Solasodine hydrochloride (90 μM; 2 days) treatment induced significant budding in P19 cells. This compound strongly stimulated the expression of various neuronal markers, including βIII-tubulin, synaptophysin, MAP2, ChAT, and the neural progenitor marker doublecortin. Predominantly, Solasodine hydrochloride directed the differentiation of P19 cells towards neuronal pathways.

Solasodine hydrochloride (90 μM; 2 days) treatment induced significant budding in P19 cells. This compound strongly stimulated the expression of various neuronal markers, including βIII-tubulin, synaptophysin, MAP2, ChAT, and the neural progenitor marker doublecortin. Predominantly, Solasodine hydrochloride directed the differentiation of P19 cells towards neuronal pathways.

Solasodine hydrochloride, administered as a single intraperitoneal injection at doses ranging from 25-100 mg/kg, significantly prolongs the latency period of the hind limb tonic extensor (HLTE) phase during convulsions induced by picrotoxin. It also significantly enhances thiopental-induced sleep in a dose-dependent manner. Additionally, when administered via intracerebroventricular injection at 375 μM consistently over two weeks, Solasodine hydrochloride markedly increases the uptake of bromodeoxyuridine in ependymal layer, subventricular zone, and cortical cells, which colocalize with doublecortin immunostaining. Treatment in rats significantly boosts the expression of cholesterol and drug-binding transport proteins in ependymal cells. The compound exhibits anticonvulsant effects and suppresses central nervous system activity. In animal models, Swiss albino mice weighing 18-25 g were used, treated with either picrotoxin or thiopental.