Neuroprotective Effects of Tectoridin in H2O2-Induced Oxidative Stress and an Amyloid-Infused Rat Model of Alzheimer's Disease.

This study aims to examine the effects of tectoridin in both in vitro and in vivo models of Alzheimer's disease. In vitro, oxidative stress was induced in PC12 cells using 400 µM of hydrogen peroxide (H2O2) to simulate cellular damage. In vivo, a rat model of Alzheimer's disease was established through repeated intracerebroventricular administration of soluble amyloid-beta (Aß1-42) to induce neurodegeneration. The effects of tectoridin on oxidative stress markers and protein expression levels were assessed. Tectoridin treatment significantly improved cell survival and enhanced antioxidant defense by increasing the activities of superoxide dismutase (SOD) and catalase (CAT), as well as glutathione (GSH) levels in H2O2-exposed PC12 cells. Polymerase chain reaction (PCR) and western blot analyses revealed that tectoridin upregulated the expression of Bcl-2 while downregulating the expression of Bax, caspase-3, and caspase-9, suggesting a reduction in apoptotic signaling. In the in vivo rat model, tectoridin mitigated Aß1-42-induced neurodegeneration, leading to improvements in spatial learning and memory performance and reduced neurofibrillary tangles. Tectoridin treatment also improved oxidative stress parameters by increasing SOD and GSH levels while reducing malondialdehyde (MDA) content. Western blot analysis further demonstrated that tectoridin downregulated the expression of amyloid-beta (Aß1-40), amyloid precursor protein (APP), tau, Bax, caspase-3, and caspase-9, while upregulating Bcl-2. These results suggest that tectoridin exerts neuroprotective effects by modulating oxidative-antioxidant balance and inhibiting apoptotic pathways, indicating its potential as a therapeutic agent for Alzheimer's disease.