CAJ | 학술논문

目的探讨氢饱和生理盐水对急性坏死性胰腺炎(ANP)大鼠肾损伤的保护作用及其机制.方法雄性Wistar大鼠54只,按数字表法随机分为假手术组、ANP组和氢饱和生理盐水处理(HRS)组,每组18只.采用胆胰管逆行注射5％牛磺胆酸钠方法制备ANP模型.HRS组在造模成功后5 min尾静脉注射HRS6 ml/kg体重,并皮下滴注HRS 20 ml/kg体重.假手术组大鼠开腹后仅翻动十二指肠和胰腺后关腹.假手术组和ANP组大鼠在术后5 min经尾静脉注射生理盐水(6 ml/kg体重),并皮下滴注生理盐水(20 ml/kg体重).术后3、12、24 h分批处死大鼠,取血检测血淀粉酶、肌酐、尿素氮含量.取新鲜肾组织制备匀浆,检测其丙二醛(MDA)含量和超氧化物歧化酶(SOD)活性.取肾脏及胰腺组织行常规病理检查,并在透射电镜下观察肾组织的超微结构.结果 ANP组12 h时的血淀粉酶、肌酐、尿素氮水平,肾脏组织病理评分,MDA含量分别为(5396±500) U/L、(80.3±11.6) U/L、(14.1±2.1)U/L、(448.3±36.8)分、(7.03±0.85) nmol/mg,均较假手术组显著升高(P值均＜0.05)；SOD活性为(35.2±5.28) U/mg,较假手术组显著降低(P＜0.05).HRS组的相应值分别为(5448±967) U/L、(41.9±8.6) U/L、(7.2±1.3)U/L、(315.2±39.6)分、(5.15±0.35) nmol/mg,较ANP组均显著下降,但仍显著高于假手术组(P值均＜0.05)；SOD活性为(49.1±6.79) U/mg,较ANP组显著升高,但仍显著低于假手术组(P值均＜0.05).结论氢饱和生理盐水对ANP大鼠的肾损伤具有一定程度的保护作用,其机制可能与抗氧化应激有关.
목적 탐토경포화생리염수대급성배사성이선염(ANP)대서신손상적보호작용급기궤제.방법 웅성Wistar대서54지,안수자표법수궤분위가수술조、ANP조화경포화생리염수처리(HRS)조,매조18지.채용담이관역행주사5％우광담산납방법제비ANP모형.HRS조재조모성공후5 min미정맥주사HRS6 ml/kg체중,병피하적주HRS 20 ml/kg체중.가수술조대서개복후부번동십이지장화이선후관복.가수술조화ANP조대서재술후5 min경미정맥주사생리염수(6 ml/kg체중),병피하적주생리염수(20 ml/kg체중).술후3、12、24 h분비처사대서,취혈검측혈정분매、기항、뇨소담함량.취신선신조직제비균장,검측기병이철(MDA)함량화초양화물기화매(SOD)활성.취신장급이선조직행상규병리검사,병재투사전경하관찰신조직적초미결구.결과 ANP조12 h시적혈정분매、기항、뇨소담수평,신장조직병리평분,MDA함량분별위(5396±500) U/L、(80.3±11.6) U/L、(14.1±2.1)U/L、(448.3±36.8)분、(7.03±0.85) nmol/mg,균교가수술조현저승고(P치균＜0.05)；SOD활성위(35.2±5.28) U/mg,교가수술조현저강저(P＜0.05).HRS조적상응치분별위(5448±967) U/L、(41.9±8.6) U/L、(7.2±1.3)U/L、(315.2±39.6)분、(5.15±0.35) nmol/mg,교ANP조균현저하강,단잉현저고우가수술조(P치균＜0.05)；SOD활성위(49.1±6.79) U/mg,교ANP조현저승고,단잉현저저우가수술조(P치균＜0.05).결론 경포화생리염수대ANP대서적신손상구유일정정도적보호작용,기궤제가능여항양화응격유관.
Objective To investigate the protective effect of hydrogen-rich saline on renal injury of rats with acute necrotizing pancreatitis and its mechanism.Methods Fifty-four male Wistar rats were randomly divided into three groups:sham operation group (SO group),acute necrotizing pancreatitis group (ANP group) and hydrogen-rich saline treatment group (HRS group),with 18 rats in each group.Acute necrotizing pancreatitis model was induced by retrograde injection of 5％ sodium taurocholate into the biliopancreatic duct.Hydrogen-rich saline was injected through the tail vein (6 ml/kg) and subcutaneously (20 ml/kg) at 5 minutes after the operation in HRS group.The rats of SO group underwent laparotomy with gentle pancreas,duodenum manipulation only.The rats of SO group and ANP group were administered with intravenous (6 ml/kg) and subcutaneous (20 ml/kg) injection with saline.Rats in each group were sacrificed at 3,12 and 24 h after the operation.The levels of serum amylase,creatinine,urea nitrogen were determined.Fresh renal tissue was prepared and renal malondialdehyde (MDA),renal superoxide dismutase (SOD) activity were measured.Pathological changes of renal and pancreas tissues were examined and pathological scores were recorded.Ultrastructural changes of renal tissues were observed under a transmission electron microscope.Results The levels of serum amylase,creatinine,urea nitrogen,renal histopathological scores,MDA were (5396 ± 500) U/L,(80.3 ± 11.6) U/L,(14.1 ± 2.1) U/L,(448.3 ± 36.8),(7.03 ± 0.85) nmol/mg,which were significantly higher than those in SO group (P ＜ 0.05),but the renal SOD activity was (35.2 ± 5.28) U/mg,which were significantly lower than that in SO group (P ＜ 0.05).The corresponding values in HRS group were (5448±967)U/L,(41.9±8.6)U/L,(7.2± 1.3)U/L,(315.2±39.6),(5.15±0.35) nmol/mg,which were significantly lower than those in ANP group,but were significantly higher than those in SO group (P ＜ 0.05).The renal SOD activity was (49.1 ± 6.79) U/rag,which were siguificantly higher than that in ANP group,but was significantly lower than that in SO group (P ＜ 0.05).Conclusions Hydrogen-rich saline has a protective effect on renal injury of ANP,and its mechanism may be related to anti-oxidative stress.