Conclusion
Ger reduced the oxidative stress status, neuroinflammation and apoptosis and activated GABAergic neurotransmission, which might clarify its anticonvulsant. Ger protects animals against PTZ prompted kindling as established by the enhancement in short term as well as long-term memory. Ger mitigated the injury induced by Glu in NGF prompted PC12 cell.
Results
Ger up to 400 μg/mL did not display any toxicity or injury in PC12 cells. Ger (100 to 200 μg/mL) reduced the injury induced by Glu, increased the gene expression of GABAA-Rα1, GAD65 and GAD67 and decreased GAT 1, GAT 3 and NMDAR1 expression in NGF-induced PC12 cells damaged by Glu. Ger (100 to 200 μg/mL) increased GABA and reduced TNF-α, IL-4 and IL-1β levels in NGF-induced PC12 cells injured by Glu. As for the in-vivo results, Ger increased GABA, GAD, GAT 1 and 3 and lowered GABA T. Ger mitigated MDA, NO, IL-1β, IL-6, TNF-α and IFN-γ, GFAP, caspase-3, and -9 levels and Bax gene expression and escalated GSH, SOD, catalase, BDNF and Bcl2 gene expression.