伤性脑损伤后(TBI)脑组织核因子NF - κB的表达、下游炎性因子水平及皮层神经细胞凋亡的调控作用.方法 72只Wistar大鼠随机分成对照组、TBI组、TBI+ rhEPO组,后两组再分为脑损伤后1d、3d、7d亚组,应用EMSA法检测挫伤灶周围脑组织NF - κB结合活性、ELISA法检测炎性因子TNF -α、IL -6水平、干湿比重法检测脑组织水含量、TUNEL法检测皮层神经细胞凋亡.结果 TBI后脑组织中NF - κB结合活性、炎性因子水平持续升高；伤后脑水肿明显；TUNEL阳性细胞显著增多.给予rhEPO治疗后,脑组织NF- κB结合活性、TNF -α、IL -6水平、伤侧脑组织水肿程度及神经细胞凋亡均比TBI组降低(P＜0.01).结论 rhEPO能够抑制TBI后脑组织NF - κB的结合活性、降低下游炎性因子的表达和脑水肿程度、减少神经细胞凋亡,明显减轻继发性脑损害.
목적 탐토중조인촉홍세포생성소(rhEPO)대대서창상성뇌손상후(TBI)뇌조직핵인자NF - κB적표체、하유염성인자수평급피층신경세포조망적조공작용.방법 72지Wistar대서수궤분성대조조、TBI조、TBI+ rhEPO조,후량조재분위뇌손상후1d、3d、7d아조,응용EMSA법검측좌상조주위뇌조직NF - κB결합활성、ELISA법검측염성인자TNF -α、IL -6수평、간습비중법검측뇌조직수함량、TUNEL법검측피층신경세포조망.결과 TBI후뇌조직중NF - κB결합활성、염성인자수평지속승고；상후뇌수종명현；TUNEL양성세포현저증다.급여rhEPO치료후,뇌조직NF- κB결합활성、TNF -α、IL -6수평、상측뇌조직수종정도급신경세포조망균비TBI조강저(P＜0.01).결론 rhEPO능구억제TBI후뇌조직NF - κB적결합활성、강저하유염성인자적표체화뇌수종정도、감소신경세포조망,명현감경계발성뇌손해.
Objective To investigate the role of rhEPO in regulating expression of nuclear factorkappaB (NF- κB)、proinflammatory cytokines and neural apoptosis in the injured brain following traumatic brain injury.Methods A total of 72 Wistar rats were randomly divided into control group,trauma group and rhEPO treatment group.TBI group and rhEPO group sacrificed at days 1,3 and 7 post injury respectively.Activity of NF - κB in the brain tissues were detected by using EMSA and levels of TNF - αand IL - 6 by ELISA.The water content of the injured brain was measured by dry -wet weight method.Furthermore,apoptosis in the cortical contusion was estimated by TUNEL method.Result The result showed a persistent up -regulation of NF- κB binding activity,expression of TNF -α,IL-6 in the area surrounding the injuried brain and significant brain edema.The TUNEL positive cells significantly increased.The level of NF - κB binding activity and inflammatory factors expression,the water content of the injury brain and apoptosis can be significantly decreased by administration of rhEPO ( P ＜ 0.01 ).Conclusion rhEPO administration can inhibit the binding activity of the NF - κB,down - regulate the expression of the inflammatory factors,alleviate the brain edema and apoptosis and decrease the secondary brain injury after TBI.