Comparative effects of dexpanthenol and thymoquinone on colistin-induced neurotoxicity in rats.

Colistin is used as a last-line treatment for multidrug-resistant gram-negative bacilli. Neurotoxicity limits clinic use of colistin. The use of colistin causes oxidative stress and inflammation. The antioxidant activities of dexpanthenol and thymoquinone are well known. The aim of this research was to investigate and compare the efficacy of dexpanthenol and thymoquinone in alleviating neurotoxicity in rats exposed to colistin therapy. The present study investigated inflammation biomarkers using enzyme-linked immunosorbent assay kits, whereas oxidative stress biomarkers were assessed using several photometric techniques. Serum and brain tissue samples were collected from rats with colistin neurotoxicity following treatment with dexpanthenol and thymoquinone. The administration of dexpanthenol markedly ameliorated colistin-induced oxidative stress indicators (except serum disulfide levels) and inflammatory biomarkers in rats. The effectiveness of thymoquinone exhibited a somewhat restricted scope. Thymoquinone demonstrated a notable enhancement in oxidative stress and inflammatory indicators in rats treated with colistin, except for serum disulfide levels, total antioxidant status (TAS), and brain tissue interleukin 6 (IL-6) levels, as these variables remained unaffected. The administration of dexpanthenol and thymoquinone has demonstrated notable neuroprotective effects in mitigating colistin-induced neurotoxicity in a rat model. A comparison of the neuroprotective properties of dexpanthenol and thymoquinone revealed that dexpanthenol had superior ameliorative effects on serum TAS and brain IL-6 levels compared to thymoquinone. The results of this study indicate that dexpanthenol may exhibit superior efficacy compared to thymoquinone in mitigating the neurotoxic adverse effects associated with colistin.