Abstract Aims:The aim of this study is to investigate the possible protective neuroprotective effects of gossypine (GOS) against cisplatin (CIS) (cis-diamminedichloroplatin [II]) toxicity. Materials and methods:CIS (In-vitro; 50 and 100 µM, In-vivo; 10 mg/kg/day) toxicity was created In-vitro and In-vivo, and GOS administration (In-vitro; 50, 75 and 100 µM, In-vivo; 5, 10 and 20 mg/kg/day). Key findings:We used different methods that supported each other. In primary neuron culture, cell proliferation was protected against CIS toxicity in a time-dependent manner with applying GOS. Oxidative/antioxidative markers were normalized in a dose-dependent manner with gossypin administration. In the mechanisms of neurotoxic/neuroprotective (iNOS/nNOS) and inhibition of inflammatory mediators (TNF-a and NF-kB), gossypin has been shown to inhibit NF-kB activation to suppress CIS-induced inflammation in primary neuron culture cells. It has been shown to have antiapoptotic effects in healthy tissues and cells by inhibiting CASP-3 and CASP-9 mRNA levels by regulating the ratio of BCL2/BAX, which are pro-apoptotic and anti-apoptotic indicators. Significance:We conclude that It has been shown that gossypin may be an ideal neuroprotective agent with potent antioxidant capacity and does not reduce the antitumor activity of the chemotherapeutic drug.
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Çınar et al. (2024) studied this question.
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