Honokiol prevents central kainic acid-induced neurodegeneration by suppressing oxidative stress, inflammation, and TGF-β1 expression.

Abstract

This study explored the neuroprotective effects of honokiol against oxidative stress, neuroinflammation and transforming growth factor-beta1 (TGF-β1) pathways in kainic acid (KA)-induced neurodegeneration in rats. The animals were divided into: control [Honokiol solvent (dimethyl sulphoxide), intraperitoneal for 7 days]; sham [single-dose KA solvent (saline, intracerebroventricular)]; KA (0,5 μg/μl, single-dose, intracerebroventricular); Honokiol [5 mg/kg-intraperitoneal) for 7 days]; and KA+Honokiol [KA single dose and Honokiol (for 7 days)]. Cerebral cortex and hippocampus tissues of the right hemispheres of rat brains were removed and examined biochemically and histopathologically. KA administration caused an increase in malondialdehyde levels and a decrease in reduced glutathione (GSH) and superoxide dismutase (SOD) levels. In addition, interleukin-1β levels and TGF-β1 expression were increased. Honokiol treatment decreased malondialdehyde levels, increased SOD and GSH levels, increased interleukin-1β levels and improved TGF-β1 expression in rats. Our data showed Honokiol has a protective potential against kainic acid-induced neurodegeneration by suppressing oxidative stress, inflammation and TGF-β1 expression.