中华围产医学杂志
中華圍產醫學雜誌
중화위산의학잡지
CHINESE JOURNAL OF PERINATAL MEDICINE
2011年
12期
735-738
,共4页
周春清%许锋%姜红%薛永梅
週春清%許鋒%薑紅%薛永梅
주춘청%허봉%강홍%설영매
血小板源性生长因子%缺氧缺血,脑%细胞凋亡%磷酸丙酮酸水合酶%大鼠
血小闆源性生長因子%缺氧缺血,腦%細胞凋亡%燐痠丙酮痠水閤酶%大鼠
혈소판원성생장인자%결양결혈,뇌%세포조망%린산병동산수합매%대서
Platelet derived growth factor%Hypoxia-ischemic, brain%Apoptosis%Phosphopyruvate hydratase%Rats
目的 研究血小板源性生长因子(platelet derived growth factor,PDGF)对缺氧缺血性脑损伤(hypoxic-ischemic brain damage,HIBD)的新生鼠神经细胞凋亡率及血清神经元特异性烯醇化酶(neuron-specific enolase,NSE)浓度的影响,进而探讨其对HIBD的神经保护作用. 方法 7日龄新生Wistar大鼠48只制备HIBD模型,并分为PDGF治疗组和生理盐水对照组,每组各24只.另取24只为假手术组.治疗组在缺氧缺血后即刻给PDGF-BB 50 ng/kg腹腔注射.对照组和假手术组腹腔注射等体积的生理盐水.每组于处置后12、24和72 h随机取8只处死,留血清标本,酶联免疫吸附法检测大鼠血清标本NSE浓度；取右侧大脑组织制备脑细胞悬液,双染法流式细胞仪检测脑细胞凋亡率.采用单因素方差分析及q检验进行统计学分析. 结果 (1)脑细胞凋亡率:治疗组[(6.09±0.70)％、(9.67±1.52)％和(14.15±1.52)％]和对照组[(8.00±1.10)％、(11.45±2.42)％和(22.90±2.03)％]3个时点的脑细胞凋亡率均较假手术组(2.11±0.54)％、(2.34±0.46)％和(2.21±0.49)％]显著增加(P均＜0.01或＜0.05),治疗组较对照组各时点脑细胞凋亡率均明显降低(P均＜0.01或＜0.05),3组大鼠在12、24、72 h时的组间比较差异均有统计学意义(F=39.01、66.60、194.20,P均＜0.01).(2)血清NSE浓度:各时点对照组[(10.04±0.19) μg/L、(9.33±0.15)μg/L和(8.36±0.16)μg/L]和治疗组[(8.43±0.17)μg/L、(6.73±0.16) μg/L和(6.12±0.13)μg/L]较假手术组[(4.22±0.53)μg/L、(3.96±0.60) μg/L和(3.59±0.55) μg/L]NSE浓度增加(P均＜0.01),治疗组较对照组各时点NSE浓度降低(P均＜0.01),3组大鼠在12、24、72h组间比较差异均有统计学意义(F=371.25、245.61、236.22,P均＜0.01). 结论 PDGF能抑制新生大鼠HIBD后神经细胞凋亡及降低血清NSE浓度,对HIBD新生大鼠有神经保护作用.
目的 研究血小闆源性生長因子(platelet derived growth factor,PDGF)對缺氧缺血性腦損傷(hypoxic-ischemic brain damage,HIBD)的新生鼠神經細胞凋亡率及血清神經元特異性烯醇化酶(neuron-specific enolase,NSE)濃度的影響,進而探討其對HIBD的神經保護作用. 方法 7日齡新生Wistar大鼠48隻製備HIBD模型,併分為PDGF治療組和生理鹽水對照組,每組各24隻.另取24隻為假手術組.治療組在缺氧缺血後即刻給PDGF-BB 50 ng/kg腹腔註射.對照組和假手術組腹腔註射等體積的生理鹽水.每組于處置後12、24和72 h隨機取8隻處死,留血清標本,酶聯免疫吸附法檢測大鼠血清標本NSE濃度；取右側大腦組織製備腦細胞懸液,雙染法流式細胞儀檢測腦細胞凋亡率.採用單因素方差分析及q檢驗進行統計學分析. 結果 (1)腦細胞凋亡率:治療組[(6.09±0.70)％、(9.67±1.52)％和(14.15±1.52)％]和對照組[(8.00±1.10)％、(11.45±2.42)％和(22.90±2.03)％]3箇時點的腦細胞凋亡率均較假手術組(2.11±0.54)％、(2.34±0.46)％和(2.21±0.49)％]顯著增加(P均＜0.01或＜0.05),治療組較對照組各時點腦細胞凋亡率均明顯降低(P均＜0.01或＜0.05),3組大鼠在12、24、72 h時的組間比較差異均有統計學意義(F=39.01、66.60、194.20,P均＜0.01).(2)血清NSE濃度:各時點對照組[(10.04±0.19) μg/L、(9.33±0.15)μg/L和(8.36±0.16)μg/L]和治療組[(8.43±0.17)μg/L、(6.73±0.16) μg/L和(6.12±0.13)μg/L]較假手術組[(4.22±0.53)μg/L、(3.96±0.60) μg/L和(3.59±0.55) μg/L]NSE濃度增加(P均＜0.01),治療組較對照組各時點NSE濃度降低(P均＜0.01),3組大鼠在12、24、72h組間比較差異均有統計學意義(F=371.25、245.61、236.22,P均＜0.01). 結論 PDGF能抑製新生大鼠HIBD後神經細胞凋亡及降低血清NSE濃度,對HIBD新生大鼠有神經保護作用.
목적 연구혈소판원성생장인자(platelet derived growth factor,PDGF)대결양결혈성뇌손상(hypoxic-ischemic brain damage,HIBD)적신생서신경세포조망솔급혈청신경원특이성희순화매(neuron-specific enolase,NSE)농도적영향,진이탐토기대HIBD적신경보호작용. 방법 7일령신생Wistar대서48지제비HIBD모형,병분위PDGF치료조화생리염수대조조,매조각24지.령취24지위가수술조.치료조재결양결혈후즉각급PDGF-BB 50 ng/kg복강주사.대조조화가수술조복강주사등체적적생리염수.매조우처치후12、24화72 h수궤취8지처사,류혈청표본,매련면역흡부법검측대서혈청표본NSE농도；취우측대뇌조직제비뇌세포현액,쌍염법류식세포의검측뇌세포조망솔.채용단인소방차분석급q검험진행통계학분석. 결과 (1)뇌세포조망솔:치료조[(6.09±0.70)％、(9.67±1.52)％화(14.15±1.52)％]화대조조[(8.00±1.10)％、(11.45±2.42)％화(22.90±2.03)％]3개시점적뇌세포조망솔균교가수술조(2.11±0.54)％、(2.34±0.46)％화(2.21±0.49)％]현저증가(P균＜0.01혹＜0.05),치료조교대조조각시점뇌세포조망솔균명현강저(P균＜0.01혹＜0.05),3조대서재12、24、72 h시적조간비교차이균유통계학의의(F=39.01、66.60、194.20,P균＜0.01).(2)혈청NSE농도:각시점대조조[(10.04±0.19) μg/L、(9.33±0.15)μg/L화(8.36±0.16)μg/L]화치료조[(8.43±0.17)μg/L、(6.73±0.16) μg/L화(6.12±0.13)μg/L]교가수술조[(4.22±0.53)μg/L、(3.96±0.60) μg/L화(3.59±0.55) μg/L]NSE농도증가(P균＜0.01),치료조교대조조각시점NSE농도강저(P균＜0.01),3조대서재12、24、72h조간비교차이균유통계학의의(F=371.25、245.61、236.22,P균＜0.01). 결론 PDGF능억제신생대서HIBD후신경세포조망급강저혈청NSE농도,대HIBD신생대서유신경보호작용.
Objective To investigate the effects of platelet derived growth factor (PDGF) on brain cell apoptosis rate and serum neuron-specific enolase (NSE) concentration after hypoxic-ischemic brain damage (HIBD) in neonatal rats. Methods Forty-eight HIBD models of 7-day old neonatal Wistar rats were established and then divided into two groups randomly:PDGF group and normal saline control group (n =24 in each).Another 24 neonatal Wistar rats were taken into the sham operation group.The treatment group received intraperitoneal injection of PDGF-BB (50 ng/kg) once,while the other two groups received normal saline at the same time.In each group,rats were randomly sacrificed immediately at 12,24 and 72 hours after injection (n=8).The serum of rats were reserved for NSE concentration determination by enzyme linked immunosorbent assay,and the right brains of the sacrificed rats were used to prepare brain cell suspension for neurocyte apoptosis rate examination by flow cytometry.Mono-variate analysis and q-test were performed for statistical analysis. Results (1) The brain cell apoptotic rates of treatment group [ (6.09 ± 0.70)％,(9.67 ± 1.52) ％ and (14.15±1.52)％] and control group [(8.00± 1.10)％,(11.45±2.42)％ and (22.90±2.03) ％] were significantly increased compared to that of sham group [(2.11 ± 0.54)％,(2.34 ±0.46)％ and (2.21±0.49)％] at all time points (all P＜0.01 or ＜0.05),the apoptotic rate of treatment group was lower than that of control group (P＜0.01 or ＜0.05).Statistical differences were found among the three groups at 12,24 and 72 hours (F =39.01,66.60 and 194.20respectively; P＜0.01).(2) Serum NSE concentration was significantly increased in the treatment group [(8.43 ± 0.17) μg/L,(6.73 ± 0.16) μg/L and (6.12 ± 0.13) μg/L] and control group [(10.04±0.19) μg/L,(9.33 0.15) μg/L and (8.36 ± 0.16) μg/L] than in the sham group [(4.22±0.53) μg/L,(3.96±0.60) μg/L and (3.59±0.55) μg/L] at all time points,and it was significantly lower in treatment group than in control group (P＜ 0.01).Statistical difference was found among three groups at 12,24 and 72 hours (F=371.25,245.61 and 236.22 respectively,P＜0.01). Conclusions PDGF might have neuroprotective effect,which could inhibit apoptosis of neural cells and decrease the serum NSE concentration.
