摘要
目的探讨氢化可的松对实验性急性坏死性胰腺炎(ANP)肺损伤的治疗作用及作用机制。方法54只健康SD大鼠随机分为3组:假手术(SO)组、ANP组及氢化可的松治疗。采用胰胆管逆行注射5%牛磺胆酸钠(1 ml/kg体重)诱导大鼠ANP模型。氢化可的松治疗组于型制作成功后10 min 给予舌下静脉注射氢化可的松(10 mg/kg体重)。各组于术后3 h、6 h和12 h分批处死动物,观察各组大鼠血浆淀粉酶、TNF-α、IL-6、血栓素B2(TXB2)、6酮前列腺素F1α(6-Keto-PGF1α)、TXB2/6-Keto-PGF1α比值、肺组织髓过氧化物酶(MPO)、肺湿干比值及胰腺、肺组织病理变化。结果ANP组血浆淀粉酶、TNF-α、IL-6、TXB2、TXB2/6-Keto-PGF1α比值、肺组织MPO均较SO组明显升高(P<0.05),6 h、12 h肺湿干比值较SO组明显升高(P<0.01);氢化可的松治疗组TNF-α、IL-6、TXB2、TXB2/6 Keto PGF1α比值、肺组织MPO均较ANP组显著降低(P<0.05),6 h、12 h肺湿干比值较ANP组明显降低(P<0.01), 肺组织病理损伤较ANP组明显减轻。结论氢化可的松可减少TXA-2、TNF-α、IL-6等炎症因子的产生而对ANP肺损伤具有重要的保护作用。
Objective To investigate the therapeutic effect and mechanism of Hydrocortisone on acute necrotic pancreatitis（ANP） associated lung injury. Methods Fifty-four SD rats were rardomized into three groups： sham operation（SO） group, ANP group and Hydrocortisone treatment group. The ANP model was induced by retrograde injection of 5% sodium taurocholate into the bili-pancreatic duct. The animals in the Hydrocortisone-treatment group were given 10mg/kg Hydrocortisone 10min after inducing ANP. Rats in the three groups were killed at 3, 6 and 12 hours after induction of the model. The levels of amylase, TNF-α, IL-6, TXB2, 6 Keto-PGF1α, TXB2/6-Keto-PGF1α in plasma, myeloperoxidase （MPO） in the lung, the wet/dry ratio of lung were measured. Histopathological changes of pancreatic and pulmonary tissues were evaluated. Results The levels of amylase, TNF-α, IL-6, TXB2, TXB2/6 Keto PGF1α and pulmonary MPO significantly increased in ANP group compared with those in SO group（P 〈 0.05）. At 6 and 12 h, the wet/dry ratio of lung also significantly increased in ANP group compared with that in SO group（P 〈 0.01 ）. Compared with ANP group, administration of Hydrocortisone significantly reduced the levels of TNF-α, IL-6, TXB2, TXB2/6-Keto-PGF1α and pulmonary MPO（P 〈 0.05）; the wet/dry ratio of lung also significantly decreased at 6 and 12 h（P 〈 0.01）. and the severity of lung injury was decreased. Conclusions Hydrocortisone may exert the therapeutic effect on ANP associated lung injury by decreasing the production of TXA2, TNF-α and IL- 6.
出处
《胰腺病学》
CAS
2005年第3期166-169,共4页
Chinese JOurnal of Pancreatology
