中华肿瘤杂志
中華腫瘤雜誌
중화종류잡지
CHINESE JOURNAL OF ONCOLOGY
2009年
10期
742-745
,共4页
王兴文%林晓燕%毕迎惠%韩俊庆
王興文%林曉燕%畢迎惠%韓俊慶
왕흥문%림효연%필영혜%한준경
大鼠%辐射损伤%凋亡%爱维治
大鼠%輻射損傷%凋亡%愛維治
대서%복사손상%조망%애유치
Rats%Radiation injuries%Apoptosis%Actovegin
目的 探讨小牛血去蛋白提取物(商品名爱维治)对急性放射性肠炎大鼠小肠黏膜的修复作用及对肠上皮细胞bcl-2、bax基因蛋白表达的影响.方法 以高能X线直线加速器给予实验大鼠全腹照射(9.0 Gy),建立辐射损伤模型.实验大鼠随机分成正常对照组、模型对照组、爱维治低、中、高剂量组.造模后连续4 d腹腔注射给药,取相应部佗的小肠制成病理切片,图像分析仪测定相关形态学指标,用免疫组化方法 检测小肠黏膜上皮细胞中凋亡相关蛋白bcl-2、bax的表达.结果 爱维治中、高剂量组小肠绒毛高度、隐窝深度、黏膜厚度和全层厚度分别为(254.66±26.71)μm、(166.47±25.31)μm、(510.44±30.27)μm、(610.38±37.56)μm和(261.71±30.12)μm、(165.41±19.89)μm、(511.71±29.64)μm、(608.98±34.23)μm,较模型对照组明显改善(P＜0.05).爱维治中、高剂量组bax的表达量分别为(24.54±8.59)%和(23.24±9.10)%,低于模型对照组(P＜0.05);爱维治中、高剂量组bcl-2的表达量分别为(55.54±8.59)%和(52.21±8.32)%,高于模型对照组(P＜0.05);爱维治中、高剂量组bcl-2/bax的比值分别为2.2632和2.1275,高于模型对照组(0.3425,P＜0.01).结论 爱维治通过促进抑凋亡蛋白bcl-2的表达,抑制促凋亡蛋白bax的表达,减少肠黏膜细胞凋亡,加速急性放射性肠炎受损肠黏膜的修复.
目的 探討小牛血去蛋白提取物(商品名愛維治)對急性放射性腸炎大鼠小腸黏膜的脩複作用及對腸上皮細胞bcl-2、bax基因蛋白錶達的影響.方法 以高能X線直線加速器給予實驗大鼠全腹照射(9.0 Gy),建立輻射損傷模型.實驗大鼠隨機分成正常對照組、模型對照組、愛維治低、中、高劑量組.造模後連續4 d腹腔註射給藥,取相應部佗的小腸製成病理切片,圖像分析儀測定相關形態學指標,用免疫組化方法 檢測小腸黏膜上皮細胞中凋亡相關蛋白bcl-2、bax的錶達.結果 愛維治中、高劑量組小腸絨毛高度、隱窩深度、黏膜厚度和全層厚度分彆為(254.66±26.71)μm、(166.47±25.31)μm、(510.44±30.27)μm、(610.38±37.56)μm和(261.71±30.12)μm、(165.41±19.89)μm、(511.71±29.64)μm、(608.98±34.23)μm,較模型對照組明顯改善(P＜0.05).愛維治中、高劑量組bax的錶達量分彆為(24.54±8.59)%和(23.24±9.10)%,低于模型對照組(P＜0.05);愛維治中、高劑量組bcl-2的錶達量分彆為(55.54±8.59)%和(52.21±8.32)%,高于模型對照組(P＜0.05);愛維治中、高劑量組bcl-2/bax的比值分彆為2.2632和2.1275,高于模型對照組(0.3425,P＜0.01).結論 愛維治通過促進抑凋亡蛋白bcl-2的錶達,抑製促凋亡蛋白bax的錶達,減少腸黏膜細胞凋亡,加速急性放射性腸炎受損腸黏膜的脩複.
목적 탐토소우혈거단백제취물(상품명애유치)대급성방사성장염대서소장점막적수복작용급대장상피세포bcl-2、bax기인단백표체적영향.방법 이고능X선직선가속기급여실험대서전복조사(9.0 Gy),건립복사손상모형.실험대서수궤분성정상대조조、모형대조조、애유치저、중、고제량조.조모후련속4 d복강주사급약,취상응부타적소장제성병리절편,도상분석의측정상관형태학지표,용면역조화방법 검측소장점막상피세포중조망상관단백bcl-2、bax적표체.결과 애유치중、고제량조소장융모고도、은와심도、점막후도화전층후도분별위(254.66±26.71)μm、(166.47±25.31)μm、(510.44±30.27)μm、(610.38±37.56)μm화(261.71±30.12)μm、(165.41±19.89)μm、(511.71±29.64)μm、(608.98±34.23)μm,교모형대조조명현개선(P＜0.05).애유치중、고제량조bax적표체량분별위(24.54±8.59)%화(23.24±9.10)%,저우모형대조조(P＜0.05);애유치중、고제량조bcl-2적표체량분별위(55.54±8.59)%화(52.21±8.32)%,고우모형대조조(P＜0.05);애유치중、고제량조bcl-2/bax적비치분별위2.2632화2.1275,고우모형대조조(0.3425,P＜0.01).결론 애유치통과촉진억조망단백bcl-2적표체,억제촉조망단백bax적표체,감소장점막세포조망,가속급성방사성장염수손장점막적수복.
Objective To evaluate the effect of actovegin ( Nycomed,deproteinized hemoderivative of calf blood injection) on intestinal mucosa in rats with acute radiation enteritis,and observe the changes of expression of apoptosis-related bcl-2/bax genes.Methods An abdominal irradiation in a dose of 9.0 Gy X-ray of linear accelerator was performed once on a group of Wistar rats to establish a model of acute intestinal radiation enteritis.The experimental rats were randomly divided into five groups.Group 1 was normal control group;group 2 was model control group;groups 3,4 and 5 were treated with low,middle and high dose of actovegin,respectively.After the model was established,actovegin injection was given intraperitoneally for successive 4 days.Coresponding intestinal tissues were taken for morphological examination with an image analysis system.The expression of apoptosis related bax and bcl-2 protein in the intestinal mucosal epithelial cells was determined by immunohistochemistry.Results The groups 4 and 5 had significantly higher height of intestinal villi,the depth of crypt,the thickness of the mucosa and entire wall ( 254.66/261.71 μm,166.47/165.41μm,510.44/511.71 μm,610.38/608.98μm),compared with those of the model control group (239.12 μm,151.45 μm,420.27 μm and 579.32 μm),respectively (P＜0.05).Treatment with middle and high doses of actovegin also significantly down-regulated the expression of activating apoptosis protein bax (24.54/23.24) compared with that of model control group (59.32)(P＜0.05) and upregulated the expression of inhibiting apoptosis protein bcl-2 (55.54/52.21) compared with that of model control group (20.32)(P＜0.05).The ratio of bcl-2/bax was significantly higher in the groups 4 and 5 (2.2632,2.1275) compared with that in the model control group (0.3425) (P＜0.01) .Conclusion Actovegin accelerates the recovery of the acute radiation-injured intestinal mucosal epithelium by decreasing apoptosis via down-regnlation of the expression of activating apoptosis protein bax and up-regulation of inhibiting apoptosis protein bcl-2.
