乙胺嗪可减轻四氯化碳（CCl₄）诱导的小鼠肝损伤中的慢性炎症和纤维化。
Diethylcarbamazine reduces chronic inflammation and fibrosis in carbon tetrachloride- (CCl₄-) induced liver injury in mice.
作者信息
Rocha Sura Wanessa Santos, de França Maria Eduarda Rocha, Rodrigues Gabriel Barros, Barbosa Karla Patrícia Sousa, Nunes Ana Karolina Santana, Pastor André Filipe, Oliveira Anne Gabrielle Vasconcelos, Oliveira Wilma Helena, Luna Rayana Leal Almeida, Peixoto Christina Alves
机构信息
Laboratory of Ultrastructure, Aggeu Magalhães Research Center (CPqAM), Avenida Professor Moraes Rego, s/n, Cidade Universitária, 50740-465 Recife, PE, Brazil ; Department of Entomology, Aggeu Magalhães Research Center (CPqAM), Avenida Professor Moraes Rego, s/n, Cidade Universitária, 50740-465 Recife, PE, Brazil.
Laboratory of Ultrastructure, Aggeu Magalhães Research Center (CPqAM), Avenida Professor Moraes Rego, s/n, Cidade Universitária, 50740-465 Recife, PE, Brazil.
出版信息
Mediators Inflamm. 2014;2014:696383. doi: 10.1155/2014/696383. Epub 2014 Oct 13.
This study investigated the anti-inflammatory effects of DEC on the CCl4-induced hepatotoxicity in C57BL/6 mice. Chronic inflammation was induced by i.p. administration of CCl4 0.5 μL/g of body weight through two injections a week for 6 weeks. DEC (50 mg/kg) was administered by gavage for 12 days before finishing the CCl4 induction. Histological analyses of the DEC-treated group exhibited reduced inflammatory process and prevented liver necrosis and fibrosis. Immunohistochemical and immunofluorescence analyses of the DEC-treated group showed reduced COX-2, IL1β, MDA, TGF-β, and αSMA immunopositivity, besides exhibiting decreased IL1β, COX-2, NFκB, IFNγ, and TGFβ expressions in the western blot analysis. The DEC group enhanced significantly the IL-10 expression. The reduction of hepatic injury in the DEC-treated group was confirmed by the COX-2 and iNOS mRNA expression levels. Based on the results of the present study, DEC can be used as a potential anti-inflammatory drug for chronic hepatic inflammation.
本研究调查了二乙氨基乙醇（DEC）对C57BL/6小鼠四氯化碳（CCl4）诱导的肝毒性的抗炎作用。通过每周两次腹腔注射0.5 μL/g体重的CCl4，持续6周来诱导慢性炎症。在完成CCl4诱导前12天，通过灌胃给予DEC（50 mg/kg）。对DEC治疗组的组织学分析显示炎症过程减轻，预防了肝坏死和纤维化。对DEC治疗组的免疫组织化学和免疫荧光分析表明，除了在蛋白质免疫印迹分析中显示白细胞介素1β（IL1β）、环氧化酶-2（COX-2）、核因子κB（NFκB）、干扰素γ（IFNγ）和转化生长因子β（TGFβ）表达降低外，COX-2、IL1β、丙二醛（MDA）、TGF-β和α平滑肌肌动蛋白（αSMA）免疫阳性也降低。DEC组显著增强了白细胞介素10（IL-10）的表达。COX-2和诱导型一氧化氮合酶（iNOS）的mRNA表达水平证实了DEC治疗组肝损伤的减轻。基于本研究结果，DEC可作为治疗慢性肝炎症的潜在抗炎药物。
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