中华实验外科杂志
中華實驗外科雜誌
중화실험외과잡지
CHINESE JOURNAL OF EXPERIMENTAL SURGERY
2014年
2期
375-377
,共3页
糖皮质激素%股骨头坏死%维生素E%脱噬作用
糖皮質激素%股骨頭壞死%維生素E%脫噬作用
당피질격소%고골두배사%유생소E%탈서작용
Glucocorticoids%Necrosis of femoral head%Vitamin E%Apoptosis
目的 观察维生素E(vitamin E)对激素性股骨头坏死早期骨细胞凋亡的影响.方法 将36.只家兔分为3组(12只/组).模型组,耳缘静脉注射大肠杆菌内毒素10 μg/kg,24h后臀肌注射甲基强的松龙,20 mg/kg,共3次,间隔24h/次.vitamin E组,同模型组方法造模,同时饲以vitamin E[0.6 g/(kg·d)].对照组:于相同时间点注射等量生理盐水.于4周和6周,分批处死家兔,观察股骨头组织病理学改变、原位末端转移酶标记(TUNEL)法检测,免疫组织化学链菌素抗生物素蛋白-过氧化物酶(SP)法检测.结果 (1)制模后4、6周vitamin E组的空骨陷窝率为(15.87±1.97)％、(25.09±2.67)％,低于模型组的(20.02±2.21)％、(27.79±1.39)％(P＜0.05).vitamin E组骨细胞凋亡指数为(20.99±2.95)％、(33.93±1.62)％,低于模型组的(26.46±3.37)％、(39.90±3.74)％(P＜0.05).(2)制模后4周,vitamin E组股骨头组织B淋巴细胞/白血病-2(bcl-2)阳性细胞比率为(9.81±1.01)％,高于模型组的(8.26±1.13)％(P＜0.05);半胱氨酰天冬氨酸特异性蛋白酶(Caspase)-3阳性染色中,vitamin E组阳性表达比率(55％)介于模型组(68％)与对照组(5％)之间.结论 vitamin E可以减少激素诱导的骨细胞凋亡,减少股骨头坏死的发生.vitamin E可能通过促进bcl-2的表达和抑制Caspase-3的表达来抑制骨细胞凋亡.
目的 觀察維生素E(vitamin E)對激素性股骨頭壞死早期骨細胞凋亡的影響.方法 將36.隻傢兔分為3組(12隻/組).模型組,耳緣靜脈註射大腸桿菌內毒素10 μg/kg,24h後臀肌註射甲基彊的鬆龍,20 mg/kg,共3次,間隔24h/次.vitamin E組,同模型組方法造模,同時飼以vitamin E[0.6 g/(kg·d)].對照組:于相同時間點註射等量生理鹽水.于4週和6週,分批處死傢兔,觀察股骨頭組織病理學改變、原位末耑轉移酶標記(TUNEL)法檢測,免疫組織化學鏈菌素抗生物素蛋白-過氧化物酶(SP)法檢測.結果 (1)製模後4、6週vitamin E組的空骨陷窩率為(15.87±1.97)％、(25.09±2.67)％,低于模型組的(20.02±2.21)％、(27.79±1.39)％(P＜0.05).vitamin E組骨細胞凋亡指數為(20.99±2.95)％、(33.93±1.62)％,低于模型組的(26.46±3.37)％、(39.90±3.74)％(P＜0.05).(2)製模後4週,vitamin E組股骨頭組織B淋巴細胞/白血病-2(bcl-2)暘性細胞比率為(9.81±1.01)％,高于模型組的(8.26±1.13)％(P＜0.05);半胱氨酰天鼕氨痠特異性蛋白酶(Caspase)-3暘性染色中,vitamin E組暘性錶達比率(55％)介于模型組(68％)與對照組(5％)之間.結論 vitamin E可以減少激素誘導的骨細胞凋亡,減少股骨頭壞死的髮生.vitamin E可能通過促進bcl-2的錶達和抑製Caspase-3的錶達來抑製骨細胞凋亡.
목적 관찰유생소E(vitamin E)대격소성고골두배사조기골세포조망적영향.방법 장36.지가토분위3조(12지/조).모형조,이연정맥주사대장간균내독소10 μg/kg,24h후둔기주사갑기강적송룡,20 mg/kg,공3차,간격24h/차.vitamin E조,동모형조방법조모,동시사이vitamin E[0.6 g/(kg·d)].대조조:우상동시간점주사등량생리염수.우4주화6주,분비처사가토,관찰고골두조직병이학개변、원위말단전이매표기(TUNEL)법검측,면역조직화학련균소항생물소단백-과양화물매(SP)법검측.결과 (1)제모후4、6주vitamin E조적공골함와솔위(15.87±1.97)％、(25.09±2.67)％,저우모형조적(20.02±2.21)％、(27.79±1.39)％(P＜0.05).vitamin E조골세포조망지수위(20.99±2.95)％、(33.93±1.62)％,저우모형조적(26.46±3.37)％、(39.90±3.74)％(P＜0.05).(2)제모후4주,vitamin E조고골두조직B림파세포/백혈병-2(bcl-2)양성세포비솔위(9.81±1.01)％,고우모형조적(8.26±1.13)％(P＜0.05);반광안선천동안산특이성단백매(Caspase)-3양성염색중,vitamin E조양성표체비솔(55％)개우모형조(68％)여대조조(5％)지간.결론 vitamin E가이감소격소유도적골세포조망,감소고골두배사적발생.vitamin E가능통과촉진bcl-2적표체화억제Caspase-3적표체래억제골세포조망.
Objective To study the anti-apoptotic effects of vitamin E on osteonecrosis of the femoral head induced by glucocorticoids.Methods The 36 rabbits were divided three groups:model group,receiving hormone and endotoxin to induce model of femoral head necrosis; vitamin E group,administered vitamin E [0.6 g/(kg· d)] orally following establishment of femoral head necrosis; control group,given sodium chloride alone.At the fouth and sixth week after the last dosing,animals were sacrificed,each n =6.The femoral heads were conventionally fixed and decalcified.Hematoxylin and eosin (HE) staining was used to examine vacant bone lacuna.TdT-mediated dUTP nick end labeling (TUNEL) assay was used to determine apoptosis.The expression of B lymphocytes/leukemia-2 (bcl-2) and cysteinyl aspartate-specific protease (Caspase)-3 was detected by using immunohistochemical method.Results (1) At the 4th and 6th week,the average percentage of empty osteocyte lacunae in vitamin E group was lower than that of the model group (P ＜0.05),and the average apoptosis index in the vitamin E group was significantly lower than that of the model group (P ＜ 0.05) ; (2) As compared with the model group,bcl-2 positive cell rate was increased in the vitamin E group (P ＜ 0.05),and the Caspase-3 positive cell rate was decreased in the vitamin E group (P ＜ 0.05).As compared with the model and vitamin E groups,bcl-2 positive cell rate was obviously increased in the control group (P ＜0.01),and the Caspase-3 positive cell rate was significantly decreased (P ＜0.01).Conclusion Vitamin E may prevent corticosteroid-induced osteonecrosis by up-regulating the expression of bcl-2 and down-regulating the expression of Caspase-3.
