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

Autor:	Gilani SJ; Department of Basic Health Sciences, Foundation Year, Princess Nourah bint Abdulrahman University, Riyadh, Saudi Arabia., Bin Jumah MN; Environment and Biomaterial Unit, Health Sciences Research Center, Princess Nourah bint Abdulrahman University, Riyadh, Saudi Arabia.; Saudi Society for Applied Science, Princess Nourah bint Abdulrahman University, Riyadh, Saudi Arabia.; Biology Department, College of Science, Princess Nourah bint Abdulrahman University, Riyadh, Riyadh, Saudi Arabia., Fatima F; Department of Pharmaceutics, College of Pharmacy, Prince Sattam Bin Abdulaziz University, Al-kharj, Saudi Arabia., Al-Abbasi FA; Department of Biochemistry, Faculty of Sciences, King Abdulaziz University, Jeddah, Saudi Arabia., Afzal M; Department of Pharmaceutical Sciences, Pharmacy Program, Batterjee Medical College, Jeddah, Saudi Arabia., Alzarea SI; Department of Pharmacology, College of Pharmacy, Jouf University, Sakaka, Saudi Arabia., Sayyed N; School of Pharmacy, Glocal University, Saharanpur, Uttar Pradesh, India., Nadeem MS; Department of Biochemistry, Faculty of Sciences, King Abdulaziz University, Jeddah, Saudi Arabia., Kazmi I; Department of Biochemistry, Faculty of Sciences, King Abdulaziz University, Jeddah, Saudi Arabia.
Jazyk:	angličtina
Zdroj:	PeerJ [PeerJ] 2024 Jan 31; Vol. 12, pp. e16795. Date of Electronic Publication: 2024 Jan 31 (Print Publication: 2024).
DOI:	10.7717/peerj.16795
Abstrakt:	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. Competing Interests: The authors declare that they have no competing interests. (© 2024 Gilani et al.)
Databáze:	MEDLINE
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