Luteolin (LUT) is a glycosylated flavonoid compound that has multiple beneficial pharmacological and biological impacts. The current investigation was undertaken to evaluate the putative neuroprotective potency of LUT against neuronal damage induced by lead acetate (PbAc). Twenty-eight rats were placed into four equal groups. Group 1: served as the control group, group 2: rats were supplemented orally with LUT (50 mg kg-1), group 3: rats were intraperitoneally injected with PbAc (20 mg kg-1), and group 4: rats were pretreated with LUT before PbAc injection with the same doses. All animals were treated for 7 days. The exposure to PbAc increased the concentration of lead in the cortical tissue, neuronal lipid peroxidation, and nitric oxide (NO) production and decreased the antioxidant enzymes. Additionally, PbAc enhanced a neuroinflammatory response in the cortical tissue through increasing the pro-inflammatory cytokines secretion and inducible NO synthase expression. Moreover, cortical cell death was recorded following PbAc intoxication as evidenced by the enhancement of the proapoptotic and inhibiting the antiapoptotic markers. Interestingly, LUT supplementation reversed the cortical adverse reactions induced by PbAc. Taken together, these findings may suggest that LUT may be useful for attenuating neuronal damage induced by PbAc through inhibiting the oxidative damage, neuroinflammation, and the cortical cell death.

中文翻译：

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木犀草素对乙酸铅诱导的大鼠皮层损伤的神经保护作用。

木犀草素（LUT）是一种糖基化的类黄酮化合物，具有多种有益的药理和生物学作用。进行了当前的研究，以评估LUT对乙酸铅（PbAc）诱导的神经元损伤的神经保护作用。将二十八只大鼠分成四个相等的组。第1组：作为对照组，第2组：对大鼠口服LUT（50 mg kg-1），第3组：对大鼠腹腔注射PbAc（20 mg kg-1），第4组：大鼠进行预处理在以相同剂量注射PbAc之前使用LUT。将所有动物治疗7天。暴露于PbAc可增加皮层组织中铅的浓度，神经元脂质过氧化和一氧化氮（NO）的产生，并减少抗氧化酶。另外，PbAc通过增加促炎性细胞因子的分泌和诱导型NO合酶的表达来增强皮质组织中的神经炎性反应。此外，PbAc中毒后记录了皮质细胞死亡，其表现为促凋亡和抑制抗凋亡标记的增强。有趣的是，补充LUT逆转了PbAc诱导的皮质不良反应。综上所述，这些发现可能暗示LUT可通过抑制氧化损伤，神经炎症和皮层细胞死亡而用于减轻由PbAc诱导的神经元损伤。PbAc中毒后记录皮质细胞死亡，其表现为促凋亡和抑制抗凋亡标志物增强。有趣的是，补充LUT逆转了PbAc诱导的皮质不良反应。综上所述，这些发现可能暗示LUT可通过抑制氧化损伤，神经炎症和皮层细胞死亡而用于减轻由PbAc诱导的神经元损伤。PbAc中毒后记录皮质细胞死亡，其表现为促凋亡和抑制抗凋亡标志物增强。有趣的是，补充LUT逆转了PbAc诱导的皮质不良反应。综上所述，这些发现可能暗示LUT可通过抑制氧化损伤，神经炎症和皮层细胞死亡而用于减轻由PbAc诱导的神经元损伤。