CAJ | 학술논문

目的观察人参皂苷Rg1(ginsenoside Rg1)对大鼠肠缺血/再灌注后肠组织损伤的影响,并探讨其机制.方法制备SD大鼠肠缺血/再灌注损伤模型.实验分为3组(n =10):假手术组、缺血/再灌注组(对照组)、人参皂苷Rg1干预组(治疗组).比较各组大鼠肠黏膜肿瘤坏死因子α(TNF-α)水平、白细胞介素6(IL-6)水平、丙二醛(MDA)含量、超氧化物歧化酶(SOD)活性的变化;用Chiu氏评分法观察肠黏膜的损伤情况.结果与假手术组相比,对照组TNF-α、IL-6水平明显升高,MDA含量明显增高,SOD活性明显降低,小肠损伤评分明显升高;与对照组相比,治疗组TNF-α、IL-6水平明显降低,MDA含量明显降低,SOD活性明显升高,小肠损伤评分明显降低.结论人参皂苷Rg1对大鼠肠缺血/再灌注后的肠道有保护作用,该保护作用可能与减少TNF-α、IL-6、MDA含量,提高SOD活性有关.
목적 관찰인삼조감Rg1(ginsenoside Rg1)대대서장결혈/재관주후장조직손상적영향,병탐토기궤제.방법 제비SD대서장결혈/재관주손상모형.실험분위3조(n =10):가수술조、결혈/재관주조(대조조)、인삼조감Rg1간예조(치료조).비교각조대서장점막종류배사인자α(TNF-α)수평、백세포개소6(IL-6)수평、병이철(MDA)함량、초양화물기화매(SOD)활성적변화;용Chiu씨평분법관찰장점막적손상정황.결과 여가수술조상비,대조조TNF-α、IL-6수평명현승고,MDA함량명현증고,SOD활성명현강저,소장손상평분명현승고;여대조조상비,치료조TNF-α、IL-6수평명현강저,MDA함량명현강저,SOD활성명현승고,소장손상평분명현강저.결론 인삼조감Rg1대대서장결혈/재관주후적장도유보호작용,해보호작용가능여감소TNF-α、IL-6、MDA함량,제고SOD활성유관.
Aim To investigate the effect of ginsenoside Rg1 on gut injury following intestinal ischemia reperfusion in rats and the possible mechanism.Methods By using rat model of intestinal I/R injury, 30 male SD rats were randomly divided into 3 groups(n =10 in each group):sham-operation group, I/R group(control group)and ginsenoside Rg1 group(treatment group).The contents of tumor necrosis factor α(TNF-α), interleukin-6(IL-6), malondialdehyde(MDA), the activity of superoxide dismutase(SOD)in intestinal mucosa were measured respectively.Chiu's count was used to assess the changes in intestinal pathological morphology.Results TNF-α, IL-6, MDA contents and the intestinal injury score in control group were significantly increased compared to those in sham-operation group, while SOD contents in control group were significantly decreased compared to sham-operation group.Inversely, TNF-α, IL-6, MDA contents and the intestinal injury score in treatment group were significantly decreased compared to those in control group, while SOD contents in treatment group were significantly increased compared to control group.Conclusion Pretreatment with ginsenoside Rg1 has protective effect on intestinal ischemia-reperfusion injury in rats, which may be attributed to decreased contents of TNF-α, IL-6, MDA and increased levels of SOD.