中华实验外科杂志
中華實驗外科雜誌
중화실험외과잡지
CHINESE JOURNAL OF EXPERIMENTAL SURGERY
2013年
9期
1886-1888
,共3页
王钟兴%方佳峰%黄婵燕%陈图锋
王鐘興%方佳峰%黃嬋燕%陳圖鋒
왕종흥%방가봉%황선연%진도봉
过氧化物酶体增殖物激活受体-γ%罗格列酮%肝门阻断%肠损伤
過氧化物酶體增殖物激活受體-γ%囉格列酮%肝門阻斷%腸損傷
과양화물매체증식물격활수체-γ%라격렬동%간문조단%장손상
Peroxisome proliferators-activated receptor-γ%Rosiglitazone%Hepatic inflow occlusion%Intestinal injury
目的 探讨过氧化物酶体增殖物激活受体-γ(PPAR-γ)激动剂罗格列酮在肝门阻断所致肠道损伤中的作用和机制.方法 将雄性SD大鼠随机分为4组:对照组(CTL)、假手术组(Sham)、肝门阻断组(HIO)和罗格列酮预处理组(Ros).采用Pringle's法行肝门阻断,持续30 min.解除阻断血流恢复2h后,测定回肠组织丙二醛(MDA)、超氧化物歧化酶(SOD)的含量,检测血清二胺氧化酶(DAO)、白细胞介素-1β(IL-1β)以及肿瘤坏死因子·α(TNF-0)的水平.结果 相对于HIO组,Ros组大鼠回肠组织MDA含量降低[(1.91 ±0.40) nmol/mg蛋白比(4.71 ±0.72) nmol/mg蛋白,P＜0.01],SOD活性升高[(217.48±37.30) U/mg蛋白比(151.13 ±30.59) U/mg蛋白,P＜0.01],血清DAO[(16.02 ±2.04) U/L比(20.83±2.46) U/L,P＜0.01]、IL-1β[(121.11±24.34) ng/L比(309.10±37.39) ng/L,P＜0.05]及TNF-t[(26.35 ±7.19) ng/L比(101.95±18.68) ng/L,P＜0.05]水平均显著下降.结论 PPAR-、γ激动剂罗格列酮通过减轻组织氧化应激反应、抑制促炎因子的过表达,对肝门阻断造成的肠道损伤具有保护作用.
目的 探討過氧化物酶體增殖物激活受體-γ(PPAR-γ)激動劑囉格列酮在肝門阻斷所緻腸道損傷中的作用和機製.方法 將雄性SD大鼠隨機分為4組:對照組(CTL)、假手術組(Sham)、肝門阻斷組(HIO)和囉格列酮預處理組(Ros).採用Pringle's法行肝門阻斷,持續30 min.解除阻斷血流恢複2h後,測定迴腸組織丙二醛(MDA)、超氧化物歧化酶(SOD)的含量,檢測血清二胺氧化酶(DAO)、白細胞介素-1β(IL-1β)以及腫瘤壞死因子·α(TNF-0)的水平.結果 相對于HIO組,Ros組大鼠迴腸組織MDA含量降低[(1.91 ±0.40) nmol/mg蛋白比(4.71 ±0.72) nmol/mg蛋白,P＜0.01],SOD活性升高[(217.48±37.30) U/mg蛋白比(151.13 ±30.59) U/mg蛋白,P＜0.01],血清DAO[(16.02 ±2.04) U/L比(20.83±2.46) U/L,P＜0.01]、IL-1β[(121.11±24.34) ng/L比(309.10±37.39) ng/L,P＜0.05]及TNF-t[(26.35 ±7.19) ng/L比(101.95±18.68) ng/L,P＜0.05]水平均顯著下降.結論 PPAR-、γ激動劑囉格列酮通過減輕組織氧化應激反應、抑製促炎因子的過錶達,對肝門阻斷造成的腸道損傷具有保護作用.
목적 탐토과양화물매체증식물격활수체-γ(PPAR-γ)격동제라격렬동재간문조단소치장도손상중적작용화궤제.방법 장웅성SD대서수궤분위4조:대조조(CTL)、가수술조(Sham)、간문조단조(HIO)화라격렬동예처리조(Ros).채용Pringle's법행간문조단,지속30 min.해제조단혈류회복2h후,측정회장조직병이철(MDA)、초양화물기화매(SOD)적함량,검측혈청이알양화매(DAO)、백세포개소-1β(IL-1β)이급종류배사인자·α(TNF-0)적수평.결과 상대우HIO조,Ros조대서회장조직MDA함량강저[(1.91 ±0.40) nmol/mg단백비(4.71 ±0.72) nmol/mg단백,P＜0.01],SOD활성승고[(217.48±37.30) U/mg단백비(151.13 ±30.59) U/mg단백,P＜0.01],혈청DAO[(16.02 ±2.04) U/L비(20.83±2.46) U/L,P＜0.01]、IL-1β[(121.11±24.34) ng/L비(309.10±37.39) ng/L,P＜0.05]급TNF-t[(26.35 ±7.19) ng/L비(101.95±18.68) ng/L,P＜0.05]수평균현저하강.결론 PPAR-、γ격동제라격렬동통과감경조직양화응격반응、억제촉염인자적과표체,대간문조단조성적장도손상구유보호작용.
Objective To investigate the effect of peroxisome proliferators-activated receptor-γ (PPAR-γ) agonist rosiglitazone on the intestinal injury induced by hepatic inflow occlusion (HIO).Methods Sprague-Dawley male rats were randomly divided into four groups:control (CTL) group,sham group,HIO group and rosiglitazone pretreatment (Ros) group.Hepatoduodenal ligament was occluded (Pringle manoeuvre) by clamp for 30 min.After allowing reperfusion for 2 h by release of the clamp,ileac tissue level of malonaldehyde (MDA),activity of superoxide dismutase (SOD) and serum content of diamine oxidase (DAO) were assessed according to the corresponding kits.Serum levels of interleukin (IL)-1β and tumor necrosis factor (TNF)-α were detected by using enzyme-linked immunosorbent assay.Results As compared with HIO group,rosiglitazone significantly reduced the tissue level of MDA [(1.91 ±0.40)nmol/mg protein vs.(4.71 ± 0.72) nmol/mg protein,P ＜ 0.01],enhanced the activity of SOD [(217.48-37.30) U/rg protein vs.(151.13 ± 30.59) U/mg protein,P ＜ 0.01],decreased the levels of DAO [(16.02-2.04) U/L vs.(20.83±2.46) U/L,P＜0.01],IL-l[β [(121.11 ±24.34) ng/L vs.(309.10±37.39) ng/L,P＜0.05] aswellasTNF-α [(26.35 ±7.19) ng/Lvs.(101.95-18.68)ng/L,P ＜ 0.05] in serum.Conclusion PPAR-γ agonist rosiglitazone can protect against intestinal injury caused by HIO though the mechanism of attenuating oxidative stress and inhibiting the overexpression of proinflammatory cytokines.
