Mustafa Saygin1, Onder Ozturk2, Ozlem Ozmen3, Ilter Ilhan4, Taner Gonca5, Nurhan Gumral6, Hikmet Orhan7, Rahime Aslankoc6. 1. Department of Physiology, Suleyman Demirel University, Faculty of Medicine, Isparta, Turkey. Electronic address: fizyolog@gmail.com. 2. Department of Chest Diseases, Suleyman Demirel University, Faculty of Medicine, Isparta, Turkey. 3. Department of Pathology Mehmet Akif Ersoy University, Faculty of Veterinary Medicine, Burdur, Turkey. 4. Department of Medical Biochemistry, Suleyman Demirel University, Faculty of Medicine, Isparta, Turkey. 5. Clinic of Chest Diseases, Isparta State Hospital, Isparta, Turkey. 6. Department of Physiology, Suleyman Demirel University, Faculty of Medicine, Isparta, Turkey. 7. Department of Biostatistics and Medical Informatics, Suleyman Demirel University, Faculty of Medicine, Isparta, Turkey.
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 PGE2, 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.
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 PGE2, 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.
Authors: Kailibinuer Aierken; Yuqing Luo; Maitinuer Maiwulanjiang; Tao Wu; H A Aisa Journal: Evid Based Complement Alternat Med Date: 2021-11-30 Impact factor: 2.629