中华实用儿科临床杂志
中華實用兒科臨床雜誌
중화실용인과림상잡지
Journal of Applied Clinical Pediatrics
2014年
17期
1349-1351
,共3页
罗宇%俞松%王健%唐诗鹏%陆建国%闫陶然%卓金伟
囉宇%俞鬆%王健%唐詩鵬%陸建國%閆陶然%卓金偉
라우%유송%왕건%당시붕%륙건국%염도연%탁금위
凋亡相关蛋白%股骨头缺血坏死%动物模型%幼兔%糖皮质激素
凋亡相關蛋白%股骨頭缺血壞死%動物模型%幼兔%糖皮質激素
조망상관단백%고골두결혈배사%동물모형%유토%당피질격소
Apoptosis-related proteins%Avascular necrosis%Animal models%Juvenile rabbit%Glucocorticoids
目的 观察各凋亡相关蛋白在激素性幼兔股骨头缺血坏死动物模型股骨头组织中的表达情况,探讨该模型中调控凋亡的主要通路.方法 选用2月龄的新西兰大白兔,制作糖皮质激素性幼兔股骨头缺血坏死模型及对照组模型,根据是否发病将激素注射组分为未发病组和发病组.取股骨头软骨及软骨下骨组织用免疫组织化学法检测凋亡通路中凋亡相关蛋白天冬氨酸特异酶切的半胱氨酸蛋白酶-3(Caspase-3)、Caspase-8、人结合凋亡蛋白酶活化因子-1(apaf-1)、钙蛋白酶-1(calpain-1)的表达情况.分别测定在单位视野中Caspase-3、Caspase-8、apaf-1、calpain-1的积分光密度(IOD)值.结果 1.Caspase-3的IOD值分别为发病组25 142.72 ±21 528.48,未发病组2 069.63±1 096.96,对照组301.80±99.66.Caspase-8的IOD值分别为发病组24 942.63±18 942.99,未发病组2016.31±1 518.70,对照组236.85±97.94.Apaf-1的IOD值分别为发病组8 514.23±6 384.20,未发病组1 118.49±1 360.59,对照组95.13±38.05.Calpain-1的IOD值分别为发病组9 636.71 ±9 123.81,未发病组1 881.10±3 277.86,对照组126.71±47.35.Caspase-3在发病组和未发病组、对照组间差异有统计学意义(H=11.470、23.996,p＜0.01);Caspase-8在发病组和对照组间差异有统计学意义(H=22.178,P＜0.01);apaf-1在发病组和对照组间差异有统计学意义(H=22.808,P＜0.01);calpain-1在发病组和对照组间差异有统计学意义(H=13.553,P ＜0.01).2.线性回归分析:Caspase-8能够显著的预测Caspase-3,且回归方程回归效应显著,回归方程能够解释40.3％的变异,而apaf-1和calpain-1对Caspase-3的回归效应不显著.结论 凋亡受体通路可能在股骨头缺血坏死的凋亡过程中发挥主要调控作用.
目的 觀察各凋亡相關蛋白在激素性幼兔股骨頭缺血壞死動物模型股骨頭組織中的錶達情況,探討該模型中調控凋亡的主要通路.方法 選用2月齡的新西蘭大白兔,製作糖皮質激素性幼兔股骨頭缺血壞死模型及對照組模型,根據是否髮病將激素註射組分為未髮病組和髮病組.取股骨頭軟骨及軟骨下骨組織用免疫組織化學法檢測凋亡通路中凋亡相關蛋白天鼕氨痠特異酶切的半胱氨痠蛋白酶-3(Caspase-3)、Caspase-8、人結閤凋亡蛋白酶活化因子-1(apaf-1)、鈣蛋白酶-1(calpain-1)的錶達情況.分彆測定在單位視野中Caspase-3、Caspase-8、apaf-1、calpain-1的積分光密度(IOD)值.結果 1.Caspase-3的IOD值分彆為髮病組25 142.72 ±21 528.48,未髮病組2 069.63±1 096.96,對照組301.80±99.66.Caspase-8的IOD值分彆為髮病組24 942.63±18 942.99,未髮病組2016.31±1 518.70,對照組236.85±97.94.Apaf-1的IOD值分彆為髮病組8 514.23±6 384.20,未髮病組1 118.49±1 360.59,對照組95.13±38.05.Calpain-1的IOD值分彆為髮病組9 636.71 ±9 123.81,未髮病組1 881.10±3 277.86,對照組126.71±47.35.Caspase-3在髮病組和未髮病組、對照組間差異有統計學意義(H=11.470、23.996,p＜0.01);Caspase-8在髮病組和對照組間差異有統計學意義(H=22.178,P＜0.01);apaf-1在髮病組和對照組間差異有統計學意義(H=22.808,P＜0.01);calpain-1在髮病組和對照組間差異有統計學意義(H=13.553,P ＜0.01).2.線性迴歸分析:Caspase-8能夠顯著的預測Caspase-3,且迴歸方程迴歸效應顯著,迴歸方程能夠解釋40.3％的變異,而apaf-1和calpain-1對Caspase-3的迴歸效應不顯著.結論 凋亡受體通路可能在股骨頭缺血壞死的凋亡過程中髮揮主要調控作用.
목적 관찰각조망상관단백재격소성유토고골두결혈배사동물모형고골두조직중적표체정황,탐토해모형중조공조망적주요통로.방법 선용2월령적신서란대백토,제작당피질격소성유토고골두결혈배사모형급대조조모형,근거시부발병장격소주사조분위미발병조화발병조.취고골두연골급연골하골조직용면역조직화학법검측조망통로중조망상관단백천동안산특이매절적반광안산단백매-3(Caspase-3)、Caspase-8、인결합조망단백매활화인자-1(apaf-1)、개단백매-1(calpain-1)적표체정황.분별측정재단위시야중Caspase-3、Caspase-8、apaf-1、calpain-1적적분광밀도(IOD)치.결과 1.Caspase-3적IOD치분별위발병조25 142.72 ±21 528.48,미발병조2 069.63±1 096.96,대조조301.80±99.66.Caspase-8적IOD치분별위발병조24 942.63±18 942.99,미발병조2016.31±1 518.70,대조조236.85±97.94.Apaf-1적IOD치분별위발병조8 514.23±6 384.20,미발병조1 118.49±1 360.59,대조조95.13±38.05.Calpain-1적IOD치분별위발병조9 636.71 ±9 123.81,미발병조1 881.10±3 277.86,대조조126.71±47.35.Caspase-3재발병조화미발병조、대조조간차이유통계학의의(H=11.470、23.996,p＜0.01);Caspase-8재발병조화대조조간차이유통계학의의(H=22.178,P＜0.01);apaf-1재발병조화대조조간차이유통계학의의(H=22.808,P＜0.01);calpain-1재발병조화대조조간차이유통계학의의(H=13.553,P ＜0.01).2.선성회귀분석:Caspase-8능구현저적예측Caspase-3,차회귀방정회귀효응현저,회귀방정능구해석40.3％적변이,이apaf-1화calpain-1대Caspase-3적회귀효응불현저.결론 조망수체통로가능재고골두결혈배사적조망과정중발휘주요조공작용.
Objective To detect the apoptosis of femoral head cartilage cells and to observe the expression of apoptosis-related proteins in the tissues of the femoral head,as well as to explore the main pathway for regulating the apoptosis in steroid induced by juvenile rabbit models with avascular necrosis of femoral head.Methods The models with avascular necrosis of the femoral head and the control group model were made in New Zealand infancy albino rabbits induced by glucocorticoid(GC).The immunohistochemical method was used to detect the expressions of Caspase3,Caspase-8,apoptosis protease activating factor-1 (apaf-1),calpain-1 in the femoral heads.Results 1.The integrated optical density(IOD) values of Caspase-3 in GC-induced subgroup,the subgroup that was not induced by GC and control group were 25 142.72 ± 21 528.48,2 069.63 ± 1 096.96 and 301.80 ± 99.66,respectively.The IOD values of Caspase-8 in GC-induced subgroup,the subgroup respectively and the control group were 24 942.63 ± 18 942.99,2 016.31 ± 1 518.70,236.85 ±97.94,respectively.The IOD values of apaf-1 in GC-induced subgroup,the subgroup that was not induced by GC and the control group were 8 5 14.23 ± 6 384.20,1 118.49 ± 1 360.59,95.13 ± 38.05,respectively.The IOD values of calpain-1 in GC-induccd subgroup,the subgroup that was not induced by GC and control group were 9 636.71 ± 9 123.81,1 881.10 ± 3 277.86,126.71 ± 47.35,respectively.The IOD value differences of the Caspase-3 between GC-induced subgroup and the subgroup that was not induced by GC,the control group were extremely significant (H =l 1.470,23.996,P ＜ 0.01).The IOD value differences of the Caspase-8,apaf-1,calpain-1 between GC-induced subgroup and the control group were extremely significant (H =22.178,22.808,13.553,P ＜ 0.01).2.The linear regression analysis results showed that under the joint action of Caspase-8,apaf-1,calpain-1,only the Caspase-8 could significantly predict Caspase-3,and its regression equation regression got significant effect and could explain 40.3％ of the variance;while the regression effects of the apaf-1 and calpain-1 to Caspase-3 were not significant.Conclusion Death receptor pathway might play a major regulation role in the apoptotic process of avascular necrosis.
