中华实验外科杂志
中華實驗外科雜誌
중화실험외과잡지
CHINESE JOURNAL OF EXPERIMENTAL SURGERY
2014年
12期
2685-2687
,共3页
陈忠宝%周江桥%邱涛%陈志远%刘修恒
陳忠寶%週江橋%邱濤%陳誌遠%劉脩恆
진충보%주강교%구도%진지원%류수항
阿托伐他汀%缺血再灌注损伤%内皮型一氧化氮合酶%一氧化氮
阿託伐他汀%缺血再灌註損傷%內皮型一氧化氮閤酶%一氧化氮
아탁벌타정%결혈재관주손상%내피형일양화담합매%일양화담
Atorvastatin preconditioning%Ischemia/reperfusion%Endothelial nitric oxide synthase%Nitric oxide
目的 观察阿托伐他汀预处理对大鼠急性肾缺血再灌注损伤的保护作用,并探讨其可能机制.方法 将18只雄性SD大鼠随机分为3组:假手术组、缺血再灌注组及阿托伐他汀组,在缺血再灌注处理前2周开始对阿托伐他汀组大鼠经腹腔注射阿托伐他汀[20 mg/(kg·d)],假手术组及缺血再灌注组同法给予等量生理盐水.分析再灌注48 h后各组大鼠血清尿素氮(BUN)、肌酐(Cr)、一氧化氮(N0)水平以及其肾脏组织中髓过氧化物酶(MPO)、内皮型一氧化氮合酶(eNOS)、超氧化物歧化酶(SOD)表达水平.结果 与缺血再灌注组比较,阿托伐他汀预处理可降低BUN(mmoL/L,78.59±10.47比128.54±6.69)及Cr(μmol/L,19.44±9.30比31.44±9.87)水平,增加NO(μmol/L,94.65±10.33比67.50±8.32)水平,减少MPO(U/g,1.25±0.14比1.68±0.12)表达,增加SOD[U/(mg·酶蛋白),139.0±10.6比109.0±4.7]及eNOS表达,差异均有统计学意义(P＜0.05).结论 阿托伐他汀预处理对大鼠肾缺血再灌注损伤有保护作用,作用其机制可能与eNOS的诱导合成增多,NO产生增多有关.
目的 觀察阿託伐他汀預處理對大鼠急性腎缺血再灌註損傷的保護作用,併探討其可能機製.方法 將18隻雄性SD大鼠隨機分為3組:假手術組、缺血再灌註組及阿託伐他汀組,在缺血再灌註處理前2週開始對阿託伐他汀組大鼠經腹腔註射阿託伐他汀[20 mg/(kg·d)],假手術組及缺血再灌註組同法給予等量生理鹽水.分析再灌註48 h後各組大鼠血清尿素氮(BUN)、肌酐(Cr)、一氧化氮(N0)水平以及其腎髒組織中髓過氧化物酶(MPO)、內皮型一氧化氮閤酶(eNOS)、超氧化物歧化酶(SOD)錶達水平.結果 與缺血再灌註組比較,阿託伐他汀預處理可降低BUN(mmoL/L,78.59±10.47比128.54±6.69)及Cr(μmol/L,19.44±9.30比31.44±9.87)水平,增加NO(μmol/L,94.65±10.33比67.50±8.32)水平,減少MPO(U/g,1.25±0.14比1.68±0.12)錶達,增加SOD[U/(mg·酶蛋白),139.0±10.6比109.0±4.7]及eNOS錶達,差異均有統計學意義(P＜0.05).結論 阿託伐他汀預處理對大鼠腎缺血再灌註損傷有保護作用,作用其機製可能與eNOS的誘導閤成增多,NO產生增多有關.
목적 관찰아탁벌타정예처리대대서급성신결혈재관주손상적보호작용,병탐토기가능궤제.방법 장18지웅성SD대서수궤분위3조:가수술조、결혈재관주조급아탁벌타정조,재결혈재관주처리전2주개시대아탁벌타정조대서경복강주사아탁벌타정[20 mg/(kg·d)],가수술조급결혈재관주조동법급여등량생리염수.분석재관주48 h후각조대서혈청뇨소담(BUN)、기항(Cr)、일양화담(N0)수평이급기신장조직중수과양화물매(MPO)、내피형일양화담합매(eNOS)、초양화물기화매(SOD)표체수평.결과 여결혈재관주조비교,아탁벌타정예처리가강저BUN(mmoL/L,78.59±10.47비128.54±6.69)급Cr(μmol/L,19.44±9.30비31.44±9.87)수평,증가NO(μmol/L,94.65±10.33비67.50±8.32)수평,감소MPO(U/g,1.25±0.14비1.68±0.12)표체,증가SOD[U/(mg·매단백),139.0±10.6비109.0±4.7]급eNOS표체,차이균유통계학의의(P＜0.05).결론 아탁벌타정예처리대대서신결혈재관주손상유보호작용,작용기궤제가능여eNOS적유도합성증다,NO산생증다유관.
Objective To investigate the protective effect of atorvastatin (ATO) preconditioning on rats with acute renal ischemia-reperfusion (I/R) injury and its effect on endothelial nitric oxide synthase (eNOS).Methods 18 male Sprague Dawley rat was randomly distributed into three groups:sham,I/R and I/R + ATO.ATO was given by intraperitoneal injection [20 mg/(kg·d)] 2 weeks before ischemia/ reperfusion operation in the I/R + ATO group.The sham group and I/R group received saline vehicle via the intraperitoneal route.Serum levels of blood urea nitrogen (BUN),creatinine (Cr),nitric oxide (NO) and expression levels of myeloperoxidase (MPO),eNOS and superoxide dismutase (SOD) in renal tissue were analyzed.Results Comparing with the sham group,ATO treatment reduced the elevation of BUN (mmol/L) (78.59±10.47 vs.128.54 ±6.69) andCr(μmol/L) (19.44±9.3vs.31.44±9.87) level,inhibited the expression of MPO (U/g) (1.25 ±0.14 vs.1.68 ±0.12),but increased the expression of SOD [U/(mg·pro)] (139 ± 10.6 vs.109 ±4.7),and enhance the elevation of NO (μmol/L)(94.65 ± 10.33 vs.67.50 ±8.32) and eNOS.All differences were significant.(P ＜0.01).Conclusion These data suggest that ATO protect renal function from ischemia-reperfusion injury probably by promote the expression of eNOS and consequently increase the production of NO.
