Neurological mechanism of the dietary supplementations of lycopene on chemotherapy-induced cognitive dysfunction/chemobrain and hippocampal toxicity in the rat model

Aspects of molecular medicine Pub Date : 2025-07-10 DOI:10.1016/j.amolm.2025.100094

Sunday Aderemi Adelakun , Jacob Adewale Siyanbade , Akwu Bala Peter , Mistura Abisola Salami , Bisade Esther Adeyeluwa , Opeyemi Zainab Kaka

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Abstract

Background

Chemo-brain signifies the memory and cognitive challenges cancer patients encounter during and after chemotherapy. Lycopene (LP) is a naturally occurring carotenoid with potent anti-reactive oxygen species (ROS) characteristics. This study investigates the effect of Lycopene on Chemotherapy-induced cognitive dysfunction and hippocampal toxicity in rat models.

Method

Thirty Adult male Sprague-Dawley rats were divided into five groups of five (n = 6) rats each. Group A control received normal saline. Group B received a single dose of 10 mg/kg bwt cisplatin (CP, i.p.) on the first day. Group C received 100 mg/kg bwt of Lycopene (LP) (i.p) once daily. Group D received a single dose of 10 mg/kg CP (i.p.) on the first day, followed by 100 mg/kg bwt of LP (i.p) once daily. Group E was treated with 100 mg/kg bwt of LP (i.p) once daily, followed by a single dose of 10 mg/kg bwt CP (i.p.) on the last day. The experiment lasted for 28 days. Hippocampus histology, oxidative stress, neuro-inflammation, apoptotic markers, brain acetylcholinesterase (AChE) activity, and levels of dopamine (DA), gamma-aminobutyric acid GABA, and serotonin 5-HT were investigated.

Results

Lycopene attenuation of malondialdehyde and nitric oxide levels with elevated glutathione levels and intensified superoxide dismutase and catalase activities. Lycopene decreased the levels of inflammatory and apoptotic markers. In addition, LP reduced AChE activity, and elevated glial fibrillary acidic proteins increased neurotransmitter and brain-derived neurotrophic factors.

Conclusion

Lycopene protected chemobrain rats, decreasing inflammation and apoptosis, increasing antioxidant enzyme activities, and attenuating lipid peroxidation.

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膳食补充番茄红素对大鼠化疗诱导的认知功能障碍/化学脑和海马毒性的神经机制

化疗脑（chemo -brain）是指癌症患者在化疗期间和化疗后遇到的记忆和认知挑战。番茄红素（LP）是一种天然存在的类胡萝卜素，具有有效的抗活性氧（ROS）特性。本研究探讨番茄红素对大鼠化疗诱导的认知功能障碍和海马毒性的影响。方法30只成年雄性Sprague-Dawley大鼠随机分为5组，每组5只（n = 6）。A组对照组给予生理盐水。B组患者第1天给予顺铂单剂量10 mg/kg bwt （CP, ig）。C组给予番茄红素（LP）（i.p） 100 mg/kg bwt，每日1次。D组在第一天给予单剂量10 mg/kg CP (i.p)，随后给予100 mg/kg bwt LP (i.p)，每日1次。E组每日给予100 mg/kg bwt LP (i.p) 1次，最后1天给予10 mg/kg bwt CP （i.p）单剂量。试验期28 d。观察海马组织、氧化应激、神经炎症、凋亡标志物、脑乙酰胆碱酯酶（AChE）活性、多巴胺（DA）、γ -氨基丁酸GABA、血清素5-HT水平。结果番茄红素抑制丙二醛和一氧化氮水平，使谷胱甘肽水平升高，超氧化物歧化酶和过氧化氢酶活性增强。番茄红素降低炎症和凋亡标志物的水平。此外，LP降低了AChE活性，升高的胶质纤维酸性蛋白增加了神经递质和脑源性神经营养因子。结论番茄红素对化学脑大鼠具有保护作用，可减少炎症和细胞凋亡，提高抗氧化酶活性，减轻脂质过氧化。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

Aspects of molecular medicine Molecular Biology, Molecular Medicine

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审稿时长

38 days