揭示菊黄素对成年雄性 Wistar 大鼠前额叶皮层的神经保护潜力

Ifeanyi Anthony Egwuatu, C. Ozoemena, Fortune Kasiemobi Onuorah
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摘要

人体内过多的自由基会使各个系统中的细胞失衡,并导致氧反应物的积累,即氧化应激。中枢神经系统也不能幸免于这些细胞和组织损伤。中枢神经系统的氧化应激可能是造成焦虑、空间记忆障碍、神经细胞耗竭和神经毒性导致的空泡组织变性的原因。多柔比星等化疗药物的使用与氧反应物和抗氧化剂之间的失衡有关。因此,寻找具有神经保护作用的抗氧化剂补充剂已成为一个研究热点。本研究旨在评估菊黄素对多柔比星诱发认知障碍的雄性 Wistar 大鼠前额叶皮层的保护潜力。35 只成年 Wistar 大鼠(180-200 克)被分为七组(1-7;n = 5)。第 1 组为正常对照组,在整个研究过程中只接受生理盐水治疗。第 2 组仅腹腔注射多柔比星 21 天。第 3 组和第 4 组分别口服低剂量和高剂量的金霉素 21 天。第 5 组、第 6 组和第 7 组分别腹腔注射和口服低、中、高剂量的多柔比星和金霉素 21 天。这与凋亡指标、炎症标志物和组织学病变的显著升高相对应,而这些都是认知障碍的表现。5,7-二羟基黄酮(金丝桃苷)能明显减轻和逆转多柔比星引起的认知障碍。这种作用可能是通过抑制氧化应激、炎症和细胞凋亡实现的。
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Unveiling the neuroprotective potential of chrysin on the pre-frontal cortex of adult male Wistar rats
Excessive free radicals in the human body predispose cells within the various systems to an imbalance and accumulation of oxygen-reactive species, known as oxidative stress. The central nervous system is not spared when it comes to these cell and tissue damages. Oxidative stress on the central nervous system may be responsible for anxiety, spatial memory impairment, neuronal cell depletion, and vacuole-tissue degeneration resulting from neurotoxicity. The use of chemotherapeutic agents such as doxorubicin has been implicated in the build-up of this imbalance between oxygen-reactive species and antioxidants. Therefore, it has become an area of research interest to seek antioxidant supplements that may offer neuroprotective effects. This study is aimed to evaluate the protective potential of chrysin on the pre-frontal cortex of male Wistar rats with doxorubicin-induced cognitive impairment. Thirty-five adult Wistar rats (180–200 g) were grouped into seven (1–7; n = 5). Group 1, the normal control, received normal saline treatment only throughout the study. Group 2 was administered with doxorubicin only for 21 days by intraperitoneal injection. Groups 3 and 4 were administered with chrysin in low and high doses for 21 days orally. Groups 5, 6 and 7 were exposed to doxorubicin and chrysin for 21 days intra-peritoneally and orally with low, medium and high doses, respectively. Anti-oxidative biomarkers analysed in Group 2 (doxorubicin-only) demonstrated a significant difference when compared to other groups. This corresponded to significant elevations in apoptotic indicators, inflammatory markers and histological lesions, which were indicative of cognitive impairment. 5, 7-dihydroxyflavone (chrysin) significantly mitigated and also reversed cognitive impairment caused by doxorubicin. The data showed that chrysin protected against doxorubicin-induced cognitive impairment. This effect is probably made possible by suppressing oxidative stress, inflammation and apoptosis.
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