中华实验外科杂志
中華實驗外科雜誌
중화실험외과잡지
CHINESE JOURNAL OF EXPERIMENTAL SURGERY
2015年
6期
1261-1263
,共3页
王宁%张燕林%Keshav raj Sigdel%王茵
王寧%張燕林%Keshav raj Sigdel%王茵
왕저%장연림%Keshav raj Sigdel%왕인
瞬时感受器电位离子通道4%肾缺血%再灌注损伤%急性肾损伤
瞬時感受器電位離子通道4%腎缺血%再灌註損傷%急性腎損傷
순시감수기전위리자통도4%신결혈%재관주손상%급성신손상
Transient receptor potential vanilloid 4%Renal ischemia%Reperfusion injury%Acute kidney injury
目的 观察瞬时感受器电位离子通道香草素受体亚家族4(TRPV4)激动剂对缺血再灌注肾损伤的保护作用,并探讨其作用机制.方法 建立大鼠肾缺血再灌注模型,将实验动物随机分为3组:假手术组、缺血再灌注组、治疗组(各8只).治疗组大鼠给TRPV4激动剂GSA1016790A(30 μg/kg),缺血再灌注组给予相同量的生理盐水,假手术组不夹闭肾蒂,余处理同缺血再灌注组.各组分别检测血清肌酐、尿素氮水平,组织病理检查,同时行免疫组织化学、Western blot及实时定量聚合酶链反应(Real-time PCR)检测肾组织中TRPV4及内皮型一氧化氮合酶(eNOS)的表达.结果 GSK1016790A可以改善缺血再灌注急性肾损伤的组织损伤.与缺血再灌注组比较,治疗组中血清肌酐及尿素氮水平显著降低[(228.4±32.62) μmol/L比(123.62±21.23) μmol/L、(35.65±13.9) μmol/L比(20.93±9.6)μmol/L,P＜0.05],免疫组织化学及Real-time PCR检测显示TRPV4及eNOS的表达明显升高(P＜0.05).结论 TRPV4激动剂GSA1016790A可通过血管舒张改善缺血再灌注急性肾损伤.
目的 觀察瞬時感受器電位離子通道香草素受體亞傢族4(TRPV4)激動劑對缺血再灌註腎損傷的保護作用,併探討其作用機製.方法 建立大鼠腎缺血再灌註模型,將實驗動物隨機分為3組:假手術組、缺血再灌註組、治療組(各8隻).治療組大鼠給TRPV4激動劑GSA1016790A(30 μg/kg),缺血再灌註組給予相同量的生理鹽水,假手術組不夾閉腎蒂,餘處理同缺血再灌註組.各組分彆檢測血清肌酐、尿素氮水平,組織病理檢查,同時行免疫組織化學、Western blot及實時定量聚閤酶鏈反應(Real-time PCR)檢測腎組織中TRPV4及內皮型一氧化氮閤酶(eNOS)的錶達.結果 GSK1016790A可以改善缺血再灌註急性腎損傷的組織損傷.與缺血再灌註組比較,治療組中血清肌酐及尿素氮水平顯著降低[(228.4±32.62) μmol/L比(123.62±21.23) μmol/L、(35.65±13.9) μmol/L比(20.93±9.6)μmol/L,P＜0.05],免疫組織化學及Real-time PCR檢測顯示TRPV4及eNOS的錶達明顯升高(P＜0.05).結論 TRPV4激動劑GSA1016790A可通過血管舒張改善缺血再灌註急性腎損傷.
목적 관찰순시감수기전위리자통도향초소수체아가족4(TRPV4)격동제대결혈재관주신손상적보호작용,병탐토기작용궤제.방법 건립대서신결혈재관주모형,장실험동물수궤분위3조:가수술조、결혈재관주조、치료조(각8지).치료조대서급TRPV4격동제GSA1016790A(30 μg/kg),결혈재관주조급여상동량적생리염수,가수술조불협폐신체,여처리동결혈재관주조.각조분별검측혈청기항、뇨소담수평,조직병리검사,동시행면역조직화학、Western blot급실시정량취합매련반응(Real-time PCR)검측신조직중TRPV4급내피형일양화담합매(eNOS)적표체.결과 GSK1016790A가이개선결혈재관주급성신손상적조직손상.여결혈재관주조비교,치료조중혈청기항급뇨소담수평현저강저[(228.4±32.62) μmol/L비(123.62±21.23) μmol/L、(35.65±13.9) μmol/L비(20.93±9.6)μmol/L,P＜0.05],면역조직화학급Real-time PCR검측현시TRPV4급eNOS적표체명현승고(P＜0.05).결론 TRPV4격동제GSA1016790A가통과혈관서장개선결혈재관주급성신손상.
Objective To study the protective effect of transient receptor potential vanilloid 4 (TRPV4) on ischemia-reperfusion (I/R) kidney injury in rats and the action mechanism.Methods I/R acute kidney injury (AKI) model was established in SD rats.Rats were randomly assigned to the following groups:(1) sham + saline group (n=8);(2) I/R + saline group (n=8);(3) I/R + GSK1016790A group (n =8).The rats were intraperitoneally injected either with solvent (sham group and I/R group),and GSK1016790A (30 μg/kg body weight) in I/R + GSK1016790A group before the start of ischemia.Respectively.The levels of blood urea nitrogen and creatinine were measured.The expression of TRPV4 and endothelial nitric oxide synthase (eNOS) was detected by immunohistochemistry,and real-time quantitative polymerase chain reaction (Real-time PCR),respectively.Results GSK1016790A ameliorated the histologic damage of rats with I/R-induced AKI.Compared to I/R + saline group,the levels of serum creatinine and urea nitrogen were significantly reduced in I/R + GSK1016790A group [(228.4 ± 32.62) μmol/L vs.(123.62 ±21.23) μmol/L,and (35.65 ± 13.9) μmol/L vs.(20.93 ±9.6) μmol/L,respectively,P ＜0.05].The TRPV4 and eNOS expression was increased after GSK1016790A treatment (P ＜ 0.05).Conclusion Activation of TRPV4 can ameliorate I/R-induced AKI by the way of eNOS-mediated vasodilation.
