Carbon Nanodots Inhibit Tumor Necrosis Factor-α-Induced Endothelial Inflammation through Scavenging Hydrogen Peroxide and Upregulating Antioxidant Gene Expression in EA.hy926 Endothelial Cells
Carbon nanodots (CNDs) are a new type of nanomaterial with a size of less than 10 nanometers and excellent biocompatibility, widely used in fields such as biological imaging, transmission, diagnosis, and drug delivery. However, its potential and mechanism to mediate endothelial inflammation have yet...
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| Format: | Article |
| Language: | English |
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MDPI AG
2024-02-01
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| Series: | Antioxidants |
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| Online Access: | https://www.mdpi.com/2076-3921/13/2/224 |
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| author | Jessica Chavez Ajmal Khan Kenna R. Watson Safeera Khan Yaru Si Alexandra Y. Deng Grant Koher Mmesoma S. Anike Xianwen Yi Zhenquan Jia |
| author_facet | Jessica Chavez Ajmal Khan Kenna R. Watson Safeera Khan Yaru Si Alexandra Y. Deng Grant Koher Mmesoma S. Anike Xianwen Yi Zhenquan Jia |
| author_sort | Jessica Chavez |
| collection | DOAJ |
| description | Carbon nanodots (CNDs) are a new type of nanomaterial with a size of less than 10 nanometers and excellent biocompatibility, widely used in fields such as biological imaging, transmission, diagnosis, and drug delivery. However, its potential and mechanism to mediate endothelial inflammation have yet to be explored. Here, we report that the uptake of CNDs by EA.hy926 endothelial cells is both time and dose dependent. The concentration of CNDs used in this experiment was found to not affect cell viability. TNF-α is a known biomarker of vascular inflammation. Cells treated with CNDs for 24 h significantly inhibited TNF-α (0.5 ng/mL)-induced expression of intracellular adhesion molecule 1 (<i>ICAM-1</i>) and interleukin 8 (<i>IL-8</i>). <i>ICAM-1</i> and <i>IL-8</i> are two key molecules responsible for the activation and the firm adhesion of monocytes to activated endothelial cells for the initiation of atherosclerosis. ROS, such as hydrogen peroxide, play an important role in TNF-α-induced inflammation. Interestingly, we found that CNDs effectively scavenged H<sub>2</sub>O<sub>2</sub> in a dose-dependent manner. CNDs treatment also increased the activity of the antioxidant enzyme NQO1 in EA.hy926 endothelial cells indicating the antioxidant properties of CNDs. These results suggest that the anti-inflammatory effects of CNDs may be due to the direct H<sub>2</sub>O<sub>2</sub> scavenging properties of CNDs and the indirect upregulation of antioxidant enzyme NQO1 activity in endothelial cells. In conclusion, CND can inhibit TNF-α-induced endothelial inflammation, possibly due to its direct scavenging of H<sub>2</sub>O<sub>2</sub> and the indirect upregulation of antioxidant enzyme NQO1 activity in endothelial cells. |
| first_indexed | 2024-03-07T22:44:57Z |
| format | Article |
| id | doaj.art-cdeb0d5da5b64d958bd96a9906429391 |
| institution | Directory Open Access Journal |
| issn | 2076-3921 |
| language | English |
| last_indexed | 2024-03-07T22:44:57Z |
| publishDate | 2024-02-01 |
| publisher | MDPI AG |
| record_format | Article |
| series | Antioxidants |
| spelling | doaj.art-cdeb0d5da5b64d958bd96a99064293912024-02-23T15:05:33ZengMDPI AGAntioxidants2076-39212024-02-0113222410.3390/antiox13020224Carbon Nanodots Inhibit Tumor Necrosis Factor-α-Induced Endothelial Inflammation through Scavenging Hydrogen Peroxide and Upregulating Antioxidant Gene Expression in EA.hy926 Endothelial CellsJessica Chavez0Ajmal Khan1Kenna R. Watson2Safeera Khan3Yaru Si4Alexandra Y. Deng5Grant Koher6Mmesoma S. Anike7Xianwen Yi8Zhenquan Jia9Department of Biology, University of North Carolina at Greensboro, Greensboro, NC 27412, USADepartment of Biology, University of North Carolina at Greensboro, Greensboro, NC 27412, USADepartment of Biology, University of North Carolina at Greensboro, Greensboro, NC 27412, USADepartment of Biology, University of North Carolina at Greensboro, Greensboro, NC 27412, USADepartment of Biology, University of North Carolina at Greensboro, Greensboro, NC 27412, USAChapel Hill High School, Chapel Hill, NC 27516, USADepartment of Biology, University of North Carolina at Greensboro, Greensboro, NC 27412, USADepartment of Biology, University of North Carolina at Greensboro, Greensboro, NC 27412, USADepartment of Surgery, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USADepartment of Biology, University of North Carolina at Greensboro, Greensboro, NC 27412, USACarbon nanodots (CNDs) are a new type of nanomaterial with a size of less than 10 nanometers and excellent biocompatibility, widely used in fields such as biological imaging, transmission, diagnosis, and drug delivery. However, its potential and mechanism to mediate endothelial inflammation have yet to be explored. Here, we report that the uptake of CNDs by EA.hy926 endothelial cells is both time and dose dependent. The concentration of CNDs used in this experiment was found to not affect cell viability. TNF-α is a known biomarker of vascular inflammation. Cells treated with CNDs for 24 h significantly inhibited TNF-α (0.5 ng/mL)-induced expression of intracellular adhesion molecule 1 (<i>ICAM-1</i>) and interleukin 8 (<i>IL-8</i>). <i>ICAM-1</i> and <i>IL-8</i> are two key molecules responsible for the activation and the firm adhesion of monocytes to activated endothelial cells for the initiation of atherosclerosis. ROS, such as hydrogen peroxide, play an important role in TNF-α-induced inflammation. Interestingly, we found that CNDs effectively scavenged H<sub>2</sub>O<sub>2</sub> in a dose-dependent manner. CNDs treatment also increased the activity of the antioxidant enzyme NQO1 in EA.hy926 endothelial cells indicating the antioxidant properties of CNDs. These results suggest that the anti-inflammatory effects of CNDs may be due to the direct H<sub>2</sub>O<sub>2</sub> scavenging properties of CNDs and the indirect upregulation of antioxidant enzyme NQO1 activity in endothelial cells. In conclusion, CND can inhibit TNF-α-induced endothelial inflammation, possibly due to its direct scavenging of H<sub>2</sub>O<sub>2</sub> and the indirect upregulation of antioxidant enzyme NQO1 activity in endothelial cells.https://www.mdpi.com/2076-3921/13/2/224carbon nanodotstumor necrosis factor-alphavascular inflammationROS |
| spellingShingle | Jessica Chavez Ajmal Khan Kenna R. Watson Safeera Khan Yaru Si Alexandra Y. Deng Grant Koher Mmesoma S. Anike Xianwen Yi Zhenquan Jia Carbon Nanodots Inhibit Tumor Necrosis Factor-α-Induced Endothelial Inflammation through Scavenging Hydrogen Peroxide and Upregulating Antioxidant Gene Expression in EA.hy926 Endothelial Cells Antioxidants carbon nanodots tumor necrosis factor-alpha vascular inflammation ROS |
| title | Carbon Nanodots Inhibit Tumor Necrosis Factor-α-Induced Endothelial Inflammation through Scavenging Hydrogen Peroxide and Upregulating Antioxidant Gene Expression in EA.hy926 Endothelial Cells |
| title_full | Carbon Nanodots Inhibit Tumor Necrosis Factor-α-Induced Endothelial Inflammation through Scavenging Hydrogen Peroxide and Upregulating Antioxidant Gene Expression in EA.hy926 Endothelial Cells |
| title_fullStr | Carbon Nanodots Inhibit Tumor Necrosis Factor-α-Induced Endothelial Inflammation through Scavenging Hydrogen Peroxide and Upregulating Antioxidant Gene Expression in EA.hy926 Endothelial Cells |
| title_full_unstemmed | Carbon Nanodots Inhibit Tumor Necrosis Factor-α-Induced Endothelial Inflammation through Scavenging Hydrogen Peroxide and Upregulating Antioxidant Gene Expression in EA.hy926 Endothelial Cells |
| title_short | Carbon Nanodots Inhibit Tumor Necrosis Factor-α-Induced Endothelial Inflammation through Scavenging Hydrogen Peroxide and Upregulating Antioxidant Gene Expression in EA.hy926 Endothelial Cells |
| title_sort | carbon nanodots inhibit tumor necrosis factor α induced endothelial inflammation through scavenging hydrogen peroxide and upregulating antioxidant gene expression in ea hy926 endothelial cells |
| topic | carbon nanodots tumor necrosis factor-alpha vascular inflammation ROS |
| url | https://www.mdpi.com/2076-3921/13/2/224 |
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