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• W2152220474 abstract "Methotrexate (MTX) is used to treat cancers, several forms of arthritis and other rheumatic conditions, although MTX may cause pulmonary toxicity related to the production of free oxygen radicals, various cytokines. Infliximab (IB) with its potent effect on tumor necrosis factor-alpha (TNF-α) inhibition also inhibits the release of endothelin-1 (ET-1). We aimed to investigate whether IB reduces pulmonary damage induced by an overdose of MTX. The rats were divided into 3 groups of 8 animals. The control group was given only saline. One dose of 20 mg/kg MTX intraperitoneal was administered in the MTX group. IB 7 mg/kg was given to the MTX + IB (MI) group. Three days after IB was administered, 20 mg/kg MTX was given. Five days after MTX was administered, all rats were sacrificed. The TNF-α, ET-1, malondialdehyde (MDA), myeloperoxidase (MPO) and caspase-3 levels in MTX group were significantly higher than in control groups of TNF-α (P=.001), ET-1 (P=.001), MDA (P=.001), MPO (P=.001) and caspase-3 levels (P=.001) and MI groups of TNF-α (P=.009), ET-1 (P=.001), MDA (P=.047), MPO (P=.007) and caspase-3 levels (P=.003). The MI group had less histopathological damage in lung tissue than the MTX group. Overdose of MTX leads to cytokine release and the formation of reactive oxygen species in addition to increased ET-1 secretion release that causes lung damage. IB, as a potent proinflammatory agent, TNF-α blocker, can decrease ET-1 release and oxidative stress, it may show significant protective effects in lung tissue against damage caused by MTX overdose. El metotrexato (MTX) se emplea para tratar el cáncer, varias formas de artritis y otras patologías reumáticas, pero puede causar toxicidad pulmonar debido a la producción de radicales libres del oxígeno y varias citocinas. Infliximab (IB) es un potente inhibidor del factor de necrosis tumoral-alfa (TNF-α) e inhibe también la liberación de endotelina-1 (ET-1). Nos propusimos investigar si IB reduce el daño pulmonar inducido por una sobredosis de MTX. Las ratas se dividieron en 3 grupos de 8 animales. Al grupo control solamente se le administró solución salina. Al grupo MTX se le administró una dosis intraperitoneal de 20 mg/kg de MTX. Al grupo de MTX + IB (MI) se le administraron 7 mg/kg de IB. Tres días después de la administración de IB se administraron 20 mg/kg de MTX. Todas las ratas se sacrificaron 5 días después de la administración de MTX. Las concentraciones de TNF-α, ET-1, malondialdehído (MDA), mieloperoxidasa (MPO) y caspasa-3 fueron significativamente más altas en el grupo MTX que en el grupo control: TNF-α (p < 0,001), ET-1 (p < 0,001), MDA (p < 0,001), MPO (p < 0,001) y caspasa-3 (p < 0,001) y en el grupo MI: TNF-α (p < 0,009), ET-1 (p < 0,001), MDA (p < 0,047), MPO (p < 0,007) y caspasa-3 (p < 0,003). El grupo MI mostró menos daño histopatológico en el tejido pulmonar que en el grupo MTX. La sobredosis de MTX induce la liberación de citocinas y la formación de especies reactivas de oxígeno, además de una mayor secreción de ET-1 que provoca daño pulmonar. IB es un agente proinflamatorio potente, bloquea el TNF-α, puede reducir la liberación de ET-1 y el estrés oxidativo y mostrar importantes efectos protectores del tejido pulmonar frente al daño causado por una sobredosis de MTX." @default.
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• W2152220474 date "2015-11-01" @default.
• W2152220474 modified "2023-09-29" @default.
• W2152220474 title "Protective Effects of Infliximab on Lung Injury Induced by Methotrexate" @default.
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• W2152220474 doi "https://doi.org/10.1016/j.arbr.2015.05.012" @default.
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