中国妇幼健康研究
中國婦幼健康研究
중국부유건강연구
CHINESE JOURNAL OF MATERNAL AND CHILD HEALTH RESEARCH
2013年
6期
804-807
,共4页
脑缺氧缺血%重组人促红细胞生成素%凋亡%流式细胞学分析
腦缺氧缺血%重組人促紅細胞生成素%凋亡%流式細胞學分析
뇌결양결혈%중조인촉홍세포생성소%조망%류식세포학분석
cerebral hypoxia ischemia%recombinant human erythropoietin (rhEPO)%apoptosis%flow cytometry (FCM)
目的：探讨重组人促红细胞生成素（ rhEPO）对新生鼠缺氧缺血性脑损伤的神经保护作用。方法57只7天龄新生鼠随机分为假手术对照（正常对照组）、缺氧缺血性脑损伤动物模型组（ HIBD模型）、rhEPO治疗组。在建立HIBD模型后， rhEPO治疗组立即一次性腹腔注射3000IU/kg剂量的rhEPO；HIBD模型组注射等量生理盐水；于处置后24h电镜观察脑组织病理形态学变化，流式细胞计检测脑受损局部神经元细胞凋亡情况，实验7天进行短期感觉运动反射评价。结果与正常对照组相比，HIBD模型组光镜下左侧大脑病理损伤明显；HIBD模型组神经细胞凋亡与正常对照组相比增加（28．30±4．80 vs 47．14±6．97，P＜0．05），存活细胞减少（72．42±7．93 vs 48．33±8．39，P＜0．05）；rhEPO治疗组细胞凋亡与HIBD模型组相比减轻（47．14±6．97 vs 36．88±9．43，P＜0．05），存活细胞增多（48．33±8．39 vs 60．06±8．32，P＜0．05）；HIBD模型组悬吊测试、翻正反射、悬崖逃避反射、趋地反射这四项反射与正常对照组相比成绩均较差，提示神经功能受损；rhEPO治疗组翻正反射及悬崖逃避反射时间与HIBD模型组相比缩短，（4．59±0．11 vs 2．84±0．13，10．84±1．26 vs 8．49±1．03，均P＜0．05），以上差异均有统计学意义。结论外源性给予rhEPO能够减轻HIBD大鼠脑组织病理损伤，稳定细胞结构，抑制细胞凋亡，改善短期行为学评价，从而发挥其神经保护作用。
目的：探討重組人促紅細胞生成素（ rhEPO）對新生鼠缺氧缺血性腦損傷的神經保護作用。方法57隻7天齡新生鼠隨機分為假手術對照（正常對照組）、缺氧缺血性腦損傷動物模型組（ HIBD模型）、rhEPO治療組。在建立HIBD模型後， rhEPO治療組立即一次性腹腔註射3000IU/kg劑量的rhEPO；HIBD模型組註射等量生理鹽水；于處置後24h電鏡觀察腦組織病理形態學變化，流式細胞計檢測腦受損跼部神經元細胞凋亡情況，實驗7天進行短期感覺運動反射評價。結果與正常對照組相比，HIBD模型組光鏡下左側大腦病理損傷明顯；HIBD模型組神經細胞凋亡與正常對照組相比增加（28．30±4．80 vs 47．14±6．97，P＜0．05），存活細胞減少（72．42±7．93 vs 48．33±8．39，P＜0．05）；rhEPO治療組細胞凋亡與HIBD模型組相比減輕（47．14±6．97 vs 36．88±9．43，P＜0．05），存活細胞增多（48．33±8．39 vs 60．06±8．32，P＜0．05）；HIBD模型組懸弔測試、翻正反射、懸崖逃避反射、趨地反射這四項反射與正常對照組相比成績均較差，提示神經功能受損；rhEPO治療組翻正反射及懸崖逃避反射時間與HIBD模型組相比縮短，（4．59±0．11 vs 2．84±0．13，10．84±1．26 vs 8．49±1．03，均P＜0．05），以上差異均有統計學意義。結論外源性給予rhEPO能夠減輕HIBD大鼠腦組織病理損傷，穩定細胞結構，抑製細胞凋亡，改善短期行為學評價，從而髮揮其神經保護作用。
목적：탐토중조인촉홍세포생성소（ rhEPO）대신생서결양결혈성뇌손상적신경보호작용。방법57지7천령신생서수궤분위가수술대조（정상대조조）、결양결혈성뇌손상동물모형조（ HIBD모형）、rhEPO치료조。재건립HIBD모형후， rhEPO치료조립즉일차성복강주사3000IU/kg제량적rhEPO；HIBD모형조주사등량생리염수；우처치후24h전경관찰뇌조직병리형태학변화，류식세포계검측뇌수손국부신경원세포조망정황，실험7천진행단기감각운동반사평개。결과여정상대조조상비，HIBD모형조광경하좌측대뇌병리손상명현；HIBD모형조신경세포조망여정상대조조상비증가（28．30±4．80 vs 47．14±6．97，P＜0．05），존활세포감소（72．42±7．93 vs 48．33±8．39，P＜0．05）；rhEPO치료조세포조망여HIBD모형조상비감경（47．14±6．97 vs 36．88±9．43，P＜0．05），존활세포증다（48．33±8．39 vs 60．06±8．32，P＜0．05）；HIBD모형조현조측시、번정반사、현애도피반사、추지반사저사항반사여정상대조조상비성적균교차，제시신경공능수손；rhEPO치료조번정반사급현애도피반사시간여HIBD모형조상비축단，（4．59±0．11 vs 2．84±0．13，10．84±1．26 vs 8．49±1．03，균P＜0．05），이상차이균유통계학의의。결론외원성급여rhEPO능구감경HIBD대서뇌조직병리손상，은정세포결구，억제세포조망，개선단기행위학평개，종이발휘기신경보호작용。
Objective To explore the protective effects of recombinant human erythropoietin ( rhEPO) on hypoxic-ischemic brain damage in neonatal rats .Methods Fifty-seven 7-day-old Sprague-Dawley rats were randomly assigned to 3 groups: sham-operated group ( control group), hypoxic-ischemic brain damage model (HIBD group) and rhEPO-intervention group.Immediately after reparation of HIBD model , the rhEPO-intervention group was injected 3 000U/kg of rhEPO into the abdominal cavity , and the HIBD group was injected the same dose of normal saline .After 24 hours histological changes in brain tissue were observed with electron microscope .Apoptosis of damage neuron was measured by flow cytometry (FCM).Four separate reflexes were evaluated at 7day.Results Compared with the sham-operated group, the rats in HIBD group showed obvious histo-pathological damage in left brain.The apoptosis of neuron increased (28.30 ±4.80 vs 47.14 ± 6.97, P<0.05) and the survived cells decreased (72.42 ±7.93 vs 48.33 ±8.39, P<0.05).Compared with the HIBD group, the neuronal apoptosis decreased (47.14 ±6.97 vs 36.88 ±9.43,P<0.05) and survived cells increased (48.33 ±8.39 vs 60.06 ±8.32, P<0.05) in rhEPO-intervention group.The evaluation on four reflections ( suspension test, righting reflex, cliff aversion reflex and tendency reflection ) in HIBD group was worse than that in the control group , which indicated nerve function injury .Compared with the HIBD group, the righting reflex and cliff aversion reflex were shortened in rhEPO-intervention group (4.59 ±0.11 vs 2.84 ±0.13, 10.84 ± 1.26 vs 8.49 ±1.03, P<0.05).The differences between groups and among groups were all significant .Conclusion Extrinsic rhEPO can reduce pathologic injury of brain tissues in HIBD rats and plays a neuroprotective role through stabilizing cell structure , inhibiting cell apoptosis and improving short-term behavioral assessment .
