Introduction: Alzheimer's disease (AD) is the most common progressive neurodegenerative disorder characterized by the formation of beta-amyloid plaques in the brain. Loss of neurons is one of the important features of this disease, which is accompanied by memory and cognitive disorders. In this study, the effect of ghrelin on different pathways of cell death, including apoptosis, necroptosis and autophagy, was investigated in AD model rats induced by β-amyloid. Methodsand Materials: Experiments were performed on male Wistar rats with a weight range of (250±20). Animals were randomly divided into five groups including sham control, ghrelin, beta-amyloid and beta-amyloid+ghrelin. Bilateral administration of β-amyloid (5 μg/10 μl) into the hippocampus was used to induce Alzheimer's disease. Ghrelin (80 µg/kg) was injected intraperitoneally for ten consecutive days. Then the memory of rats was evaluated by the passive avoidance method and the Morris water maze. In the end, the hippocampal tissue was extracted and subjected to histopathological study. Also, the expression of Bax protein (apoptosis), Bcl-2 protein (anti-apoptotic), necroptosis proteins RIP1K and RIP3K, and autophagic marker Beclin-1 were investigated by western blot method. Results: The findings of this study showed that ghrelin improves memory impairment in Alzheimer's rats and reduces the expression of Bax (apoptotic), RIP1K and RIP3K (necrotic) proteins. It also increases the expression of Bcl-2 (anti-apoptotic) and the Bax/Bcl-2 ratio. Beclin-1 protein expression is also significantly increased by ghrelin treatment (p<0.05). Conclusion: These results show that peripheral administration of ghrelin can prevent cell death and protect neurons by inhibiting apoptosis and necroptosis and autophagy promotion. Therefore, it should play a role in preventing the progression of Alzheimer's disease.
Naseri F, Sirati-Sabet M, Shahsavari Z, Goshadrou F. Ghrelin prevents cell death of hippocampal neurons in Alzheimer's disease model rats. Koomesh 2023; 25 (5) :693-693 URL: http://koomeshjournal.semums.ac.ir/article-1-8886-en.html