Pretreatment with Liposome-Encapsulated Shrimp Shell Extract Attenuated Neuronal Damage and Death in Aβ1-42-Induced Memory Deficits in Rats

• Published in: Neurochemical research Vol. 49; no. 5; pp. 1166 - 1187
• Main Authors: Kuedo, Zulkiflee, Binlateh, Thunwa, Benjakul, Soottawat, Hutamekalin, Pilaiwanwadee
• Format: Journal Article
• Language: English
• Published: New York Springer US 01.05.2024; Springer Nature B.V
• Subjects: Alzheimer's disease; Apoptosis; Astaxanthin; Bcl-2 protein; Biochemistry; Biomarkers; Biomedical and Life Sciences; Biomedicine; Carotenoids; Caspase-3; Cell Biology; Cell death; Cytokines; Damage accumulation; Degeneration; Disease; Encapsulation; Ethanol; Glial fibrillary acidic protein; Hippocampus; Inflammation; Lipid peroxidation; Lipids; Liposomes; Memory; Microglia; Mortality; Neurochemistry; Neurodegenerative diseases; Neurology; Neuroprotection; Neurosciences; Neurotoxicity; NF-κB protein; Object recognition; Original Paper; Oxidative stress; Pattern recognition; Peptides; Peroxidation; Pretreatment; Proteins; Shrimps; Tumor necrosis factor-TNF; Tumor necrosis factor-α; β-Amyloid; Liposome; Oxidative stress; Neuroprotection; Neuroinflammation; Shrimp extract; Amyloid-beta
• ISSN: 0364-3190; 1573-6903; 1573-6903
• DOI: 10.1007/s11064-024-04103-1

The accumulation of amyloid-beta (Aβ) peptides is a crucial factor in the neuronal degeneration of Alzheimer’s disease (AD). The current study investigated the underlying neuroprotective mechanisms of shrimp shell extract (SSE) and liposome-encapsulated SSE (SSE/L) against Aβ 1-42 -induced neuronal damage and death in rats. Intracerebroventricular infusion of Aβ 1-42 effectively induced memory decline, as observed in a reduction of the rat’s discriminating ability in the novel object recognition and novel object location tasks. Oral pretreatment with 100 mg/kg of SSE demonstrated no preventive effect on the memory decline induced by Aβ 1-42 infusion. However, treatment with SSE/L 100 mg/kg BW effectively attenuated memory deficits in both behavioral assessments following two and four weeks after Aβ 1-42 infusion. Moreover, SSE/L exerted neuroprotective effects by reducing lipid peroxidation and increasing Nrf2/HO-1 expression. There was a significant decrease in Iba1 and GFAP (biomarkers of microglia and astrocyte activity, respectively), as well as a decrease in the levels of NF-κB expression and the inflammatory cytokines TNF-α and IL-6 in the cortical and hippocampal tissues. Treatment with SSE/L also reduced the pro-apoptotic proteins Bax and cleaved caspase-3 while raising the anti-apoptotic protein Bcl2. In addition, the beneficial effects of SSE/L were along with the effects of a positive control commercial astaxanthin (AST). The findings of this study indicated that SSE/L provided neuroprotective effects on Aβ 1-42 -induced AD rats by ameliorating oxidative stress, neuroinflammation and apoptotic cell death. Therefore, SSE/L might be employed to prevent and mitigate Aβ accumulation-induced neurotoxicity in AD.