The ameliorative effects of Honokiol on intracerebroventricular Kainic acid-induced spinal cord neurotoxicity.

Kainic acid (Ka) is a neuroexcitatory agent commonly utilized in the modeling of excitotoxicity. The study aims to investigate both the neurotoxic effects of intracerebroventricular (icv) Ka injections in rats on the cervical spinal cord and the therapeutic role of honokiol. Fifty male Wistar Albino rats (n = 10) are divided into five groups. The control group of rats received normal saline by intraperitoneal (ip) injection for a duration of 7 days. The sham group of rats was administered a single dose of icv normal saline on the first day. Rats in the Ka group received a single icv dosage of Ka (0.5 μg/μl). Honokiol (Hnl) group rats Hnl for 7 days (ip-5 mg/kg), while Ka + Hnl group rats were administered Ka (single dose) and Hnl (7 days). Exhibited substantial histopathological alterations and an increase in glial fibrillary acidic protein (GFAP) positive (+) cells in the rats in the Ka group. In the Ka + Hnl group of rats, an improvement in histological structure and a reduction in GFAP (+) cells compared to the Ka group. The central canal lumen diameters were significantly expanded in the Ka group rats. It was observed that malondialdehyde (MDA) and tumor necrosis factor-α (TNF-α) levels increased and glutathione (GSH) levels decreased in the spinal cord of rats in the Ka group. Hnl treatment caused a significant improvement in MDA and GSH levels and a decrease in TNF-α levels in rats with the excitotoxicity model. In conclusion, the findings showed that Hnl treatment attenuated Ka-induced neurotoxicity by reducing oxidative tissue damage, inflammatory response, and GFAP expression.