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

IF 2.4 4区医学 Q2 PHARMACOLOGY & PHARMACY

Toxicon Pub Date : 2025-09-10 DOI:10.1016/j.toxicon.2025.108568

Tansu Kuşat , Feyza Başak , Emine Ümran Örsçeli̇k , Oğuzhan Koca , Güngör Çağdaş Di̇nçel

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Abstract

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.

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厚朴酚对脑室内凯尼克酸所致脊髓神经毒性的改善作用

Kainic acid （Ka）是一种神经兴奋剂，通常用于兴奋性毒性的建模。本研究旨在探讨大鼠脑室注射Ka对颈脊髓的神经毒性作用及本木酚的治疗作用。50只雄性Wistar Albino大鼠（n = 10）分为5组。对照组大鼠腹腔注射生理盐水，持续7 d。假手术组大鼠第1天给予单剂量生理盐水。Ka组大鼠给予单icv剂量的Ka （0.5 μg/μl）。本木酚（Hnl）组大鼠给药Hnl 7 d (ip-5 mg/kg)， Ka + Hnl组大鼠给药Ka（单剂量）和Hnl （7 d）。Ka组大鼠表现出明显的组织病理学改变，胶质纤维酸性蛋白（GFAP）阳性（+）细胞增多。与Ka组相比，Ka + Hnl组大鼠组织学结构改善，GFAP（+）细胞减少。Ka组大鼠中央管腔直径明显扩大。结果显示，Ka组大鼠脊髓内丙二醛（MDA）和肿瘤坏死因子-α (TNF-α)水平升高，谷胱甘肽（GSH）水平降低。Hnl处理引起兴奋性毒性模型大鼠MDA和GSH水平的显著改善和TNF-α水平的降低。总之，研究结果表明，Hnl治疗通过减少氧化组织损伤、炎症反应和GFAP表达来减轻ka诱导的神经毒性。

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来源期刊

Toxicon 医学-毒理学

CiteScore

4.80

自引率

10.70%

发文量

358

审稿时长

68 days

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