Applied Biotechnology Research Center, Baqiyatallah University of Medical Sciences, Tehran, Iran.
J Pharm Pharmacol. 2013 Jun;65(6):868-73. doi: 10.1111/jphp.12048. Epub 2013 Mar 11.
The purpose of this study was to demonstrate the effect of methyl-3-O-methyl gallate (M3OMG), a rare polyphenolic natural product with a potent in-vitro antioxidant effect, against sodium fluoride (NaF)-induced oxidative stress in rat erythrocytes in vivo.
Male Wistar rats were treated daily with either M3OMG (10 and 20 mg/kg) obtained through synthesis, vitamin C (10 mg/kg) or vehicle intraperitoneally for 7 days. Oxidative stress was then induced by exposing animals to NaF (600 ppm) through drinking water for 7 days. At the end of intoxication period, rats were killed and erythrocytes isolated. The activity of antioxidant enzymes (catalase and superoxide dismutase) and levels of reduced glutathione and thiobarbituric acid reactive substances were measured in erythrocyte haemolysates.
NaF intoxication resulted in a 1.9-fold increase in erythrocyte lipid peroxidation associated with significant (P < 0.001) depletion of reduced glutathione level. Superoxide dismutase and catalase activity was suppressed by NaF treatment by 3.069 and 2.3 fold when compared with untreated control groups. Pretreatment of rats with M3OMG or vitamin C afforded protection against NaF-induced oxidative stress as assessed through the measured oxidant/antioxidant markers.
This finding provided in-vivo evidence for the therapeutic potential of M3OMG in combating fluoride-induced oxidative damage in cellular systems.
本研究旨在证明甲氧基-3-O-甲基没食子酸(M3OMG)的作用,M3OMG 是一种具有强大体外抗氧化作用的罕见多酚天然产物,对抗体内氟化物(NaF)诱导的大鼠红细胞氧化应激。
雄性 Wistar 大鼠每天通过合成、维生素 C(10mg/kg)或腹腔内注射 M3OMG(10 和 20mg/kg)、载体进行治疗,持续 7 天。然后通过饮用水使动物暴露于 NaF(600ppm)7 天来诱导氧化应激。在中毒期结束时,处死大鼠并分离红细胞。在红细胞溶血物中测量抗氧化酶(过氧化氢酶和超氧化物歧化酶)的活性以及还原型谷胱甘肽和硫代巴比妥酸反应物质的水平。
NaF 中毒导致红细胞脂质过氧化增加 1.9 倍,与还原型谷胱甘肽水平显著(P<0.001)降低有关。超氧化物歧化酶和过氧化氢酶的活性分别被 NaF 处理抑制了 3.069 和 2.3 倍,与未处理的对照组相比。用 M3OMG 或维生素 C 预处理大鼠可防止 NaF 诱导的氧化应激,这可通过测量的氧化剂/抗氧化剂标志物来评估。
该发现为 M3OMG 在对抗细胞系统中氟化物诱导的氧化损伤方面的治疗潜力提供了体内证据。