Sinensetin Shows Neuroprotective Effects in Aluminum Chloride-induced Alzheimer’s Disease in Rats by Regulating BDNF/PPAR-γ/p38MAPK/NF-κB Pathways

Background Alzheimer’s disease (AD) is a neurological disorder characterized by behavioral and memory deficits, along with cognitive impairments. The majority of AD cases are often present in individuals aged 60 and above. Objectives The present work was conducted to investigate the neuroprotective properties of sinensetin against aluminum chloride (AlCl3)-induced Alzheimer’s disease (AD) in rats. Materials and Methods The rats were given AlCl 3 (175 mg/kg) orally for 25 days to induce AD. Sinensetin (20 and 40 mg/kg) was orally given to the AD rats from the 25th to the 36th day. After treatments, behavioral changes were evaluated using the open-field and Morris water maze assays. The inflammatory cytokines, oxidative stress markers, acetylcholinesterase (AChE), and Aβ protein were evaluated using assay kits. The histopathology study was conducted on brain tissues. Results The findings of the behavioral assessments revealed that sinensetin improved the memory and learning capacity of the AD rats. The levels of oxidative and inflammatory markers were decreased, while antioxidant enzyme activities were elevated in the brain tissues of the sinensetin-treated AD rats. The increase in BDNF and PPAR-γ levels and the reduction in p38MAPK and NF-κB levels were noted in the sinensetin-treated AD rats. The results of histopathological analysis revealed the neuroprotective properties of sinensetin. The outcomes of this work exhibited that the sinensetin treatment of the AD rats resulted in improved memory and learning, reduced oxidative stress and inflammation, an increase in BDNF/PPAR-γ levels, and a reduction in p38MAPK/NF-κB levels in the brain tissues. Conclusion Therefore, it can be concluded that sinensetin shows promise as a therapeutic candidate to treat AD in the future.