基础医学与临床
基礎醫學與臨床
기출의학여림상
BASIC MEDICAL SCIENCES AND CLINICS
2009年
11期
1207-1210
,共4页
心力衰竭%血管紧张素Ⅱ%细胞凋亡%BAX%BCL-2
心力衰竭%血管緊張素Ⅱ%細胞凋亡%BAX%BCL-2
심력쇠갈%혈관긴장소Ⅱ%세포조망%BAX%BCL-2
heart failure%angiotensin Ⅱ%apoptosis%BAX%BCL-2
目的 观察氯沙坦对心力衰竭大鼠心肌细胞凋亡的影响.方法 选8周龄雄性SD大鼠,分为对照组(C组)、心衰组(HF组)和治疗组(LS组).采用腹腔注射阿霉素造模,LS组同时氯沙坦灌胃.透射电镜观察心肌超微结构,检测血清中CPK、CK-MB及LDH的含量.用原位脱氧核糖核酸酶末端标记法(TUNEL法)检测大鼠心肌细胞凋亡,免疫组化法检测大鼠心肌BAX、BCL-2蛋白的表达.结果 HF组与C组相比,心肌细胞损伤明显,并可见凋亡小体,血清中CPK、CK-MB和LDH升高;LS组与HF组相比,心肌细胞凋亡指数下调(P＜0.01),心肌细胞BCL-2表达增加,BAX表达减少.结论 氯沙坦可有效抑制心力衰竭过程中发生的心肌细胞凋亡,逆转心肌损伤,改善心衰进程.
目的 觀察氯沙坦對心力衰竭大鼠心肌細胞凋亡的影響.方法 選8週齡雄性SD大鼠,分為對照組(C組)、心衰組(HF組)和治療組(LS組).採用腹腔註射阿黴素造模,LS組同時氯沙坦灌胃.透射電鏡觀察心肌超微結構,檢測血清中CPK、CK-MB及LDH的含量.用原位脫氧覈糖覈痠酶末耑標記法(TUNEL法)檢測大鼠心肌細胞凋亡,免疫組化法檢測大鼠心肌BAX、BCL-2蛋白的錶達.結果 HF組與C組相比,心肌細胞損傷明顯,併可見凋亡小體,血清中CPK、CK-MB和LDH升高;LS組與HF組相比,心肌細胞凋亡指數下調(P＜0.01),心肌細胞BCL-2錶達增加,BAX錶達減少.結論 氯沙坦可有效抑製心力衰竭過程中髮生的心肌細胞凋亡,逆轉心肌損傷,改善心衰進程.
목적 관찰록사탄대심력쇠갈대서심기세포조망적영향.방법 선8주령웅성SD대서,분위대조조(C조)、심쇠조(HF조)화치료조(LS조).채용복강주사아매소조모,LS조동시록사탄관위.투사전경관찰심기초미결구,검측혈청중CPK、CK-MB급LDH적함량.용원위탈양핵당핵산매말단표기법(TUNEL법)검측대서심기세포조망,면역조화법검측대서심기BAX、BCL-2단백적표체.결과 HF조여C조상비,심기세포손상명현,병가견조망소체,혈청중CPK、CK-MB화LDH승고;LS조여HF조상비,심기세포조망지수하조(P＜0.01),심기세포BCL-2표체증가,BAX표체감소.결론 록사탄가유효억제심력쇠갈과정중발생적심기세포조망,역전심기손상,개선심쇠진정.
Objective To find the inpact(s) of Losartan on myocardial apoptosis in rats with heart failure. Methods Eight-week-old male SD rats were divided into control group (group C) , heart failure (group HF) and treatment group (group LS). Use of doxorubicin injection model, group LS at the same time in a row to the oral losartan, myocardial ultrastructure was examined by TEM. DNA-situ terminal labeling (TUNEL method) was used to detect myocardial apoptosis and myocardial BAX, BCL-2 protein expression was detected by immunohistochemistry. Results Group HF showed significant myocardial cell injury, and apoptotic bodies were found, serum CPK, CK-MB and LDH were increased. In LS group, myocardial apoptosis index was lower (P <0. 01) , myocardial cells BCL-2 expression, BAX expression reduced as compared with those in HF group. Conclusion Losartan can effectively inhibit the process of heart failure occurred in cardiomyocyte apoptosis, reverse myocardial damage and improve the prognosis of heart failure.
