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Eplingiella fruticosa leaf essential oil complexed with β-cyclodextrin exerts a neuroprotective effect in an Alzheimer’s disease animal model induced by Streptozotocin

  • Vanessa Alexandre-Silva,
  • Beatriz Soares-Silva,
  • Gabrielle Christine Pereira,
  • Ana Claúdia Custódio-Silva,
  • Patrícia Santos Carvalhinho-Lopes,
  • Luciana Oliveira Taliano,
  • Rafael Herling Lambertucci,
  • Marcelo Duarte Cavalcante,
  • Adriano Antunes de Souza Araújo,
  • Lucindo Quintans-Júnior,
  • José Ronaldo dos Santos,
  • Alessandra Mussi Ribeiro

摘要

Alzheimer’s Disease (AD) is physiopathologically marked by an accumulation of beta-amyloid peptide (Aβ), hyperphosphorylation of tau protein, inflammation, and oxidative stress in the brain tissue. While new drugs for AD have been approved, novel treatments are still needed. Eplingiella fruticosa (EF) has demonstrated anti-inflammatory and antioxidant properties, which may be beneficial against AD. This study aimed to evaluate the effects of EF leaf essential oil complexed with β-cyclodextrin in a sporadic AD model induced by streptozotocin (STZ). Male Wistar rats (5–6 months old) received an intracerebroventricular STZ injection (3 mg/kg) or vehicle, and were orally treated with vehicle, EF (5 mg/kg), or donepezil (5 mg/kg) for 14 days. Behavioral tests included olfactory discrimination, open field, novel object recognition, sucrose preference, and spontaneous alternation. Upon completion, rats were euthanatized, and their brains were analyzed for Aβ, tau, and IL-1β via immunohistochemistry, and for oxidative stress markers. STZ-treated rats showed memory deficits and anhedonia, accompanied by increased Aβ, tau, and IL-1β immunoreactivity in the olfactory bulb, cortex, hippocampus, and increased TBARS levels in the hippocampus. On the other hand, EF treatment improved short-term and working memory (p < 0.001), and reduced depressive-like behavior (p = 0.02). Additionally, EF treatment decreased Aβ, tau, and IL-1β immunoreactivity in the olfactory bulb, hippocampus and cortex (p < 0.05), and reduced TBARS levels (p = 0.04) and total oxidant status in the hippocampus (p = 0.03), and increased total antioxidant status in the cortex (p = 0.04). These findings suggest EF has neuroprotective effects against STZ-induced damage, indicating its potential as a novel compound for AD treatment.