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Chemotherapy-induced neurotoxicity is a common side effect experienced by cancer patients, leading principally to chemotherapy induced cognitive impairment or chemofog (CICI) and chemotherapy induced peripheral neuropathy (CIPN). In recent years, there has been a significant increase in the investigation and exploration of the nutritional values, health benefits, and biological actions of natural products and their bioactive compounds. Thymoquinone (TQ), a bioactive compound extracted from Nigella sativa, has attracted considerable interest due to its neuroprotective activities. This review comprehensively analyzes TQ’s mechanisms in reducing chemotherapy-induced neurotoxicity, primarily by regulating oxidative stress, inflammatory responses, and apoptosis. Furthermore, this review discusses the synergistic effects of TQ when used in combination with certain anticancer drugs, enhancing both neuroprotection and overall treatment outcomes. While substantial preclinical data support TQ’s effectiveness in mitigating acute neurotoxicity, its impact on chronic neurotoxicity remains insufficiently studied. Thus, further preclinical investigations are imperative to evaluate TQ’s potential in addressing chemotherapy-induced chronic neurotoxicity.
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