Chronic exposure to lead (Pb) induces neurodegenerative changes in animals and humans. Drugs with strong antioxidant properties are effective against Pb-mediated neurotoxicity. In a prior study, we identified 5,7-dihydroxy-3′,4′,5′-trimethoxyflavone (TMF) from L. leaves as a potent antioxidant and neuroprotective compound. This research explores TMF's neuroprotective effects against Pb-induced brain toxicity in rats to establish it as a therapeutic agent. Rats received lead acetate (100 mg/kg, orally, once daily) for 30 days to induce brain injury, followed by TMF treatment (5 and 10 mg/kg, oral, once daily) 30 min later. Cognitive and motor functions were assessed using Morris Water Maze and horizontal bar tests. Lead, monoamine oxidase (MAO) A and B enzymes, reduced glutathione (GSH), thiobarbituric acid reactive species (TBARS), Tumor necrosis factor-alpha (TNF-α), and IL-6 levels were measured in the hippocampus and cerebellum. Pb exposure impaired cognitive and motor functions, increased Pb, TBARS, TNF-α, and IL-6 levels, and compromised MAO A & B and GSH levels. TMF reversed Pb-induced memory and motor deficits and normalized biochemical anomalies. TMF's neuroprotective effects against lead involve chelating, antioxidant, anti-inflammatory, and monoaminergic properties, suggesting its potential as a treatment for metal-induced brain injury.

中文翻译：

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5,7-二羟基-3',4',5'-三甲氧基黄酮通过其螯合、抗氧化、抗炎和单胺能特性减轻铅诱导的大鼠神经毒性


长期接触铅 (Pb) 会引起动物和人类的神经退行性变化。具有强抗氧化特性的药物可有效对抗铅介导的神经毒性。在之前的研究中，我们从百合叶中鉴定出 5,7-二羟基-3',4',5'-三甲氧基黄酮 (TMF) 是一种有效的抗氧化剂和神经保护化合物。本研究探讨了 TMF 对铅引起的大鼠脑毒性的神经保护作用，以确立其作为治疗剂的地位。大鼠接受醋酸铅（100 mg/kg，口服，每日一次）30 天以诱导脑损伤，30 分钟后进行 TMF 治疗（5 和 10 mg/kg，口服，每日一次）。使用莫里斯水迷宫和单杠测试评估认知和运动功能。测量海马和小脑中的铅、单胺氧化酶 (MAO) A 和 B 酶、还原型谷胱甘肽 (GSH)、硫代巴比妥酸反应物 (TBARS)、肿瘤坏死因子-α (TNF-α) 和 IL-6 水平。 Pb 暴露会损害认知和运动功能，增加 Pb、TBARS、TNF-α 和 IL-6 水平，并降低 MAO A 和 B 以及 GSH 水平。 TMF 逆转了铅引起的记忆和运动缺陷，并使生化异常正常化。 TMF 对铅的神经保护作用涉及螯合、抗氧化、抗炎和单胺能特性，表明其具有治疗金属引起的脑损伤的潜力。