Yilmaz Mustafa, Topsakal Senay, Herek Ozkan, Ozmen Ozlem, Sahinduran Sima, Buyukoglu Tulay, Yonetci Nadir
Department of Internal Medicine, University of Pamukkale, Denizli, Turkey.
Transl Res. 2009 Nov;154(5):241-9. doi: 10.1016/j.trsl.2009.07.009. Epub 2009 Aug 9.
In this study, we examined the effects of etanercept (ETA) on experimentally induced pancreatitis. Acute pancreatitis was induced with Na taurocholate. ETA was simultaneously administered to treatment groups. Serum amylase and lipase activity, pancreatic histopathology, apoptosis, malondialdehyde (MDA), and myeloperoxidase enzyme activity (MPO) were assessed. Although rats in the groups 1, 2, and 3 were sacrificed 24h later, groups 4, 5, and 6 were sacrificed 5 days later. ETA treatment significantly decreased serum amylase activity (nontreated, 2636.16+/-191.94; treated, 1898.71+/-262.53; control, 506.28+/-17.31 U/L, P<0.001), lipase activity (nontreated, 3049.67+/-972.65; treated, 2538.85+/-660.45; control, 88.57+/-7.54 U/L, P<0.001), histopathologic score (nontreated, 5.43+/-0.43; treated, 2.57+/-0.20; control, 0.71+/-0.18, P<0.001), MDA (nontreated, 105.77+/-13.29; treated, 92.89+/-10.39; control, 41.26+/-2.54 nmol/g, P<0.001), and MPO (nontreated, 0.64+/-1.15; treated, 0.59+/-0.13; control, 0.17+/-0.02 units/g/wet weight, P<0.001) activity in 24-h groups. In 5-day groups, ETA treatment decreased amylase activity (nontreated, 738.67+/-48.60; treated, 497.14+/-47.25; control, 389.00+/-9.17 U/L, P<0.001), lipase activity (nontreated, 101.33+/-39.32; treated, 34.57+/-7.29; control, 23.42+/-2.12 U/L, P<0.001), histopathologic score (nontreated, 5.43+/-0.43; treated, 3.71+/-0.68; control, 0.00+/-0.00, P<0.001), MDA (nontreated, 67.91+/-4.28; treated, 60.91+/-3.57; control, 14.85+/-1.16 nmol/g, P<0.001), and MPO (nontreated, 0.36+/-0.04; treated, 0.27+/-0.02; control, 0.14+/-0.02 units/g/wet weight, P<0.001) activity. Caspase-positive cells numbers around the necrosis significantly decreased by ETA treatment in both 24-h groups (nontreated, 74.28+/-3.26; treated, 67.00+/-1.15; control, 3.85+/-0.63, P<0.001) and 5-day groups (nontreated, 79.85+/-3.01; treated, 47.85+/-5.76; control, 2.22+/-0.63, P<0.001). These results showed that ETA has an ameliorating effect on sodium taurocholate-induced acute necrotic pancreatitis.
在本研究中,我们检测了依那西普(ETA)对实验性诱导胰腺炎的影响。用牛磺胆酸钠诱导急性胰腺炎。ETA同时给予治疗组。评估血清淀粉酶和脂肪酶活性、胰腺组织病理学、细胞凋亡、丙二醛(MDA)和髓过氧化物酶活性(MPO)。虽然第1、2和3组大鼠在24小时后处死,但第4、5和6组在5天后处死。ETA治疗显著降低了24小时组的血清淀粉酶活性(未治疗组,2636.16±191.94;治疗组,1898.71±262.53;对照组,506.28±17.31 U/L,P<0.001)、脂肪酶活性(未治疗组,3049.67±972.65;治疗组,2538.85±660.45;对照组,88.57±7.54 U/L,P<0.001)、组织病理学评分(未治疗组,5.43±0.43;治疗组,2.57±0.20;对照组,0.71±0.18,P<0.001)、MDA(未治疗组,105.77±13.29;治疗组,92.89±10.39;对照组,41.26±2.54 nmol/g,P<0.001)和MPO(未治疗组,0.64±1.15;治疗组,0.59±0.13;对照组,0.17±0.02单位/g/湿重,P<0.001)活性。在5天组中,ETA治疗降低了淀粉酶活性(未治疗组,738.67±48.60;治疗组,497.14±47.25;对照组,389.00±9.17 U/L,P<0.001)、脂肪酶活性(未治疗组,101.33±39.32;治疗组,34.57±7.29;对照组,23.42±2.12 U/L,P<0.001)、组织病理学评分(未治疗组,5.43±0.43;治疗组,3.71±0.68;对照组,0.00±0.00,P<0.001)、MDA(未治疗组,67.91±4.28;治疗组,60.91±3.57;对照组,14.85±1.16 nmol/g,P<0.001)和MPO(未治疗组,0.36±0.04;治疗组,0.27±0.02;对照组,0.14±0.02单位/g/湿重,P<0.001)活性。在24小时组(未治疗组,74.28±3.26;治疗组,67.00±1.15;对照组,3.85±0.63,P<0.001)和5天组(未治疗组,79.85±3.01;治疗组,47.85±5.76;对照组,2.22±0.63,P<0.001)中,ETA治疗均显著降低了坏死周围半胱天冬酶阳性细胞数量。这些结果表明,ETA对牛磺胆酸钠诱导的急性坏死性胰腺炎具有改善作用。