Unveiling the neuroprotective potential of chrysin on the pre-frontal cortex of adult male Wistar rats

Abstract

Objectives 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. Material and Methods 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. Results 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. Conclusion The data showed that chrysin protected against doxorubicin-induced cognitive impairment. This effect is probably made possible by suppressing oxidative stress, inflammation and apoptosis.