Hibiscetin attenuates lipopolysaccharide-evoked memory impairment by inhibiting BDNF/caspase-3/NF-κB pathway in rodents

PeerJ. 2024 Jan 31:12:e16795. doi: 10.7717/peerj.16795. eCollection 2024.

Abstract

This study explores the neuroprotective potential of hibiscetin concerning memory deficits induced by lipopolysaccharide (LPS) injection in rats. The aim of this study is to evaluate the effect of hibiscetin against LPS-injected memory deficits in rats. The behavioral paradigms were conducted to access LPS-induced memory deficits. Various biochemical parameters such as acetyl-cholinesterase activity, choline-acetyltransferase, antioxidant (superoxide dismutase, glutathione transferase, catalase), oxidative stress (malonaldehyde), and nitric oxide levels were examined. Furthermore, neuroinflammatory parameters such as tumor necrosis factor-α, interleukin-1β (IL-1β), IL-6, and nuclear factor-kappa B expression and brain-derived neurotrophic factor as well as apoptosis marker i.e., caspase-3 were evaluated. The results demonstrated that the hibiscetin-treated group exhibited significant recovery in LPS-induced memory deficits in rats by using behavioral paradigms, biochemical parameters, antioxidant levels, oxidative stress, neuroinflammatory markers, and apoptosis markers. Recent research suggested that hibiscetin may serve as a promising neuroprotective agent in experimental animals and could offer an alternative in LPS-injected memory deficits in rodent models.

Keywords: Hibiscetin; Lipopolysaccharide; Memory; Neuroinflammatory; Oxidative stress.

MeSH terms

  • Animals
  • Antioxidants / metabolism
  • Biological Products* / pharmacology
  • Brain-Derived Neurotrophic Factor / metabolism
  • Caspase 3 / metabolism
  • Lipopolysaccharides / toxicity
  • Memory Disorders* / chemically induced
  • Memory Disorders* / drug therapy
  • NF-kappa B* / metabolism
  • Rats

Substances

  • Antioxidants
  • Brain-Derived Neurotrophic Factor
  • Caspase 3
  • Lipopolysaccharides
  • NF-kappa B
  • Biological Products

Grants and funding

This research project was supported by the Princess Nourah bint Abdulrahman University Researchers Supporting Project number (PNURSP2023R108), Princess Nourah bint Abdulrahman University, Riyadh, Saudi Arabia. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.