中国医师杂志
中國醫師雜誌
중국의사잡지
JOURNAL OF CHINESE PHYSICIAN
2009年
1期
73-76
,共4页
陈芾珩%刘元生%苏永忠%陈惜遂%江美銮%李回军%谭凤娇%侯展文
陳芾珩%劉元生%囌永忠%陳惜遂%江美鑾%李迴軍%譚鳳嬌%侯展文
진비형%류원생%소영충%진석수%강미란%리회군%담봉교%후전문
血小板生成素/药理学%心肌疾病%肌细胞,心脏/药物作用%氧化性应激
血小闆生成素/藥理學%心肌疾病%肌細胞,心髒/藥物作用%氧化性應激
혈소판생성소/약이학%심기질병%기세포,심장/약물작용%양화성응격
Thrombopoietin/PD%Cardiomyopathies%Myocytes,cardiac/DE%Oxidative stress
目的 研究血小板生成素(TPO)对大鼠阿霉素(ADM)心肌细胞损伤的拮抗作用并探讨其机制.方法 32只Wistar 大鼠被随机分成4组.分别为对照组、ADM组、ADM+TPOL组、ADM+TPOH组.对照组给予生理盐水,其余各组给予ADM 20 mg/kg腹腔内注射,TPO干预组则加用不同剂量的TPO(10μg或30μg/kg,隔天1次,共3次).采用ELISA法测大鼠血清CK-MB及cTNI;观察电子显微镜下心肌细胞超微结构的变化;利用免疫组织化学染色观察心肌细胞组织学改变及DNA氧化损伤产物8-羟基脱氧鸟苷(8-OHdG)表达情况,应用IPP6.0软件,计算累积光密度(IOD)及8-OHdG index.结果 加用TPO干预后CK-MB、cTNI的活力较ADM组明显下降(P<0.01);电子显微镜下ADM组心肌细胞超微结构损害较TPO干预组严重;TPO干预组心肌组织病理损伤减轻,IOD、8-OHdG index值较其他各组明显降低(P<0.01)上述指标在ADM+TPOL组及ADM+TPOH组闻差异无统计学意义(P>0.05).结论 TPO通过拮抗阿霉素对心肌的氧化损伤来发挥心脏保护作用.
目的 研究血小闆生成素(TPO)對大鼠阿黴素(ADM)心肌細胞損傷的拮抗作用併探討其機製.方法 32隻Wistar 大鼠被隨機分成4組.分彆為對照組、ADM組、ADM+TPOL組、ADM+TPOH組.對照組給予生理鹽水,其餘各組給予ADM 20 mg/kg腹腔內註射,TPO榦預組則加用不同劑量的TPO(10μg或30μg/kg,隔天1次,共3次).採用ELISA法測大鼠血清CK-MB及cTNI;觀察電子顯微鏡下心肌細胞超微結構的變化;利用免疫組織化學染色觀察心肌細胞組織學改變及DNA氧化損傷產物8-羥基脫氧鳥苷(8-OHdG)錶達情況,應用IPP6.0軟件,計算纍積光密度(IOD)及8-OHdG index.結果 加用TPO榦預後CK-MB、cTNI的活力較ADM組明顯下降(P<0.01);電子顯微鏡下ADM組心肌細胞超微結構損害較TPO榦預組嚴重;TPO榦預組心肌組織病理損傷減輕,IOD、8-OHdG index值較其他各組明顯降低(P<0.01)上述指標在ADM+TPOL組及ADM+TPOH組聞差異無統計學意義(P>0.05).結論 TPO通過拮抗阿黴素對心肌的氧化損傷來髮揮心髒保護作用.
목적 연구혈소판생성소(TPO)대대서아매소(ADM)심기세포손상적길항작용병탐토기궤제.방법 32지Wistar 대서피수궤분성4조.분별위대조조、ADM조、ADM+TPOL조、ADM+TPOH조.대조조급여생리염수,기여각조급여ADM 20 mg/kg복강내주사,TPO간예조칙가용불동제량적TPO(10μg혹30μg/kg,격천1차,공3차).채용ELISA법측대서혈청CK-MB급cTNI;관찰전자현미경하심기세포초미결구적변화;이용면역조직화학염색관찰심기세포조직학개변급DNA양화손상산물8-간기탈양조감(8-OHdG)표체정황,응용IPP6.0연건,계산루적광밀도(IOD)급8-OHdG index.결과 가용TPO간예후CK-MB、cTNI적활력교ADM조명현하강(P<0.01);전자현미경하ADM조심기세포초미결구손해교TPO간예조엄중;TPO간예조심기조직병리손상감경,IOD、8-OHdG index치교기타각조명현강저(P<0.01)상술지표재ADM+TPOL조급ADM+TPOH조문차이무통계학의의(P>0.05).결론 TPO통과길항아매소대심기적양화손상래발휘심장보호작용.
Objective To inwst the antagonistic effect of thrombopoietin on adriamycin induced myocardium injury in rats and explore the mechanism.Methods 32 Wistar rats were randomized into four groups(n=8):Control group,ADM group,ADM+TPOL group and ADM+TPOH group.All agents were given by intraperitoneal injection.The control group was given saline.While the other three groups were given adriamycin at the dosage of20mg/kg.TPO group were injected TPO at the dosages of 10μg/kg or 30μg/kg three times on alternale days.ELISA was used to detect the concentration of CK-MB and cTnI in the serum of rats.The change of cardiocyte ultrastructure was observed by the electron microscope,and pathological change Was observed by immunohistochemistry staining.The expression level of 8- hydroxy-2'-deoxyguanosin(8-OHdG)produced by DNA oxidative damage in myocard tissue were detected.IPP6.0 software was used to detect IOD and calculate the 8-OHdG index.Results The energy of CK-MB and cTNI of TPO group was obviously lower than that in ADM group(P<0.01).The ultragtrueture of cardiocyte in the ADM group Wag damaged more severely than that in TPO group.Pathological Score,IOD and 8-OHdG index of TPO groups were lower than ADM group(P<0.05).These indexes had no significant statistics difference between ADM+TPOL group and ADM+TPOH group.Conclusions TPO can provide heart protection by antagonizing oxidative damage of myocardial cell induced by edriamycin.