Neuroprotective Effect of Alkaloid-Rich Extract of Cyperus esculentus on Pentylenetetrazole-Induced Neurotoxicity in Wistar Rats

Abstract

Cyperus esculentus commonly called tiger nut has been used traditionally for its medicinal properties. This study aimed to investigate the ameliorative effect of alkaloid-rich extract of Cyperus esculentus on pentylenetetrazole (PTZ)-induced cerebral toxicity in rats. Twenty adults male Wistar rats were randomly divided into four groups (A – D) of five animals each. Group A (Normal control) was administered normal saline only without any treatment. Groups B – D were administered PTZ as a single intraperitoneal dose of 35 mg/kg. Groups C and D were further treated with alkaloid-rich extract of Cyperus esculentus at 50 and 100 mg/kg, respectively once daily per oral for 28 days. On day 29, serum levels of oxidative stress, inflammatory, and anti-inflammatory markers, including Malondialdehyde (MDA), Glutathione (GSH), interleukin-10 (IL-10), interleukin-1beta (IL-1β), and Tumor Necrosis Factor Alpha (TNF-α) were evaluated. Rats’ cerebrum was harvested and used for histological examination and immunohistochemistry for marker of cellular proliferative (Ki-67). PTZ exposure resulted in significant elevation of MDA, reduction in GSH, increased IL-1β and TNF-α, and decreased IL-10 levels, signifying increased oxidative stress, and inflammation. Histopathological examination revealed notable alterations in cerebral tissue architecture and disrupted neuronal fiber, while immunohistochemistry showed increased Ki-67 expression in PTZ-exposed rats. However, treatment with the alkaloid-rich extract of Cyperus esculentus significantly attenuated these effects by maintaining oxidative balance, reduced inflammation, restored normal histoarchitecture, and improved cellular proliferation. These findings indicate that the alkaloid-rich extract of Cyperus esculentus exerts neuroprotective effect against PTZ-induced cerebral toxicity, likely through antioxidant, anti-inflammatory, and proliferative mechanisms.