The effect of taxifolin on cisplatin-induced oxidative pulmonary damage was investigated biochemically and histopathologically in\nmale albino Wistar rats. There were four groups, with six animals in each group: 50 mg/kg of taxifolin plus 2.5 mg/kg of cisplatin\n(TC) group, 2.5 mg/kg of cisplatin only (CIS) group, 50 mg/kg of taxifolin only (TG) group, and a healthy control group (HG). In\nterms of the experimental procedure, the animals in the TC and TG groups were first treated via oral gavage. The CIS and HG\ngroups received distilled water as solvent, respectively. One hour later, the TC and CIS groups received cisplatin at a dose of\n2.5 mg/kg (injected intraperitoneally). Taxifolin, cisplatin, and the distilled water were administered at the indicated dose and\nvolume, using the same method daily for 14 d. At the end of this period, the animals were killed with a high dosage of\nthiopental anaesthesia (50 mg/kg). Blood and lung tissue samples were taken for biochemical (malondialdehyde (MDA),\nmyeloperoxidase (MPO), total glutathione (tGSH), and 8-hydroxy-2 deoxyguanosine (8-OHdG)) analyses and histopathological\nexaminations. The biochemical and histopathological results in the TC and HG groups were then compared with those in the\nCIS group. Cisplatin increased the levels of MDA, myeloperoxidase, and 8-OHdG, a marker of oxidative DNA damage, and\nreduced the amount of tGSH in the lung tissue. Moreover, severe alveolar damage, including oedema and extensive alveolar\nseptal fibrosis, in addition to infiltration of polymorphic nuclear leucocytes and haemorrhagic foci, was observed in the CIS\ngroup. These histopathological findings demonstrate that taxifolin provides protection against pulmonary oxidative stress by\npreventing increases in oxidant parameters and decreases in antioxidants.
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