重庆医学
重慶醫學
중경의학
CHONGQING MEDICAL JOURNAL
2015年
14期
1882-1884
,共3页
心肌梗死%血管生成%功能恢复%基质细胞衍生因子-1%作用分析
心肌梗死%血管生成%功能恢複%基質細胞衍生因子-1%作用分析
심기경사%혈관생성%공능회복%기질세포연생인자-1%작용분석
myocardial infarction%angiogenesis%functional recovery%stromal cell derived factor-1%effect analysis
目的：研究依赖基质细胞衍生因子‐1（SDF‐1）对心肌梗死血管生成及功能恢复的作用。方法将大鼠随机分成检测组（n＝65）和处理组（n＝64），其中检测组在心肌梗死前后的1、2、4、7、14、28 d分别随机处死5只大鼠（梗死组），进行SDF‐1蛋白水平测定，同时设置5只大鼠为假手术对照。处理组的64只大鼠另随机分成4个小组，每组16只：分别为梗死＋ SDF‐1组、梗死＋抗SDF‐1组、梗死＋生理盐水组、正常＋生理盐水组。对各组进行相应处理后，对比心肌梗死后的SDF‐1蛋白水平情况，对比各组骨髓间质干细胞（MSCs）归巢量及新生血管的密度水平，对比各组大鼠的心肌缩短分数（EF）和射血分数（FS）变化水平。结果梗死组的SDF‐1水平在1～7 d后显著高于假手术组，并达到峰值水平，随后逐渐下降，在14 d时恢复至正常，差异有统计学意义（P＜0．05）。经过SDF‐1处理后的组别MSCs归巢量和新生血管的密度水平显著高于其他各组，梗死＋抗SDF‐1组的水平则明显低于梗死＋生理盐水组的水平，差异有统计学意义（均 P＜0．05）。梗死＋SDF‐1组大鼠的心功能改善情况显著优于其他各组，差异有统计学意义（P＜0．05）。结论 SDF‐1可促使心肌梗死血管生成，改善心功能。
目的：研究依賴基質細胞衍生因子‐1（SDF‐1）對心肌梗死血管生成及功能恢複的作用。方法將大鼠隨機分成檢測組（n＝65）和處理組（n＝64），其中檢測組在心肌梗死前後的1、2、4、7、14、28 d分彆隨機處死5隻大鼠（梗死組），進行SDF‐1蛋白水平測定，同時設置5隻大鼠為假手術對照。處理組的64隻大鼠另隨機分成4箇小組，每組16隻：分彆為梗死＋ SDF‐1組、梗死＋抗SDF‐1組、梗死＋生理鹽水組、正常＋生理鹽水組。對各組進行相應處理後，對比心肌梗死後的SDF‐1蛋白水平情況，對比各組骨髓間質榦細胞（MSCs）歸巢量及新生血管的密度水平，對比各組大鼠的心肌縮短分數（EF）和射血分數（FS）變化水平。結果梗死組的SDF‐1水平在1～7 d後顯著高于假手術組，併達到峰值水平，隨後逐漸下降，在14 d時恢複至正常，差異有統計學意義（P＜0．05）。經過SDF‐1處理後的組彆MSCs歸巢量和新生血管的密度水平顯著高于其他各組，梗死＋抗SDF‐1組的水平則明顯低于梗死＋生理鹽水組的水平，差異有統計學意義（均 P＜0．05）。梗死＋SDF‐1組大鼠的心功能改善情況顯著優于其他各組，差異有統計學意義（P＜0．05）。結論 SDF‐1可促使心肌梗死血管生成，改善心功能。
목적：연구의뢰기질세포연생인자‐1（SDF‐1）대심기경사혈관생성급공능회복적작용。방법장대서수궤분성검측조（n＝65）화처리조（n＝64），기중검측조재심기경사전후적1、2、4、7、14、28 d분별수궤처사5지대서（경사조），진행SDF‐1단백수평측정，동시설치5지대서위가수술대조。처리조적64지대서령수궤분성4개소조，매조16지：분별위경사＋ SDF‐1조、경사＋항SDF‐1조、경사＋생리염수조、정상＋생리염수조。대각조진행상응처리후，대비심기경사후적SDF‐1단백수평정황，대비각조골수간질간세포（MSCs）귀소량급신생혈관적밀도수평，대비각조대서적심기축단분수（EF）화사혈분수（FS）변화수평。결과경사조적SDF‐1수평재1～7 d후현저고우가수술조，병체도봉치수평，수후축점하강，재14 d시회복지정상，차이유통계학의의（P＜0．05）。경과SDF‐1처리후적조별MSCs귀소량화신생혈관적밀도수평현저고우기타각조，경사＋항SDF‐1조적수평칙명현저우경사＋생리염수조적수평，차이유통계학의의（균 P＜0．05）。경사＋SDF‐1조대서적심공능개선정황현저우우기타각조，차이유통계학의의（P＜0．05）。결론 SDF‐1가촉사심기경사혈관생성，개선심공능。
Objective To study the role of dependence of stromal cell derived factor‐1(SDF‐1) on myocardial infarction an‐giogenesis and function recovery .Methods The rats were randomly divided into the test group (65 cases) and the treatment group (64 cases) ,in which 5 rats in the test group were randomly killed on 1 ,2 ,4 ,7 ,14 ,28 d before and after myocardial infarction(infarc‐tion group) and the SDF‐1 protein level was detected .At the same time the sham operation group(5 cases) was set up;64 rats in the treatment group were randomly divided into four groups ,16 cases in each group ,which were infarction+SDF‐1 group ,infarct+anti‐SDF‐1 group ,infarct+normal saline group and normal+normal saline group .After the corresponding processing in each group ,the SDF‐1 levels after myocardial infarction ,MSCs homing amount ,neovascularization density ,EF and FS levels were compared among various groups .Results The SDF‐1 level after 1-7 d in the infarction group was significantly higher than that in the sham opera‐tion group ,and reached a peak level ,then decreased gradually and restored to normal on 14 d ,the difference was statistically signifi‐cant (P<0 .05) .The MSCs homing amount and neovascularization density level in the SDF‐1 treatment groups were significantly higher than those in other groups ,which in the infarction+anti‐SDF‐1 group were significantly lower than those in the infarction+normal saline group ,the differences were statistically significant (all P<0 .05) .The cardiac function improvement situation in the infarction +SDF‐1 group was significantly better than that in other groups ,the difference was statistically significant (P<0 .05) . Conclusion SDF‐1 can promote angiogenesis in myocardial infarction ,also improve the heart function .
