Aβ<sub>1-40</sub>-Induced Platelet Adhesion Is Ameliorated by Rosmarinic Acid through Inhibition of NADPH Oxidase/PKC-δ/Integrin α<sub>IIb</sub>β<sub>3</sub> Signaling
In platelets, oxidative stress reportedly increases platelet adhesion to vessels, thus promoting the vascular pathology of various neurodegenerative diseases, including Alzheimer's disease (AD). Recently, it has been shown that β-amyloid (Aβ) can increase oxidative stress in platelets; however,...
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Main Authors: | , , |
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Format: | Book |
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MDPI AG,
2021-10-01T00:00:00Z.
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Summary: | In platelets, oxidative stress reportedly increases platelet adhesion to vessels, thus promoting the vascular pathology of various neurodegenerative diseases, including Alzheimer's disease (AD). Recently, it has been shown that β-amyloid (Aβ) can increase oxidative stress in platelets; however, the underlying mechanism remains elusive. In the present study, we aimed to elucidate the signaling pathway of platelet adhesion induced by Aβ<sub>1-40</sub>, the major form of circulating Aβ, through Western blotting, immunofluorescence confocal microscopy, and fluorescence-activated cell sorting analysis. Additionally, we examined whether rosmarinic acid (RA), a natural polyphenol antioxidant, can modulate these processes. Our results show that Aβ<sub>1-40</sub>-induced platelet adhesion is mediated through NADPH oxidase/ROS/PKC-δ/integrin α<sub>IIb</sub>β<sub>3</sub> signaling, and these signaling pathways are significantly inhibited by RA. Collectively, these results suggest that RA may have beneficial effects on platelet-associated vascular pathology in AD. |
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Item Description: | 10.3390/antiox10111671 2076-3921 |