中华实验外科杂志
中華實驗外科雜誌
중화실험외과잡지
CHINESE JOURNAL OF EXPERIMENTAL SURGERY
2013年
5期
992-994
,共3页
吕俊杰%武雅琴%蒋峰%冯冬杰%张治%尹荣%许林
呂俊傑%武雅琴%蔣峰%馮鼕傑%張治%尹榮%許林
려준걸%무아금%장봉%풍동걸%장치%윤영%허림
姜黄素%肺缺血%再灌注损伤%肺泡Ⅱ型细胞%磷脂酰肌醇3激酶/丝氨酸苏氨酸蛋白激酶信号通路
薑黃素%肺缺血%再灌註損傷%肺泡Ⅱ型細胞%燐脂酰肌醇3激酶/絲氨痠囌氨痠蛋白激酶信號通路
강황소%폐결혈%재관주손상%폐포Ⅱ형세포%린지선기순3격매/사안산소안산단백격매신호통로
Curcumin%Lung ischemia%Reperfusion injury%Alveolar type Ⅱ cells%Phosphatidylinositol 3 kinase/serine/threonine kinase pathway
目的 探讨姜黄素对大鼠肺缺血再灌注损伤(LIRI)肺泡Ⅱ型细胞(AT Ⅱ)的保护作用及其机制.方法 建立大鼠肺缺血再灌注损伤长期存活模型,研究分为假手术组、缺血再灌注损伤(I/R)组、姜黄素低浓度组和姜黄素高浓度组;分别于开胸后、肺门阻断后0、4h、1、3、7d5个时间点收集血及肺组织标本,检测各组如下指标:血氧分压(Pa02)、肺组织苏木素-伊红(HE)染色、肺组织肺泡表面活性物质C(SP-C)表达及磷脂酰肌醇3激酶(PI3K)/丝氨酸苏氨酸蛋白激酶(Akt)信号通路中相关蛋白的表达.结果 成功建立大鼠肺缺血再灌注损伤长期存活模型,与I/R组比较,在I/R前(7 d)给予姜黄素(50 mg/kg和200 mg/kg)可以使动脉血氧分压值显著升高(P<0.05),缓解肺组织损伤,并上调SP-C、磷酸化Akt(p-Akt)及下游增殖相关蛋白磷酸化P70(p-P70)水平,同时下调凋亡蛋白半胱氨酰天冬氨酸特异性蛋白酶(Caspase)-3水平,两者差异有统计学意义(P<0.01);其中姜黄素高浓度组(200 mg/kg)的保护作用更为明显.结论 姜黄素可缓解LIRI,从而起到保护ATⅡ的作用,且具有剂量依赖性,其保护机制与PI3K/Akt信号通路有关.
目的 探討薑黃素對大鼠肺缺血再灌註損傷(LIRI)肺泡Ⅱ型細胞(AT Ⅱ)的保護作用及其機製.方法 建立大鼠肺缺血再灌註損傷長期存活模型,研究分為假手術組、缺血再灌註損傷(I/R)組、薑黃素低濃度組和薑黃素高濃度組;分彆于開胸後、肺門阻斷後0、4h、1、3、7d5箇時間點收集血及肺組織標本,檢測各組如下指標:血氧分壓(Pa02)、肺組織囌木素-伊紅(HE)染色、肺組織肺泡錶麵活性物質C(SP-C)錶達及燐脂酰肌醇3激酶(PI3K)/絲氨痠囌氨痠蛋白激酶(Akt)信號通路中相關蛋白的錶達.結果 成功建立大鼠肺缺血再灌註損傷長期存活模型,與I/R組比較,在I/R前(7 d)給予薑黃素(50 mg/kg和200 mg/kg)可以使動脈血氧分壓值顯著升高(P<0.05),緩解肺組織損傷,併上調SP-C、燐痠化Akt(p-Akt)及下遊增殖相關蛋白燐痠化P70(p-P70)水平,同時下調凋亡蛋白半胱氨酰天鼕氨痠特異性蛋白酶(Caspase)-3水平,兩者差異有統計學意義(P<0.01);其中薑黃素高濃度組(200 mg/kg)的保護作用更為明顯.結論 薑黃素可緩解LIRI,從而起到保護ATⅡ的作用,且具有劑量依賴性,其保護機製與PI3K/Akt信號通路有關.
목적 탐토강황소대대서폐결혈재관주손상(LIRI)폐포Ⅱ형세포(AT Ⅱ)적보호작용급기궤제.방법 건립대서폐결혈재관주손상장기존활모형,연구분위가수술조、결혈재관주손상(I/R)조、강황소저농도조화강황소고농도조;분별우개흉후、폐문조단후0、4h、1、3、7d5개시간점수집혈급폐조직표본,검측각조여하지표:혈양분압(Pa02)、폐조직소목소-이홍(HE)염색、폐조직폐포표면활성물질C(SP-C)표체급린지선기순3격매(PI3K)/사안산소안산단백격매(Akt)신호통로중상관단백적표체.결과 성공건립대서폐결혈재관주손상장기존활모형,여I/R조비교,재I/R전(7 d)급여강황소(50 mg/kg화200 mg/kg)가이사동맥혈양분압치현저승고(P<0.05),완해폐조직손상,병상조SP-C、린산화Akt(p-Akt)급하유증식상관단백린산화P70(p-P70)수평,동시하조조망단백반광안선천동안산특이성단백매(Caspase)-3수평,량자차이유통계학의의(P<0.01);기중강황소고농도조(200 mg/kg)적보호작용경위명현.결론 강황소가완해LIRI,종이기도보호ATⅡ적작용,차구유제량의뢰성,기보호궤제여PI3K/Akt신호통로유관.
Objective To investigate the protective effects and the mechanisms of curcumin preconditioning in a rat lung ischemia-reperfusion injury (LIRI) long-term survival model.Methods 100 healthy SD rats were randomly divided into 4 gronps:the sham group,LIRI group,low dose curcumin group and high dose curcumin group.The lung tissue and blood samples were collected at baseline before hilar occlusion and 1 h after ischemia,4 h,1 day,3 days and 7 days after reperfusion respectively.The indices were determined as follows:the arterial partial pressure of oxygen,the hematoxylin and eosin (HE)staining,pulmonary surfactant-C (SP-C) protein expression and phosphatidylinositol 3 kinase (PI3K)/serine/threonine kinase (Akt) signaling pathway related proteins.Results The rat LIRI long-term survival model wag successfully established.As compared with I/R group,pretreatment with curcumin (50 mg/kg and 200 mg/kg) for 7 days could significantly increased PaO2 (P < 0.05),and attenuate rat lung tissue injury.Also,protein levels of SP-C,p-Akt and p-P70 were significantly increased,but Caspase-3 protein level was decreased (P < 0.01).Conclusion Our data suggested that curcumin could attenuate rat LIRI and protect AT Ⅱ cells,which may be mediated by activation of intracellular PI3K/Akt signaling pathway.