Cerebroprotective potential of ceftriaxone against cadmium chloride-induced cerebral inflammatory changes and...

Cadmium (Cd) is a potent neurotoxic heavy metal associated with cerebral oxidative disturbances. The beta-lactam antibiotic ceftriaxone has been known to modulate the expression of GLT-1, the primary glutamate transporter. This research has been framed to evaluate the potential neurodefensive activity of ceftriaxone against cadmium chloride (CdCl₂)-elicited toxic alterations in Swiss albino mice. Thirty animals were arbitrarily divided into five groups, i.e., Group I (control), Group II (ceftriaxone per se-100 mg kg^-1 alone), Group III (CdCl₂-5 mg kg^-1), Group IV and Group V (CdCl₂ with ceftriaxone 50 mg kg^-1 and 100 mg kg^-1). Assessments include behavioral tasks (stress-coping behavior, cognition), markers of oxidative damage (thiobarbituric acid reactive substances (TBARS) and glutathione (GSH), and indicators of neuronal inflammation (myeloperoxidase, interleukin-6, 10, and tumor necrosis factor-α) in the brain, which were also estimated. Furthermore, cerebral markers (cAMP response element-binding protein (CREB) and brain-derived neurotrophic factor (BDNF)) were assessed to evaluate cerebral health. Mice treated with CdCl₂ exhibited stress-coping behavior, cognitive deficits, disturbed antioxidant status (raised TBARS and diminished GSH), increased neuroinflammatory markers, and diminished concentrations of CREB and BDNF. Observations indicated that ceftriaxone administration was associated with an improvement in stress-coping behavior, cognitive deficits, and restoration of the antioxidant and inflammatory markers. Furthermore, ceftriaxone treatment improved the levels of CREB and BDNF. The results suggest that ceftriaxone exhibits symptomatic improvement against CdCl₂-elicited toxic outcomes in mice. Whereas the exact mechanism needs further validation, these outcomes direct a potential therapeutic role for ceftriaxone in recuperating Cd-induced neurological damage.