模拟铝神经毒性时海马体内的氧化还原失衡和氧化应激,启动辅酶А的生物合成过程

N. Kanunnikova, D. Semenovich, I. N. Katkovskaya, O. V. Titko, E. P. Lukiyenko, V. Gurinovich, A. Moiseenok
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摘要

使用氯化铝(200 毫克/千克,胃内注射,6 周)诱导成熟雌性 Wistar CRL:(WI) WUBR大鼠,以建立海马氧化还原失衡和氧化应激(OS)模型,并研究每周服用辅酶A生物合成调节剂(泛醇-PL、泛酸-PT、同泛酸盐-HP)的可能性。在过氧化过程被激活和乙酰胆碱酯酶活性降低的背景下,观察到谷胱甘肽的还原电位和 CoA 酸溶性部分的水平下降,同时谷胱甘肽代谢酶(GR、GPx、GST)的活性、蛋白质的 S-谷胱甘肽化过程和蛋白质硫醇的水平上升。完全(PL、PT)或部分(HP)摄入 CoA 生物合成的前体具有抗氧化作用,可恢复 AChE 的活性、谷胱甘肽和谷胱甘肽代谢酶的水平和还原电位、S-谷胱甘肽化过程,并刺激产生 NADPH+ 的酶的活性。考虑到辅酶前体对海马体内 CoA 水平的调节作用较低,而其氧化还原药理活性较高,因此假定其对氧化还原机制的非酶作用可导致还原当量生物利用率和能量状态的提高。
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Modelling the redox imbalance and oxidative stress in the hippocampus at aluminum neurotoxicity and initiating the coenzyme А biosynthesis
An Alzheimer-like pathological process was induced in mature female Wistar CRL: (WI) WUBR rats using aluminum chloride (200 mg/kg, intragastrically, 6 weeks) in order to model redox imbalance and oxidative stress (OS) in the hippocampus and study the possibilities of their correction 2 weekly administration of coenzyme A biosynthesis modulators (panthenol – PL, pantethine – PT, homopantothenate – HP) at a dose of 200 mg/kg intragastrically for 2 weeks). Against the background of activation of peroxidation processes and a decrease in acetylcholinesterase activity, a decrease in the reduction potential of glutathione and the level of the acid-soluble fraction of CoA was observed with a simultaneous increase in the activity of glutathione-metabolizing enzymes (GR, GPx, GST), the process of S-glutathionylation of proteins and the level of protein thiols. The consumption of the precursors of CoA biosynthesis in full (PL, PT) or in part (HP) had an antioxidant effect, restored the activity of AChE, the level and reduction potential of glutathione and glutathione-metabolizing enzymes, the process of S-glutathionylation, and stimulated the activity of enzymes generating NADPH+. Taking into account the low modulating effect of coenzyme precursors on the level of CoA in the hippocampus and their high redox pharmacological activity, their non-coenzymatic effect on redox mechanisms leading to an increase in the bioavailability of reducing equivalents and energy status is assumed.
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