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目的:观察氨甲蝶呤(MTX)对急性胰腺炎时炎症性细胞因子和抗炎症细胞因子的调节作用,从免疫的角度探讨氨甲蝶呤治疗急性胰腺炎的作用机制.方法:实验用♂SD大鼠共分3组:1组为正常对照组(n=6);2组为采用开腹胰管注射5%牛黄胆酸钠(1.0m/kg)制备急性胰腺炎模型(n=8);3组为胰腺炎诱导成功后0.5h静脉注射氨甲蝶呤(1.2mg/kg),手术后2,6和24h处死动物(每时段n=7),分别抽血查TNFα,IL-1,IL-6,IL-10和TGF-β及胰淀粉酶、胰腺湿质量和白细胞计数.结果:在急性胰腺炎时血中的炎症性细胞因子和抗炎症细胞因子均显著升高,在使用MTX治疗后,上述因子均下降.其中TNFα,IL-1,IL-6在2、6和24h均明显下降(P<0.05),IL-10和TGF-β在24h段下降最为明显(P<0.05).1、2和3组动物24h胰腺湿质量分别为0.53±0.09g,1.53±0.13g和0.85±0.22g;三组24h淀粉酶分别为374.±93U/L,1817±459U/L和766±373U/L,对比MTX治疗前后,可见反映胰腺炎病情的胰腺湿质量和淀粉酶2项指标均明显好转(P<0.05).结论:MTX可以同时抑制急性胰腺炎时血中过高的炎症性细胞因子和抗炎症细胞因子,从而可能通过免疫调节的方式缓解胰腺炎的病理生理异常,达到治疗目的.
Objective: To investigate the regulation of methotrexate (MTX) for anti-inflammatory cytokines and inflammatory cytokine acute pancreatitis, explore the mechanism of methotrexate treatment of acute immunological method from the perspective of: experimental ♂ SD rats were divided into 3 groups: 1 group was normal control group (n = 6); 2 groups were prepared acute pancreatitis model (n = 8) by using open pancreatic duct injection of 5% sodium taurocholate (1.0m / kg) ); 3 groups were given methotrexate (1.2mg / kg) 0.5h after successful induction of pancreatitis, and animals were sacrificed at 2, 6 and 24h after operation (n = 7 for each time period) 1, IL-6, IL-10, TGF-β and pancreatic amylase, pancreas wet weight and white blood cell count.Results: The levels of inflammatory cytokines and anti-inflammatory cytokines in acute pancreatitis were significantly increased The levels of TNFα, IL-1 and IL-6 decreased significantly at 2, 6 and 24 hours after treatment with MTX (P <0.05), while the levels of IL-10 and TGF- <0.05) .While the pancreas wet weights in the 1, 2 and 3 groups were 0.53 ± 0.09g, 1.53 ± 0.13g and 0.85 ± 0.22g respectively, the 24h groups were 374. ± 93U / L, 1817 ± 459U / L and 766 ± 373U / L, compared with MTX before and after treatment, we can see that pancreatitis disease (P <0.05) .Conclusion: MTX can inhibit both hyperinflammatory cytokines and anti-inflammatory cytokines in acute pancreatitis at the same time, which may be mediated by immunomodulatory Way to alleviate the pathophysiology of pancreatitis anomalies, to achieve the purpose of treatment.