AI Article Synopsis
- - The study aimed to assess how methotrexate (MTX) impacts the lungs through markers of inflammation and cell death, and to explore if gallic acid (GA) can offer protective effects.
- - Twenty-four male rats were divided into three groups: one receiving saline (control), one given MTX, and one treated with both MTX and GA. Various analyses assessed DNA damage, oxidative stress, and inflammation.
- - Results indicated that MTX significantly increased DNA damage and inflammatory markers in the lungs, while GA treatment reduced these harmful effects, suggesting that GA may have a protective role against MTX-induced lung damage.
Article Abstract
Backgrounds: The aim of this study was to investigate the effects of methotrexate (MTX) on the lung via inflammatory and apoptotic pathway biomarkers and the role of gallic acid (GA).
Methods: In this study, twenty four male Wistar-Albino rats weighing 300-350g were divided into 3 groups as follows; Control group (0.1ml/oral saline, for 7 days+2nd day i.p.). MTX group (20mg/kg, single dose, on 2nd day). MTX+GA group (15mg/kg, orally, for 7 days). Comet analysis, oxidant-antioxidant status, IMA were conducted. Histopathological analyses were evaluated.
Results: Comet assay on the blood, TOS and OSI values in the lung were increased in the group II compared with the control group (p<0.05). GA significantly reduced the comet score and IMA levels in the blood, TOS and OSI values in the lung tissue in group III compared with group II (p<0.05). Immunohistochemically PGE, TNF-α, CRP, serum SAA, Caspase 3 and Caspase 9 expressions significantly increased in group II compared with the control group (p<0.001) and GA treatment ameliorated these parameters significantly in group III compared with group II (p<0.001).
Conclusions: MTX caused oxidative stress and DNA damage in the blood tissue and caused oxidative damage, inflammation and apoptosis in the lung tissue.
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| http://dx.doi.org/10.1016/j.biopha.2016.10.077 | DOI Listing |
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