Microparticles-Mediated Vascular Inflammation and its Amelioration by Antioxidant Activity of Baicalin
Microparticles (MPs) are extracellular vesicles (0.1–1.0 μm in size), released in response to cell activation or apoptosis. Endothelial microparticles (EC-MP), vascular smooth muscle cell microparticles (VSMC-MP), and macrophage microparticles (MØ-MP) are key hallmarks of atherosclerosis progression...
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| Format: | Article |
| Language: | English |
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MDPI AG
2020-09-01
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| Series: | Antioxidants |
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| Online Access: | https://www.mdpi.com/2076-3921/9/9/890 |
| _version_ | 1797553145437487104 |
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| author | Keshav Raj Paudel Dong-Wook Kim |
| author_facet | Keshav Raj Paudel Dong-Wook Kim |
| author_sort | Keshav Raj Paudel |
| collection | DOAJ |
| description | Microparticles (MPs) are extracellular vesicles (0.1–1.0 μm in size), released in response to cell activation or apoptosis. Endothelial microparticles (EC-MP), vascular smooth muscle cell microparticles (VSMC-MP), and macrophage microparticles (MØ-MP) are key hallmarks of atherosclerosis progression. In our current study, we investigated the potent antioxidant activity of baicalin to ameliorate MP-induced vascular smooth muscle cell (VSMC) dysfunction and endothelial cell (EC) dysfunction, as well as the production of inflammatory mediators in macrophage (RAW264.7). In our study, baicalin suppressed the apoptosis, reactive oxygen species (ROS) generation, NO production, foam cell formation, protein expression of inducible nitric oxide synthase and cyclooxygenase-2 in MØ-MP-induced RAW264.7. In addition, VSMC migration induced by VSMC-MP was dose-dependently inhibited by baicalin. Likewise, baicalin inhibits metalloproteinase-9 expression and suppresses VSMC-MP-induced VSMC proliferation by down-regulation of mitogen-activated protein kinase and proliferating cell nuclear antigen protein expressions. Baicalin also inhibited ROS production and apoptosis in VSMC. In EC, the marker of endothelial dysfunction (endothelial senescence, upregulation of ICAM, and ROS production) induced by EC-MP was halted by baicalin. Our results suggested that baicalin exerts potent biological activity to restore the function of EC and VSMC altered by their corresponding microparticles and inhibits the release of inflammation markers from activated macrophages. |
| first_indexed | 2024-03-10T16:11:16Z |
| format | Article |
| id | doaj.art-09b57d8d1514415e8e3b92aad03d806d |
| institution | Directory Open Access Journal |
| issn | 2076-3921 |
| language | English |
| last_indexed | 2024-03-10T16:11:16Z |
| publishDate | 2020-09-01 |
| publisher | MDPI AG |
| record_format | Article |
| series | Antioxidants |
| spelling | doaj.art-09b57d8d1514415e8e3b92aad03d806d2023-11-20T14:24:16ZengMDPI AGAntioxidants2076-39212020-09-019989010.3390/antiox9090890Microparticles-Mediated Vascular Inflammation and its Amelioration by Antioxidant Activity of BaicalinKeshav Raj Paudel0Dong-Wook Kim1Department of Oriental Medicine Resources, Mokpo National University, Muan-gun, Jeonnam 534-729, KoreaDepartment of Oriental Medicine Resources, Mokpo National University, Muan-gun, Jeonnam 534-729, KoreaMicroparticles (MPs) are extracellular vesicles (0.1–1.0 μm in size), released in response to cell activation or apoptosis. Endothelial microparticles (EC-MP), vascular smooth muscle cell microparticles (VSMC-MP), and macrophage microparticles (MØ-MP) are key hallmarks of atherosclerosis progression. In our current study, we investigated the potent antioxidant activity of baicalin to ameliorate MP-induced vascular smooth muscle cell (VSMC) dysfunction and endothelial cell (EC) dysfunction, as well as the production of inflammatory mediators in macrophage (RAW264.7). In our study, baicalin suppressed the apoptosis, reactive oxygen species (ROS) generation, NO production, foam cell formation, protein expression of inducible nitric oxide synthase and cyclooxygenase-2 in MØ-MP-induced RAW264.7. In addition, VSMC migration induced by VSMC-MP was dose-dependently inhibited by baicalin. Likewise, baicalin inhibits metalloproteinase-9 expression and suppresses VSMC-MP-induced VSMC proliferation by down-regulation of mitogen-activated protein kinase and proliferating cell nuclear antigen protein expressions. Baicalin also inhibited ROS production and apoptosis in VSMC. In EC, the marker of endothelial dysfunction (endothelial senescence, upregulation of ICAM, and ROS production) induced by EC-MP was halted by baicalin. Our results suggested that baicalin exerts potent biological activity to restore the function of EC and VSMC altered by their corresponding microparticles and inhibits the release of inflammation markers from activated macrophages.https://www.mdpi.com/2076-3921/9/9/890microparticlesbaicalinatherosclerosismigrationproliferationinflammation |
| spellingShingle | Keshav Raj Paudel Dong-Wook Kim Microparticles-Mediated Vascular Inflammation and its Amelioration by Antioxidant Activity of Baicalin Antioxidants microparticles baicalin atherosclerosis migration proliferation inflammation |
| title | Microparticles-Mediated Vascular Inflammation and its Amelioration by Antioxidant Activity of Baicalin |
| title_full | Microparticles-Mediated Vascular Inflammation and its Amelioration by Antioxidant Activity of Baicalin |
| title_fullStr | Microparticles-Mediated Vascular Inflammation and its Amelioration by Antioxidant Activity of Baicalin |
| title_full_unstemmed | Microparticles-Mediated Vascular Inflammation and its Amelioration by Antioxidant Activity of Baicalin |
| title_short | Microparticles-Mediated Vascular Inflammation and its Amelioration by Antioxidant Activity of Baicalin |
| title_sort | microparticles mediated vascular inflammation and its amelioration by antioxidant activity of baicalin |
| topic | microparticles baicalin atherosclerosis migration proliferation inflammation |
| url | https://www.mdpi.com/2076-3921/9/9/890 |
| work_keys_str_mv | AT keshavrajpaudel microparticlesmediatedvascularinflammationanditsameliorationbyantioxidantactivityofbaicalin AT dongwookkim microparticlesmediatedvascularinflammationanditsameliorationbyantioxidantactivityofbaicalin |