中华神经医学杂志
中華神經醫學雜誌
중화신경의학잡지
Chinese Journal of Neuromedicine
2015年
10期
989-993
,共5页
徐进旺%李爱民%刘希光%陈慧珍%李宁%孙勇%颜士卫%王端磊
徐進旺%李愛民%劉希光%陳慧珍%李寧%孫勇%顏士衛%王耑磊
서진왕%리애민%류희광%진혜진%리저%손용%안사위%왕단뢰
米诺环素%面神经%缺血损伤%细胞凋亡%胶质细胞源性神经营养因子
米諾環素%麵神經%缺血損傷%細胞凋亡%膠質細胞源性神經營養因子
미낙배소%면신경%결혈손상%세포조망%효질세포원성신경영양인자
Minocycline%Facial nerve%Ischemia injury%Apoptosis%Glial cell line-derived neurotrophic factor
目的 观察米诺环素对大鼠面神经缺血损伤后运动神经元胶质细胞源性神经营养因子(GDNF)表达的影响,探讨其对面神经缺血损伤的保护作用. 方法 120只成年雄性SD大鼠按照随机数字表法分为假手术组(40只)、面神经损伤组(简称损伤组,40只)及米诺环素组(40只).显微手术阻断后2组大鼠鼓室段岩动脉建立大鼠面神经缺血损伤模型,米诺环素组术后每天灌胃给予米诺环素60 mg/kg,假手术组和损伤组给予等量生理盐水.分别于建模后3d、7d、14d、28 d取面神经核组织进行HE染色,原位末端转移酶标记(TUNEL)法检测凋亡的面神经元,免疫组织化学染色和Western blotting检测面神经元中GDNF蛋白的表达. 结果 HE染色结果显示米诺环素组面神经元胞体缩小、胞浆浓缩,轴突不明显等病变均轻于损伤组;TUNEL检测示各时间点米诺环素组面神经元凋亡数量明显低于损伤组,差异有统计学意义(P<0.05);免疫组化染色和Westernblotting显示米诺环素组和损伤组面神经元内GDNF蛋白表达增高,且米诺环素组GDNF表达明显高于损伤组,差异有统计学意义(P<0.05). 结论 米诺环素在面神经缺血损伤后通过增强GDNF表达,减少面运动神经元的凋亡,从而对面神经元发挥保护作用.
目的 觀察米諾環素對大鼠麵神經缺血損傷後運動神經元膠質細胞源性神經營養因子(GDNF)錶達的影響,探討其對麵神經缺血損傷的保護作用. 方法 120隻成年雄性SD大鼠按照隨機數字錶法分為假手術組(40隻)、麵神經損傷組(簡稱損傷組,40隻)及米諾環素組(40隻).顯微手術阻斷後2組大鼠鼓室段巖動脈建立大鼠麵神經缺血損傷模型,米諾環素組術後每天灌胃給予米諾環素60 mg/kg,假手術組和損傷組給予等量生理鹽水.分彆于建模後3d、7d、14d、28 d取麵神經覈組織進行HE染色,原位末耑轉移酶標記(TUNEL)法檢測凋亡的麵神經元,免疫組織化學染色和Western blotting檢測麵神經元中GDNF蛋白的錶達. 結果 HE染色結果顯示米諾環素組麵神經元胞體縮小、胞漿濃縮,軸突不明顯等病變均輕于損傷組;TUNEL檢測示各時間點米諾環素組麵神經元凋亡數量明顯低于損傷組,差異有統計學意義(P<0.05);免疫組化染色和Westernblotting顯示米諾環素組和損傷組麵神經元內GDNF蛋白錶達增高,且米諾環素組GDNF錶達明顯高于損傷組,差異有統計學意義(P<0.05). 結論 米諾環素在麵神經缺血損傷後通過增彊GDNF錶達,減少麵運動神經元的凋亡,從而對麵神經元髮揮保護作用.
목적 관찰미낙배소대대서면신경결혈손상후운동신경원효질세포원성신경영양인자(GDNF)표체적영향,탐토기대면신경결혈손상적보호작용. 방법 120지성년웅성SD대서안조수궤수자표법분위가수술조(40지)、면신경손상조(간칭손상조,40지)급미낙배소조(40지).현미수술조단후2조대서고실단암동맥건립대서면신경결혈손상모형,미낙배소조술후매천관위급여미낙배소60 mg/kg,가수술조화손상조급여등량생리염수.분별우건모후3d、7d、14d、28 d취면신경핵조직진행HE염색,원위말단전이매표기(TUNEL)법검측조망적면신경원,면역조직화학염색화Western blotting검측면신경원중GDNF단백적표체. 결과 HE염색결과현시미낙배소조면신경원포체축소、포장농축,축돌불명현등병변균경우손상조;TUNEL검측시각시간점미낙배소조면신경원조망수량명현저우손상조,차이유통계학의의(P<0.05);면역조화염색화Westernblotting현시미낙배소조화손상조면신경원내GDNF단백표체증고,차미낙배소조GDNF표체명현고우손상조,차이유통계학의의(P<0.05). 결론 미낙배소재면신경결혈손상후통과증강GDNF표체,감소면운동신경원적조망,종이대면신경원발휘보호작용.
Objective To explore the neuroprotective mechanism of minocycline in facial motoneurons by studying the neuroprotective effect of minocycline on expression of glial cell-derived neurotrophic factor (GDNF) in rats after facial nerve ischemia.Methods One hundred and twenty male Sprague-Dawley rats were randomly divided into sham-operated (SH) group, petrosal artery interruption (PAI) group and minocyline treated (MC) group (n=40).Facial nerve ischemia models in the later two groups were established by occluding the tympanic segment of the petrosal artery.The rats in MC group were given intragastric injection of minocycline (60 mg/kg) each day, while rats in the PAI and SH groups were given the same amount of normal saline.The animals were executed 3, 7, 14, 28 days after ischemia.The histopathological changes of facial neurons were observed by hematoxylin and eosin (HE) staining.The apoptosis changes in facial motoneurons were detected by Terminal deoxynucleoside transferase mediated-dUTP nick end labeling (TUNEL).The protein expression of GDNF was measured by immunohistochemistry staining and Western blotting.Results HE staining results showed that MC group had less severe nerve damage (shrank neuronal somas, condensation of cytoplasm and unconspicuous axon) than PAI group.The TUNEL results showed that the number ofapoptotic cells in MC group was significantly fewer than that in PAI group at each time point (P<0.05).Immunohistochemistry and Western blotting indicated increased GDNF protein expression in the PAI group and MC group as compared with that in the SH group, and the GDNF expression in MC group was significantly higher than that in PAI group (P<0.05).Conclusion Minocycline could play a strong neuroprotective effect on facial motoneurons of rats after facial nerve ischemia by enhancing GDNF expression and inhibiting facial motoneurons apoptosis.