Protective Role Of Apigenin Against Aβ25-35 Toxicity Via Inhibition Of Mitochondrial Cytochrome C Release

Abstract

Cognitive dysfunction is the most common problem of patients with Alzheimer Disease (AD). The pathological mechanism of cognitive impairment in AD may contribute to neuronal loss, synaptic dysfunction, and alteration in neurotransmitters receptors. Mitochondrial synapses dysfunction due to the accumulation of Amyloid Beta (Aβ) is one of the earliest pathological features of AD. The flavone apigenin has been reported to play some protective roles in AD through the anti-oxidative and anti-inflammatory properties. This study aimed at investigating the effects of apigenin on spatial working memory and neural protection by restoring mitochondrial dysfunction and inhibition of caspase 9. Methods: Intracerebroventricular (ICV) microinjection of Aβ 25-35 was used for AD modeling. Working memory was assessed 21 days later using the Y maze test. Neuronal loss was detected in the hilar area of the hippocampus using Nissl and Fluoro-jade B staining, whereas immunohistochemistry was used to illustrate cytochrome c positive cells and caspase 9. Results: The results revealed that apigenin significantly ameliorated spatial working memory. It also significantly reduced the number of degenerative neurons in the hilus area. Apigenin almost completely blocked the release of cytochrome c and caspase 9 in hilus. Conclusion: Apigenin may improve the spatial working memory deficits and neuronal degeneration through the amelioration of the mitochondrial dysfunction.

Apigenin Ameliorates Scopolamine-Induced Cognitive Dysfunction and Neuronal Damage in Mice

“…As shown in Figure 3D, the time to reach the exposed platform was not significantly different among all the groups, suggesting that the effect of apigenin on cognitive improvement was not related to visual or swimming abilities, but learning and memory abilities. Similarly, previous studies also demonstrated that apigenin improved spatial working memory function in behavioral tasks such as the Ymaze and Morris water maze tests in Aβ 25-35 -or isoflurane-induced in vivo model [33,34]. These findings demonstrated that apigenin could ameliorate cognitive dysfunction induced by scopolamine.…”

Ameliorative Effects of Rhoifolin in Scopolamine-Induced Amnesic Zebrafish (Danio rerio) Model

“…Hashemi et al [ 32 ] demonstrated that apigenin might have a protective effect on memory deficiency in specific behavioral tasks such as the Y-maze and Morris water maze, caused by kainite through anticonvulsant and anti-apoptosis activity. In another study, Nikbakht et al [ 33 ] reported that apigenin significantly ameliorated spatial working memory impairment induced by Aβ25-35 in the Y-maze test. Chen et al [ 34 ] identified apigenin as a potent suppressor of isoflurane exposure-induced learning and memory dysfunction in rats when tested within the Morris water maze test.…”

Unearthing of Key Genes Driving the Pathogenesis of Alzheimer’s Disease via Bioinformatics

“…The main symptom of patients with AD is cognitive dysfunction. The cognitive impairment in AD may cause synaptic dysfunction, neuronal loss, and modification of neurotransmitter receptors (Nikbakht et al, 2019). Previous work reported that abnormal synaptic and dysfunction of network synchronous activity might contribute to hippocampal-dependent memory deficits in early AD models (Mayordomo-Cava et al, 2020).…”