Kinetin mitigate neurodegenerative damage of Alzheimer induced by beta-amyloid in male rats by antioxidant and antithrombotic effects.

Alzheimer’s disease (AD) is a neurodegenerative disease that is charactrized by impaired memory and cognitive function. Kinetin (Kn) is a drug that possesses antioxidant and antithrombotic properties. This study aimed to evaluate the effects Kn as a potential treatment for AD in a rat model. Thirty-five Wistar rats were randomly divided into five groups: sham, Aβ, Aβ + 0.5 mg/kg Kn, Aβ + 1 mg/kg Kn, and 1 mg/kg Kn. Beta-amyloid was administered via bilateral intraventricular injection of 10 µl. KN was injected intraperitoneally for two weeks. Subsequently, behavioral tests were conducted, and plasma was used for the thrombolytic test. Hippocampal tissue was analyzed for oxidative stress markers, inflammatory cytokine expression, apoptosis-related gene expression, and neuronal damage. In the Aβ group, behavioral tests demonstrated impaired memory. Levels of plasminogen activator inhibitor-1 (PAI-1), malondialdehyde (MDA), the expression of tumor necrosis factor-alpha (TNF-α) and BAX genes, and the number of degenerated neurons in the hippocampus were significantly increased compared to the sham group. Conversely, glutathione (GSH), superoxide dismutase (SOD), catalase (CAT), plasma tissue plasminogen activator (t-PA) level, and bcl-2 gene expression were significantly decreased in the Aβ group relative to sham controls. Treatment with kinetin improved memory performance and significantly reduced plasma level of PAI-1, MDA, and TNF-α, BAX expression, and neuronal degeneration. Additionally, kinetin significantly increased GSH, SOD, CAT, t-PA levels, and bcl-2 gene expression. Our study showed that kinetin, especially at a dose of 1 mg/kg, with its antioxidant and antithrombotic properties, reduces hippocampal tissue damage following Aβ-induced Alzheimer’s disease, thereby alleviating memory and learning impairments in rats.