Ahiskali Ibrahim, Pinar Can Lokman, Kiki Murat, Cankaya Murat, Kunak Celaleddin Semih, Altuner Durdu
Department of Ophthalmology, Palandoken State Hospital , Erzurum , Turkey.
Department of Biology, Faculty of Science and Art, Erzincan Binali Yıldırım University , Erzincan , Turkey.
Cutan Ocul Toxicol. 2019 Dec;38(4):384-389. doi: 10.1080/15569527.2019.1637348. Epub 2019 Jul 12.
Oxidative stress and inflammation have been demonstrated in the pathogenesis of methanol toxicity. Taxifolin has antioxidant and anti-inflammatory properties. In this study, we examined the protective effect of taxifolin against methanol-induced optic nerve toxicity. Animals were divided into four groups ( = 6): healthy control group (HG), methotrexate (MTX) treated group, methotrexate + methanol treated group (MTX + M), and methotrexate + methanol + taxifolin treated group (MTX + M+T). MTX was administered to all groups except HG group 3 mg/kg oral gavage for 7 d. After that 20% methanol was orally administered to the MTX + M and MTX + M+T group at a dose of 3 g/kg. After 4 h, taxifolin was orally administered to MTX + M+T group 50 mg/kg. Animals were sacrificed by high-dose thiopental anaesthesia, 8 h after taxifolin administration and biochemical studies were performed. Malondialdehyde (MDA), total oxidant system, nuclear factor kappa B (NF-κB), and tumour necrosis factor-alpha levels were significantly higher in the optic nerve of MTX and MTX + M groups compared to HG group. Otherwise, total glutathione (tGSH) and total antioxidant system levels decreased in MTX and MTX + M groups according to the HG group. MDA, total oxidant system, NF-κB, and tumour necrosis factor-alpha levels were decreased in the MTX + M+T group and tGSH, and total antioxidant system levels increased in the MTX + M+T group according to the MTX + M group. These results indicate that taxifolin prevents oxidative and inflammatory optic nerve damage due to methanol exposure.
氧化应激和炎症已在甲醇毒性的发病机制中得到证实。花旗松素具有抗氧化和抗炎特性。在本研究中，我们研究了花旗松素对甲醇诱导的视神经毒性的保护作用。将动物分为四组（每组n = 6）：健康对照组（HG）、甲氨蝶呤（MTX）治疗组、甲氨蝶呤 + 甲醇治疗组（MTX + M）和甲氨蝶呤 + 甲醇 + 花旗松素治疗组（MTX + M+T）。除HG组外，所有组均以3 mg/kg的剂量口服灌胃甲氨蝶呤，持续7天。之后，以3 g/kg的剂量对MTX + M组和MTX + M+T组口服给予20%甲醇。4小时后，以50 mg/kg的剂量对MTX + M+T组口服给予花旗松素。在给予花旗松素8小时后，通过大剂量硫喷妥钠麻醉处死动物，并进行生化研究。与HG组相比，MTX组和MTX + M组视神经中的丙二醛（MDA）、总氧化系统、核因子κB（NF-κB）和肿瘤坏死因子-α水平显著更高。否则，与HG组相比，MTX组和MTX + M组中的总谷胱甘肽（tGSH）和总抗氧化系统水平降低。与MTX + M组相比，MTX + M+T组中的MDA、总氧化系统、NF-κB和肿瘤坏死因子-α水平降低，而MTX + M+T组中的tGSH和总抗氧化系统水平升高。这些结果表明，花旗松素可预防因接触甲醇而导致的氧化和炎症性视神经损伤。
