Rosinidin attenuates scopolamine-induced memory impairment in rats via modulation of oxidative stress and BDNF/NF-κB/Nrf2/ TLR4 signaling pathway
Küçük Resim Yok
Tarih
2025
Dergi Başlığı
Dergi ISSN
Cilt Başlığı
Yayıncı
Academic Press Inc Elsevier Science
Erişim Hakkı
info:eu-repo/semantics/closedAccess
Özet
Objectives: This research aimed to assess the potential outcome of rosinidin on Scopolamine (SCOP)-induced memory dysfunction in a rat model. Methods: Adult Wistar rats were grouped (n = 6) as: Groups 1 (normal control) and 2 (SCOP control) received 0.5 percent SCMC (vehicle, 3 mL) orally; Groups 3 and 4 administered rosinidin (10 and 20 mg/k g) orally. Over 14 days of therapeutic intervention, Group 1 received normal saline one h after the above-mentioned oral treatments, and the remaining group of rats were given SCOP (1 mg/kg, i.p.). Rats were tested for spontaneous movement, learning, and memory capacities. The hippocampus of rats were collected and analyzed for oxidative stress markers [reduced glutathione (GSH), superoxide dismutase (SOD), catalase, and malondialdehyde (MDA)], pro-inflammatory markers [(Interleukin-1 beta (IL-1 beta), interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-alpha)], acetylcholinesterase (AChE), choline acetyltransferase activity (ChAT), brain-derived neurotrophic factor (BDNF), nuclear factor-kappa B (NF-kappa B), and nuclear factor erythroid 2-related factor 2 (Nrf2), and D] Toll-like Receptor 4 (TLR4). Results: Rosinidin significantly improved spatial learning and memory in SCOP-treated rats, as shown by reduced escape latency in the Morris water maze (MWM) test and increased SAP% in the Y-maze test (P < 0.001). Additionally, SCOP caused memory loss in animals, decreased GSH, SOD, and catalase, altered AChE and ChAT activity, increased malondialdehyde (MDA), nitrate, TNF-alpha, NF-kappa B, IL-1 beta, IL-6, and TLR4, as well as decreased IL-6, BDNF, and Nrf2 (P < 0.001). Rosinidin administration at both doses (10 and 20 mg/kg) restored the SCOP-induced behavioral deficits and biochemical markers to normal (P < 0.001). These findings indicate its potential to reverse SCOP-induced cognitive deficits. Conclusions: The findings suggest that rosinidin effectively ameliorates SCOP-induced memory deficits in rats. This improvement may be linked to restored cholinergic function, modulated oxidative stress, and suppressed neuroinflammation.
Açıklama
Anahtar Kelimeler
Apoptosis, Cytokines, Oxidative Stress, Learning, Memory, Scopolamine
Kaynak
Learning and Motivation
WoS Q Değeri
Q3
Scopus Q Değeri
Q2
Cilt
92
