中国组织工程研究
中國組織工程研究
중국조직공정연구
Journal of Clinical Rehabilitative Tissue Engineering Research
2015年
5期
674-680
,共7页
宋扬%吴荣%曾越灿%张振勇%杜红梅
宋颺%吳榮%曾越燦%張振勇%杜紅梅
송양%오영%증월찬%장진용%두홍매
实验动物%心脏及血管损伤动物模型%放射治疗%放射性心肌损伤%过氧化物酶体增殖物活化受体γ%过氧化物酶体增殖物活化受体γ激动剂%吡格列酮%血管紧张素Ⅱ%血管紧张素Ⅱ1型受体%国家自然科学基金
實驗動物%心髒及血管損傷動物模型%放射治療%放射性心肌損傷%過氧化物酶體增殖物活化受體γ%過氧化物酶體增殖物活化受體γ激動劑%吡格列酮%血管緊張素Ⅱ%血管緊張素Ⅱ1型受體%國傢自然科學基金
실험동물%심장급혈관손상동물모형%방사치료%방사성심기손상%과양화물매체증식물활화수체γ%과양화물매체증식물활화수체γ격동제%필격렬동%혈관긴장소Ⅱ%혈관긴장소Ⅱ1형수체%국가자연과학기금
Radiotherapy Injury%Heart Injury%Angiotensin II%Peroxisome Proliferator Activated Receptor
背景：激活过氧化物酶体增殖物活化受体γ信号途径在心血管系统有许多正效应。血管紧张素Ⅱ与心肌的纤维化密切相关，然而却很少有研究关注激活过氧化物酶体增殖物活化受体γ途径能否通过减弱血管紧张素Ⅱ的表达从而改善放射性心肌损伤。
<br> 目的：探索激活过氧化物酶体增殖物活化受体γ后血管紧张素Ⅱ1型受体对放射性心脏损伤模型大鼠的作用。方法：60只大鼠随机等分为对照组、吡格列酮组、模型组及照射+低、高剂量吡格列酮组。模型组及照射+低、高剂量吡格列酮组大鼠采用前后对穿照射方法接受6 MV高能X射线照射野心前1.5 cm×1.5 cm，照射剂量300 cGy/min。照射完后6 h时，低、高剂量吡格列酮组大鼠分别接受10，20 mg/kg吡格列酮灌胃，此后每天灌胃1次，连续灌胃30 d；模型组大鼠灌胃2 mL蒸馏水。吡格列酮组大鼠在对应时间灌胃10 mg/kg吡格列酮。
<br> 结果与结论：给予吡格列酮干预后，受照射大鼠的心脏组织损伤减轻，心脏纤维化减轻，心脏组织中血管紧张素Ⅱ1型受体蛋白及mRNA表达水平减少。提示吡格列酮干预可降低血管紧张素Ⅱ1型受体在大鼠放射性心脏损伤中的表达，提示激活过氧化物酶体增殖物活化受体γ途径可能对放射性心脏损伤有保护作用。
揹景：激活過氧化物酶體增殖物活化受體γ信號途徑在心血管繫統有許多正效應。血管緊張素Ⅱ與心肌的纖維化密切相關，然而卻很少有研究關註激活過氧化物酶體增殖物活化受體γ途徑能否通過減弱血管緊張素Ⅱ的錶達從而改善放射性心肌損傷。
<br> 目的：探索激活過氧化物酶體增殖物活化受體γ後血管緊張素Ⅱ1型受體對放射性心髒損傷模型大鼠的作用。方法：60隻大鼠隨機等分為對照組、吡格列酮組、模型組及照射+低、高劑量吡格列酮組。模型組及照射+低、高劑量吡格列酮組大鼠採用前後對穿照射方法接受6 MV高能X射線照射野心前1.5 cm×1.5 cm，照射劑量300 cGy/min。照射完後6 h時，低、高劑量吡格列酮組大鼠分彆接受10，20 mg/kg吡格列酮灌胃，此後每天灌胃1次，連續灌胃30 d；模型組大鼠灌胃2 mL蒸餾水。吡格列酮組大鼠在對應時間灌胃10 mg/kg吡格列酮。
<br> 結果與結論：給予吡格列酮榦預後，受照射大鼠的心髒組織損傷減輕，心髒纖維化減輕，心髒組織中血管緊張素Ⅱ1型受體蛋白及mRNA錶達水平減少。提示吡格列酮榦預可降低血管緊張素Ⅱ1型受體在大鼠放射性心髒損傷中的錶達，提示激活過氧化物酶體增殖物活化受體γ途徑可能對放射性心髒損傷有保護作用。
배경：격활과양화물매체증식물활화수체γ신호도경재심혈관계통유허다정효응。혈관긴장소Ⅱ여심기적섬유화밀절상관，연이각흔소유연구관주격활과양화물매체증식물활화수체γ도경능부통과감약혈관긴장소Ⅱ적표체종이개선방사성심기손상。
<br> 목적：탐색격활과양화물매체증식물활화수체γ후혈관긴장소Ⅱ1형수체대방사성심장손상모형대서적작용。방법：60지대서수궤등분위대조조、필격렬동조、모형조급조사+저、고제량필격렬동조。모형조급조사+저、고제량필격렬동조대서채용전후대천조사방법접수6 MV고능X사선조사야심전1.5 cm×1.5 cm，조사제량300 cGy/min。조사완후6 h시，저、고제량필격렬동조대서분별접수10，20 mg/kg필격렬동관위，차후매천관위1차，련속관위30 d；모형조대서관위2 mL증류수。필격렬동조대서재대응시간관위10 mg/kg필격렬동。
<br> 결과여결론：급여필격렬동간예후，수조사대서적심장조직손상감경，심장섬유화감경，심장조직중혈관긴장소Ⅱ1형수체단백급mRNA표체수평감소。제시필격렬동간예가강저혈관긴장소Ⅱ1형수체재대서방사성심장손상중적표체，제시격활과양화물매체증식물활화수체γ도경가능대방사성심장손상유보호작용。
BACKGROUND:There are many positive effects by activation of peroxisome proliferator activated receptor-gamma (PPARγ) signal pathway in cardiovascular system. Angiotensin II is closely related with myocardial fibrosis, however, there are few articles demonstrating that the activation of PPARγsignal pathway can weaken the expression of angiotensin II to improve the radiation-induced heart injury. OBJECTIVE:To evaluate the effect of angiotensin II type 1 receptor in the rat model of radiation-induced heart injury after PPARγsignal pathway is activated. METHODS:Sixty rats were randomly and equal y divided into five groups:control, pioglitazone, model, radiation+low-dose pioglitazone, radiation+high-dose pioglitazone. In the model, radiation+low-dose pioglitazone, radiation+high-dose pioglitazone groups, rats received 6 MV high energy X-ray irradiation at the range of 1.5 cm × 1.5 cm and the irradiation dose of 300 cGy/min, for 6 hours. Furthermore, rats in the radiation+low-dose pioglitazone and radiation+high-dose pioglitazone groups were given 10 and 20 mg/kg pioglitazone by lavage, for 30 days;rats in the model group were given 2 mL distil ed water. In the pioglitazone group, rats were treated with 10 mg/kg pioglitazone by lavage. RESULTS AND CONCLUSION:After rats were treated with pioglitazone, the heart injury and the heart fibrosis in the irradiated rats were decreased. The expressions of angiotensin II type 1 receptor mRNA and protein in the heart tissue were down-regulated. Experimental findings indicate that, pioglitazone intervention downregulates the expression of angiotensin II type 1 receptor in the rat models of radiation-induced heart injury and activation of PPARγsignal pathway al eviates the radiation-induced heart injury.
