中国医师杂志
中國醫師雜誌
중국의사잡지
JOURNAL OF CHINESE PHYSICIAN
2014年
12期
1645-1648
,共4页
余伟军%余智%卢波达%刘凯的%方来明
餘偉軍%餘智%盧波達%劉凱的%方來明
여위군%여지%로파체%류개적%방래명
脑源性神经营养因子%脑缺血%再灌注损伤%NF-κB%肿瘤坏死因子α%细胞凋亡
腦源性神經營養因子%腦缺血%再灌註損傷%NF-κB%腫瘤壞死因子α%細胞凋亡
뇌원성신경영양인자%뇌결혈%재관주손상%NF-κB%종류배사인자α%세포조망
Brain-derived neurotrophic factor%Brain ischemia%Reperfusion injury%NF-kappa B%Tumor necrosis factor-alpha%Apoptosis
目的 探讨脑源性神经营养因子(BDNF)干预对脑缺血再灌注损伤大鼠脑组织中NF-κB、TNF-α和细胞凋亡的变化及其可能机制.方法 84只健康雄性SD大鼠按随机数字法分为BDNF组(n=42)及对照组(n=42),前者通过改良Zea-longa法建立脑缺血再灌注损伤模型后立即予以腹腔注射0.5μg/μl BDNF,对照组则用同等剂量的生理盐水代替BDNF,以后各组分别每24小时腹腔注射一次等量BDNF/生理盐水,直至大鼠被处死,根据伤后处死时间分为l、3、6、12、24 h、3d和7d共7个亚组,每亚组各6只.取缺血灶周围组织采用免疫组织化学方法检测并比较脑组织中NF-κB及TNF-α蛋白表达水平,同时采用原位末端标记(TUNEL)法观察并比较细胞凋亡情况.结果 BDNF组NF-κB及TNF-α蛋白表达水平较对照组均明显下降,差异有统计学意义(P＜0.05),且两组中二者均呈正相关(P ＜0.001);同时BDNF组脑组织细胞凋亡数量较对照组也有所下降(P＜0.05).结论 脑缺血再灌注损伤后脑源性神经营养因子可能通过降低NF-κB活性,控制炎症反应,减少细胞凋亡,从而发挥对脑缺血再灌注损伤后的神经细胞发挥保护作用.
目的 探討腦源性神經營養因子(BDNF)榦預對腦缺血再灌註損傷大鼠腦組織中NF-κB、TNF-α和細胞凋亡的變化及其可能機製.方法 84隻健康雄性SD大鼠按隨機數字法分為BDNF組(n=42)及對照組(n=42),前者通過改良Zea-longa法建立腦缺血再灌註損傷模型後立即予以腹腔註射0.5μg/μl BDNF,對照組則用同等劑量的生理鹽水代替BDNF,以後各組分彆每24小時腹腔註射一次等量BDNF/生理鹽水,直至大鼠被處死,根據傷後處死時間分為l、3、6、12、24 h、3d和7d共7箇亞組,每亞組各6隻.取缺血竈週圍組織採用免疫組織化學方法檢測併比較腦組織中NF-κB及TNF-α蛋白錶達水平,同時採用原位末耑標記(TUNEL)法觀察併比較細胞凋亡情況.結果 BDNF組NF-κB及TNF-α蛋白錶達水平較對照組均明顯下降,差異有統計學意義(P＜0.05),且兩組中二者均呈正相關(P ＜0.001);同時BDNF組腦組織細胞凋亡數量較對照組也有所下降(P＜0.05).結論 腦缺血再灌註損傷後腦源性神經營養因子可能通過降低NF-κB活性,控製炎癥反應,減少細胞凋亡,從而髮揮對腦缺血再灌註損傷後的神經細胞髮揮保護作用.
목적 탐토뇌원성신경영양인자(BDNF)간예대뇌결혈재관주손상대서뇌조직중NF-κB、TNF-α화세포조망적변화급기가능궤제.방법 84지건강웅성SD대서안수궤수자법분위BDNF조(n=42)급대조조(n=42),전자통과개량Zea-longa법건립뇌결혈재관주손상모형후립즉여이복강주사0.5μg/μl BDNF,대조조칙용동등제량적생리염수대체BDNF,이후각조분별매24소시복강주사일차등량BDNF/생리염수,직지대서피처사,근거상후처사시간분위l、3、6、12、24 h、3d화7d공7개아조,매아조각6지.취결혈조주위조직채용면역조직화학방법검측병비교뇌조직중NF-κB급TNF-α단백표체수평,동시채용원위말단표기(TUNEL)법관찰병비교세포조망정황.결과 BDNF조NF-κB급TNF-α단백표체수평교대조조균명현하강,차이유통계학의의(P＜0.05),차량조중이자균정정상관(P ＜0.001);동시BDNF조뇌조직세포조망수량교대조조야유소하강(P＜0.05).결론 뇌결혈재관주손상후뇌원성신경영양인자가능통과강저NF-κB활성,공제염증반응,감소세포조망,종이발휘대뇌결혈재관주손상후적신경세포발휘보호작용.
Objective To investigate the changes of nuclear factor-κB (NF-κB),tumor necrosis factor-α(TNF-α),and cell apoptosis of cerebral ischemia-reperfusion injury and the influence of brain-derived neutrophic factor(BDNF) on these parameters in rats.Methods Eighty-four male Sprague-Dawley (SD) rats were randomly divided into two groups:BDNF (n =42) and control (n =42) groups.The BDNF group was induced using the improved Zea-longa method and were received abdominal injections of BDNF (0.5 μg/μl) immediately after injury.The control group was received abdominal injections with the same dose sodium chloride injection immediately after injury and repeated one time everyday until the rats was killed.Each group was divided into seven subgroups by sacrificed time after injury,including subgroups 1 h,3 h,6 h,12 h,24 h,3 d,and 7 d; each subgroup got 6 rats.Each subgroup were randomly selected three rats after being killed.The expressions of NF-κB and TNF-α of rats contusion peri tissues brain tissue were detected by immunohistochemical methods.Terminal deoxynucleotidyl transferase (TUNEL) method was used to observe the peri cell apoptosis after brain contusion.Results The expressions of NF-κB and TNF-α in BDNF group was significantly decreased relative to the control group (P ＜ 0.05),with a significant positive correlation between two parameters in two groups (P ＜ 0.001).The number of apoptotic cells was significantly decreased in the BDNF group relative to control group (P ＜ 0.05).Conclusions Brain-derived neutrophic factor probably relieves inflammation response,reduces the change of secondary brain injury after traumatic brain injury,and decreases neural cell apoptosis,and finally provides protection of neurocytes.
