Anti-inflammatory and anti-oxidative effects of vanadium on motor and cerebellar cortices of juvenile hydrocephalic mice.

Hydrocephalus presents a significant clinical neurology challenge, manifesting complications such as neuronal degeneration, cognitive impairments and motor deficits. Ventricular shunting is the primary recourse for treatment, but it is fraught with complications such as infection and obstruction. Due to the need for alternative therapeutic modalities, vanadium, a ubiquitous transition metal known for its promising therapeutic potential in neurological conditions, has recently been studied. This study investigates the anti-inflammatory and anti-oxidative effects of vanadium on the motor and cerebellar cortices in juvenile hydrocephalic mice following treatment with two doses of vanadium. Forty juvenile mice were divided into four cohorts (n = 10 each): control, hydrocephalus-only, low (0.3 mg/kg) and high (3 mg/kg) dose vanadium groups. Hydrocephalus was induced by intracisternal injection of kaolin, and sodium metavanadate was administered daily by intraperitoneal injection for 14 days. Neurobehavioral assessments: Inverted square grid test and pole test were conducted to evaluate muscular strength, motor coordination/balance, learning and memory, respectively. The cerebral motor and cerebellar cortices underwent cresyl violet staining and immunohistochemistry targeting inflammatory markers- Aquaporin-4 (AQP4), Tumor Necrosis Factor-α (TNF-α) and the astrocytic marker -Glial Fibrillary Acidic Protein (GFAP). Additionally, biochemical assays measuring TNF-α, Interleukin 1-β (IL-1β), Superoxide Dismutase (SOD), and Glutathione-S-Transferase (GST) activities were performed. Hydrocephalic mice exhibited significant weight loss and pronounced neurobehavioral deficits, characterized by diminished motor function and impaired cognitive function. Histological staining, AQP4, GFAP and TNF-α immunostaining revealed pyknotic cells, reactive astrocytes, and increased AQP4 and TNF-α expression. Biochemical analyses revealed increased TNF-α and IL-1β levels, accompanied by reduced SOD and GST activities in hydrocephalus-only group. These were all ameliorated in both vanadium-treated groups. In conclusion, this study highlights promising anti-inflammatory and anti-oxidative effects of vanadium treatment in mitigating neuroinflammation and oxidative stress associated with hydrocephalus.