中华实验外科杂志
中華實驗外科雜誌
중화실험외과잡지
Chinese Journal of Experimental Surgery
2015年
10期
2411-2413
,共3页
夏华%池信锦%李玺%吴珊%高婉菱%关健强%蔡珺%黑子清
夏華%池信錦%李璽%吳珊%高婉蔆%關健彊%蔡珺%黑子清
하화%지신금%리새%오산%고완릉%관건강%채군%흑자청
过氧化物酶体增殖物激活受体-γ%罗格列酮%自体原位肝移植%肠损伤
過氧化物酶體增殖物激活受體-γ%囉格列酮%自體原位肝移植%腸損傷
과양화물매체증식물격활수체-γ%라격렬동%자체원위간이식%장손상
Peroxisome proliferator activated receptor γ%Rosiglitazone%Orthotopic autologous liver transplantation%Intestine injury
目的 观察过氧化物酶体增殖物激活受体-γ(PPARγ)激动剂罗格列酮在自体原位肝移植(OALT)围术期肠氧化应激的影响及肠损伤的保护作用.方法 将24只雄性SD大鼠随机分为4组:对照组(CTL)、假手术组(Sham)、自体原位肝移植模型组(OALT)和罗格列酮预处理组(ROS).建立自体肝移植模型,无肝期持续20 min,肝脏再灌注8h后,观察回肠组织病理学变化,检测血清二胺氧化酶(DAO)、脂肪酸结合蛋白2(FABP2)水平和肠组织PPARγ蛋白表达、转录因子NF-E2相关因子2(Nrf2)激活、总抗氧化能力(T-AOC)、超氧化物歧化酶(SOD)、羟自由基(·OH)、丙二醛(MDA)的含量.结果 相对于OALT组,ROS组大鼠回肠组织PPARγ蛋白表达上调(P＜0.01)和Nrf2激活增加(P＜0.01),肠损伤减轻(P＜0.01);肠组织T-AOC、SOD活性升高[(3.01±0.80) nmol/g蛋白比(0.64 ±0.06) nmol/g蛋白,P＜0.01;(111.6 ±9.9)U/mg蛋白比(61.9±5.1) U/mg蛋白,P＜0.01],·OH和MDA含量降低[(180±44) nmoL/g蛋白比(508±106) nmol/g蛋白,P＜0.01;(92±22) nmol/g蛋白比(162±30) nmol/g蛋白,P＜0.01)];血清DAO和FABP2水平显著下降[(61.7±25.2) μg/L比(158.7±30.5) μg/L,P＜0.01;(42.0±32.5) ng/L比(65.3±51.0),P＜0.01].结论 PPARγ激动剂罗格列酮通过上调肠组织PPARγ蛋白表达和Nrf2激活,增强机体抗氧化能力,减轻肠组织氧化损伤,对OLAT造成的肠道损伤具有保护作用.
目的 觀察過氧化物酶體增殖物激活受體-γ(PPARγ)激動劑囉格列酮在自體原位肝移植(OALT)圍術期腸氧化應激的影響及腸損傷的保護作用.方法 將24隻雄性SD大鼠隨機分為4組:對照組(CTL)、假手術組(Sham)、自體原位肝移植模型組(OALT)和囉格列酮預處理組(ROS).建立自體肝移植模型,無肝期持續20 min,肝髒再灌註8h後,觀察迴腸組織病理學變化,檢測血清二胺氧化酶(DAO)、脂肪痠結閤蛋白2(FABP2)水平和腸組織PPARγ蛋白錶達、轉錄因子NF-E2相關因子2(Nrf2)激活、總抗氧化能力(T-AOC)、超氧化物歧化酶(SOD)、羥自由基(·OH)、丙二醛(MDA)的含量.結果 相對于OALT組,ROS組大鼠迴腸組織PPARγ蛋白錶達上調(P＜0.01)和Nrf2激活增加(P＜0.01),腸損傷減輕(P＜0.01);腸組織T-AOC、SOD活性升高[(3.01±0.80) nmol/g蛋白比(0.64 ±0.06) nmol/g蛋白,P＜0.01;(111.6 ±9.9)U/mg蛋白比(61.9±5.1) U/mg蛋白,P＜0.01],·OH和MDA含量降低[(180±44) nmoL/g蛋白比(508±106) nmol/g蛋白,P＜0.01;(92±22) nmol/g蛋白比(162±30) nmol/g蛋白,P＜0.01)];血清DAO和FABP2水平顯著下降[(61.7±25.2) μg/L比(158.7±30.5) μg/L,P＜0.01;(42.0±32.5) ng/L比(65.3±51.0),P＜0.01].結論 PPARγ激動劑囉格列酮通過上調腸組織PPARγ蛋白錶達和Nrf2激活,增彊機體抗氧化能力,減輕腸組織氧化損傷,對OLAT造成的腸道損傷具有保護作用.
목적 관찰과양화물매체증식물격활수체-γ(PPARγ)격동제라격렬동재자체원위간이식(OALT)위술기장양화응격적영향급장손상적보호작용.방법 장24지웅성SD대서수궤분위4조:대조조(CTL)、가수술조(Sham)、자체원위간이식모형조(OALT)화라격렬동예처리조(ROS).건립자체간이식모형,무간기지속20 min,간장재관주8h후,관찰회장조직병이학변화,검측혈청이알양화매(DAO)、지방산결합단백2(FABP2)수평화장조직PPARγ단백표체、전록인자NF-E2상관인자2(Nrf2)격활、총항양화능력(T-AOC)、초양화물기화매(SOD)、간자유기(·OH)、병이철(MDA)적함량.결과 상대우OALT조,ROS조대서회장조직PPARγ단백표체상조(P＜0.01)화Nrf2격활증가(P＜0.01),장손상감경(P＜0.01);장조직T-AOC、SOD활성승고[(3.01±0.80) nmol/g단백비(0.64 ±0.06) nmol/g단백,P＜0.01;(111.6 ±9.9)U/mg단백비(61.9±5.1) U/mg단백,P＜0.01],·OH화MDA함량강저[(180±44) nmoL/g단백비(508±106) nmol/g단백,P＜0.01;(92±22) nmol/g단백비(162±30) nmol/g단백,P＜0.01)];혈청DAO화FABP2수평현저하강[(61.7±25.2) μg/L비(158.7±30.5) μg/L,P＜0.01;(42.0±32.5) ng/L비(65.3±51.0),P＜0.01].결론 PPARγ격동제라격렬동통과상조장조직PPARγ단백표체화Nrf2격활,증강궤체항양화능력,감경장조직양화손상,대OLAT조성적장도손상구유보호작용.
Objective To investigate the effecof peroxisome proliferators-activated receptor-γ (PPARγ) agonisrosiglitazone on intestine injury and intestinal oxidative stresin ratundergoing orthotopiautologoulivetransplantation (OALT).MethodSprague-Dawley male ratwere randomly divided into fougroups: control group (CTL), sham group (Sham), OALgroup and rosiglitazone pretreatmengroup (ROS).ROgroup received rosiglitazone (0.3 mg/kg) 30 min before OALT, and CTL group, Sham group and OALgroup received the same amounof normal saline, respectively.Intestine tissue sectionwere stained with hematoxylin and eosin (HE) to visualize the damage.The expression of PPARγand NF-E2-related facto2 (Nrf2) awell amarkerof oxidative streswere measured.ResultRosiglitazone pretreatmentcould significantly upregulate the expression of PPARγand Nrf2, and attenuate the intestine injury induced by OAL(P ＜0.01).Compared to OALgroup, the activity of total antioxidancapacity, and superoxide dismutase in intestinal tissue waenhanced in ROgroup [(3.01 ± 0.80) nmol/g protein vs.(0.64 ± 0.06) nmol/g protein, P ＜ 0.01;(111.6 ± 9.9) U/mg protein vs.(61.9 ±5.1) U/mg protein,P ＜0.01], whereathe tissue levelof malondialdehyde and hydroxyl radical were significantly decreased [(180 ± 44) nmol/g protein vs.(508 ± 106) nmol/g protein, P ＜ 0.01;(92 ± 22) nmol/g protein vs.(162 ± 30) nmol/g protein, P ＜ 0.01)] awell diamine oxidase and fatty acid-binding protein 2 in serum [(61.7 ±25.2) μg/L vs.(158.7 ±30.5) μg/L,P＜0.01;(42.0 ± 32.5) ng/L vs.(65.3 ±51.0),P＜0.01].Conclusion PPARγ agonisrosiglitazone could protecagainsintestinal injury induced by OALthrough upregulating the PPARγ and Nrf2 expression, and attenuating oxidative stress.
