The use of chemotherapeutic drugs is associated with oxidative damage, cognitive dysfunction, and brain damage. This study sought to investigate the neuroprotective effect of curcumin against cognitive problems associated with treatment with cyclophosphamide via assessment of biomolecules associated with cognitive function in rats’ brain homogenates. Rats were divided in to five groups: Control (vehicle), CUR (curcumin [20 mg/kg]), CPA (cyclophosphamide [150 mg/kg]), CUR1 + CPA (curcumin [20 mg/kg] and cyclophosphamide [150 mg/kg]), and CPA + CUR2 (cyclophosphamide [150 mg/kg] and curcumin [20 mg/kg]). After the treatment, cognitive behavior was assessed and enzymes [cholinesterases, purinergic enzymes, arginase, and angiotensin I-converting enzyme] associated with cognitive function were examined. Oxidative stress parameters [total thiol, non-protein thiol, malondialdehyde, and nitric oxide] including the expression of caspase-3 were also assessed in rats’ brain. Our results showed that curcumin improved cognitive behavior, attenuated cholinergic deficit as revealed by the inhibition of cholinesterases, and improved purinergic signaling in cyclophosphamide-treated rats. Furthermore, curcumin reduced angiotensin-I-converting enzyme and arginase activities before and after treatment with cyclophosphamide. Curcumin also improved redox balance and showed protection against cyclophosphamide-induced oxidative damage to rats’ brain via an increase in protein and non-protein thiols and nitric oxide levels as well as a significant reduction in malondialdehyde levels. Curcumin also prevented neuronal degeneration in different brain regions and reduced caspase-3 expression. Hence this study suggests that pre and post-treatment with curcumin improved neurobehavior, modulates some biomarkers associated with cognitive function and exhibit neuroprotection against cyclophosphamide-induced neurotoxicity in rats.

中文翻译：

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姜黄素给药可减轻环磷酰胺引起的氧化损伤，并恢复大鼠脑中与认知功能相关的酶的变化。

化疗药物的使用与氧化损伤，认知功能障碍和脑损伤有关。这项研究试图通过评估大鼠脑匀浆中与认知功能相关的生物分子，研究姜黄素对与环磷酰胺治疗相关的认知问题的神经保护作用。将大鼠分为五组：对照组（车辆），CUR（姜黄素[20 mg / kg]），CPA（环磷酰胺[150 mg / kg]），CUR1 + CPA（姜黄素[20 mg / kg]和环磷酰胺[150]毫克/千克]和CPA + CUR2（环磷酰胺[150毫克/千克]和姜黄素[20毫克/千克]）。治疗后，评估认知行为并检查与认知功能相关的酶[胆碱酯酶，嘌呤能酶，精氨酸酶和血管紧张素I转化酶]。氧化应激参数[总硫醇，还评估了大鼠大脑中非蛋白硫醇，丙二醛和一氧化氮的表达，包括caspase-3的表达。我们的结果表明，姜黄素改善了认知行为，减轻了胆碱能缺陷，这是通过抑制胆碱酯酶表现出来的，并改善了环磷酰胺治疗大鼠的嘌呤能信号传导。此外，姜黄素在用环磷酰胺治疗之前和之后降低了血管紧张素-I转化酶和精氨酸酶的活性。姜黄素还改善了氧化还原平衡，并通过增加蛋白质和非蛋白质硫醇和一氧化氮的含量以及明显降低丙二醛的含量，显示出对环磷酰胺诱导的对大鼠大脑的氧化损伤的保护作用。姜黄素还可以防止不同大脑区域的神经元变性，并降低caspase-3的表达。