CAJ | 학술논문

目的探讨七氟醚对大鼠肾缺血再灌注损伤的影响及Na+-2Cl--K+协同转运蛋白1(BSC1)和水通道蛋白2(AQP2)在其中的作用.方法健康雄性SD大鼠24只,8～12周龄,体重125 ～145 g,采用随机数字表法,将大鼠随机分为3组(n=8)∶假手术组(S组)、肾缺血再灌注组(I/R组)和七氟醚组(Sev组).采用夹闭肾动脉45 min再灌注24 h的方法制备双侧肾脏缺血再灌注损伤模型.Sev组吸入1 MAC(2.2％)七氟醚,意识消失后开始制备模型,并吸入1 MAC(2.2％)七氟醚3h.于模型制备前24 h(T1)和再灌注24 h(T2)时采集尿样,记录尿量,测定尿比重、肌酐(Cr)水平,计算内生肌酐清除率(Ccr)；T2时采集下腔静脉血样,测定血清BUN和Cr、MDA浓度、SOD和髓过氧化物酶(MPO)活性浓度；取血后取左侧肾脏,观察肾组织病理学结果,进行肾小管损伤程度评分,测定肾组织SOD和MPO活性、MDA含量,分别采用免疫组化法和Western blot法测定AQP2和BSC1的表达.结果与S组比较,I/R组和Sev组T2时尿量增加,血清BUN和Cr浓度升高,尿比重和Ccr降低,血清和肾组织MPO、MDA水平升高,SOD活性降低,肾小管损伤评分升高,肾组织AQP2和BSC1表达水平下调(P＜0.05)；与I/R组比较,Sev组Ccr升高,血清BUN和Cr浓度降低,血清和肾组织MPO、MDA水平降低,SOD活性升高,肾小管损伤评分降低,肾组织AQP2和BSC1表达水平上调(P＜0.05),尿量和尿比重差异无统计学意义(P＞0.05),肾组织病理学损伤减轻.结论七氟醚可减轻大鼠肾缺血再灌注损伤,其机制与上调BSC1和AQP2的表达有关.
목적 탐토칠불미대대서신결혈재관주손상적영향급Na+-2Cl--K+협동전운단백1(BSC1)화수통도단백2(AQP2)재기중적작용.방법 건강웅성SD대서24지,8～12주령,체중125 ～145 g,채용수궤수자표법,장대서수궤분위3조(n=8)∶가수술조(S조)、신결혈재관주조(I/R조)화칠불미조(Sev조).채용협폐신동맥45 min재관주24 h적방법제비쌍측신장결혈재관주손상모형.Sev조흡입1 MAC(2.2％)칠불미,의식소실후개시제비모형,병흡입1 MAC(2.2％)칠불미3h.우모형제비전24 h(T1)화재관주24 h(T2)시채집뇨양,기록뇨량,측정뇨비중、기항(Cr)수평,계산내생기항청제솔(Ccr)；T2시채집하강정맥혈양,측정혈청BUN화Cr、MDA농도、SOD화수과양화물매(MPO)활성농도；취혈후취좌측신장,관찰신조직병이학결과,진행신소관손상정도평분,측정신조직SOD화MPO활성、MDA함량,분별채용면역조화법화Western blot법측정AQP2화BSC1적표체.결과 여S조비교,I/R조화Sev조T2시뇨량증가,혈청BUN화Cr농도승고,뇨비중화Ccr강저,혈청화신조직MPO、MDA수평승고,SOD활성강저,신소관손상평분승고,신조직AQP2화BSC1표체수평하조(P＜0.05)；여I/R조비교,Sev조Ccr승고,혈청BUN화Cr농도강저,혈청화신조직MPO、MDA수평강저,SOD활성승고,신소관손상평분강저,신조직AQP2화BSC1표체수평상조(P＜0.05),뇨량화뇨비중차이무통계학의의(P＞0.05),신조직병이학손상감경.결론 칠불미가감경대서신결혈재관주손상,기궤제여상조BSC1화AQP2적표체유관.
Objective To investigate the effects of sevoflurane on renal ischemia-reperfusion (I/R) injury in rats and the role of Na+-2Cl--K+ cotransporter 1 (BSC1) and aquaporin 2 (AQP2) in it.Methods Twentyfour male Sprague-Dawley rats,aged 8-12 weeks,weighing 125-145 g,were randomly divided into 3 groups (n =8 each) ∶ sham operation group (S group),I/R group and sevoflurane group (Sev group).Renal ischemia was induced by occlusion of the renal artery for 45 min with atraumatic microclips followed by 24 h reperfusion.In group Sev,the rats inhaled 1 MAC (2.2％) sevoflurane,renal ischemia was induced after loss of consciousness and 1 MAC (2.2％) sevoflurane was inhaled for 1 h.The urine were collected at 24 h before I/R (T1) and 24 h of reperfusion (T2) for detection of urine specific gravity and creatinine (Cr) level.The urine volume was recorded.The endogenous creatinine clearance rate (Ccr) was calculated.Blood samples were taken from the irferior vena cava at T2 for determination of concentrations of serum blood urea nitrogen (BUN) and Cr and activities of superoxide dismutase (SOD) and myeloperoxidase (MPO),malondialdehyde (MDA) concentration.The left kidney was removed for determination of MPO and SOD activities and MDA content and for microscopic examination and the pathological changes of the renal tubule were scored.The expression of AQP2 and BSC1 was detected by immunohistochemistry and Western blot.Results Compared with group S,the urine volume was enlarged,concentrations of serum BUN and Cr were significantly increased,urine specific gravity and Ccr were significantly decreased,MPO and MDA levels were significantly increased,SOD activity was significantly decreased,the pathological score was significantly increased,and the expression of AQP2 and BSC1 was down-regulated in groups I/R and Sev (P ＜ 0.05).Cer was significantly higher,conceutratious of serum BUN and Cr and MPO and MDA levels were lower,SOD activity was higher,the pathological score was lower,and the expression of AQP2 and BSC1 was higher in group Sev than in group I/R (P ＜ 0.05).Sevoflurane inhalation significantly attenuated the pathological changes.Conclusion Sevoflurane can attenuate renal I/R injury in rats through up-regulating the expression of BSC1 and AQP2.