CAJ | 학술논문

目的：：比较白藜芦醇后处理与缺血后处理(IPTC)对大鼠肝脏缺血再灌注损伤(HIRI)的保护作用,并探讨其作用机制。方法：40只健康雄性 SD 大鼠随机分成假手术对照组(SC)、缺血再灌注组(I/R)、缺血后处理组(IPTC)、白藜芦醇后处理组(Res),每组10只。建立大鼠在体肝脏缺血再灌注模型,各组于再灌注6 h 经下腔静脉取血,用于检测血清谷丙转氨酶(ALT)、谷草转氨酶(AST)和碱性磷酸酶(AKP)；取肝匀浆低温离心后测定肝组织中超氧化物歧化酶(SOD)、丙二醛(MDA)含量变化；同时取肝脏组织作病理切片观察。结果：与 I/R 组比较,Res 组和 IPTC 组 ALT、AST、AKP、MDA 均明显下降,而SOD 明显升高(P <0.01)。与 IPTC 组比较,Res 组 ALT、AST、AKP、SOD、MDA 变化无显著性差异。结论：白藜芦醇后处理组和缺血后处理组对减轻大鼠 HIRI 的保护效果一致,其可能的机制与提高机体抗氧化能力,减轻活性氧的损伤作用有关。
목적：：비교백려호순후처리여결혈후처리(IPTC)대대서간장결혈재관주손상(HIRI)적보호작용,병탐토기작용궤제。방법：40지건강웅성 SD 대서수궤분성가수술대조조(SC)、결혈재관주조(I/R)、결혈후처리조(IPTC)、백려호순후처리조(Res),매조10지。건립대서재체간장결혈재관주모형,각조우재관주6 h 경하강정맥취혈,용우검측혈청곡병전안매(ALT)、곡초전안매(AST)화감성린산매(AKP)；취간균장저온리심후측정간조직중초양화물기화매(SOD)、병이철(MDA)함량변화；동시취간장조직작병리절편관찰。결과：여 I/R 조비교,Res 조화 IPTC 조 ALT、AST、AKP、MDA 균명현하강,이SOD 명현승고(P <0.01)。여 IPTC 조비교,Res 조 ALT、AST、AKP、SOD、MDA 변화무현저성차이。결론：백려호순후처리조화결혈후처리조대감경대서 HIRI 적보호효과일치,기가능적궤제여제고궤체항양화능력,감경활성양적손상작용유관。
Objective:To compare the protective effects of resveratrol and ischemic postconditioning on hepatic ischemia-reperfusion injury in rats,and investigate their mechanisms.Methods:40 healthy male Sprague-Dawley (SD)rats were randomly divided into 4 groups:sham control (SC)group,ischemic/reperfusion (I/R)group,ischemic postconditioning group,and postdisposal treatment of resveratrol group. The activity of alanine aminotransferase (ALT),aspartate aminotransferase (AST)and alkaline phosphatase (AKP)in serum were determined;The activity of superoxidase dismutase (SOD)and content of malondialdehyde (MDA)in live tissue were measured.Meanwhile, the liver tissue section was observed by HE staining.Results:As compared with I/R group,the concentrations of serum AST,ALT and AKP were decreased markedly in Res group and IPTC group(P<0.01).The activity of SOD were higher but content of MDA were lower in both Res group and IPTC group(P<0.01).Meanwhile,the injury of hepatic was improved,Res group and IPTC group have no significant difference.Conclusion:Both resveratrol and ischemic postconditioning have similar protective effects on hepatic ischemia-reperfusion injury in rats.Its possible mechanisms might include strengthening the antioxidant capacity of organisms and ptotecting against from rective oxygen species injury.