FOXO1 regulates NLRP3 inflammasome proteins in LPS-induced cardiotoxicity
AJTR Copyright © 2023..
OBJECTIVE: Forkhead box protein O1 (FOXO1) has been shown to regulate multiple proteins in various cardiovascular disease processes. However, the effect of FOXO1 on lipopolysaccharide (LPS)-induced cardiotoxicity remains unknown. The aim of this study was to explore the impact of FOXO1 on LPS-induced cardiotoxicity.
METHODS: Rat-derived H9c2 cells were subjected to LPS, and the manipulation of FOXO1 was achieved through overexpression and knockdown using the adeno-associated virus system and siRNA, respectively. Western blotting and quantitative real-time polymerase chain reaction were utilized to examine the inhibitory effect of FOXO1. Cell viability was examined utilizing Cell Counting Kit-8 assay. The changes of apoptosis were examined utilizing Annexin V-FITC/PI method. The levels of pro-inflammatory cytokines, including interleukin (IL)-1β, IL-18, and tumor necrosis factor-α in the H9c2 cells were measured using ELISA kits. Reactive oxygen species (ROS) generation was quantified using the 2'-7'dichlorofluorescin diacetate assay kit.
RESULTS: In H9c2 cells treated with LPS, FOXO1 expression was downregulated in a dose-dependent and time-dependent manner. Overexpression of FOXO1 attenuated LPS-induced apoptosis, oxidative stress injury, and cardiomyocyte inflammation, while FOXO1 inhibition aggravated these processes. Additionally, FOXO1 was found to regulate LPS-related myocardial injury by downregulating the expression of NLR family pyrin domain-containing 3 (NLRP3).
CONCLUSION: FOXO1 overexpression attenuated apoptosis, ROS generation, and inflammation, whereas FOXO1 inhibition aggravated LPS-induced cardiomyocyte injury via the NLRP3 inflammasome signaling pathway.
| Medienart: |
Artikel |
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| Erscheinungsjahr: |
2023 |
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| Erschienen: |
2023 |
| Enthalten in: |
Zur Gesamtaufnahme - volume:15 |
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| Enthalten in: |
American journal of translational research - 15(2023), 8 vom: 24., Seite 5446-5456 |
| Sprache: |
Englisch |
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| Beteiligte Personen: |
Zhao, Hui [VerfasserIn] |
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| Themen: |
Cardiomyopathy |
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| Anmerkungen: |
Date Revised 13.09.2023 published: Electronic-eCollection Citation Status PubMed-not-MEDLINE |
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| Förderinstitution / Projekttitel: |
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| PPN (Katalog-ID): |
NLM361904231 |
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| 245 | 1 | 0 | |a FOXO1 regulates NLRP3 inflammasome proteins in LPS-induced cardiotoxicity |
| 264 | 1 | |c 2023 | |
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| 500 | |a Date Revised 13.09.2023 | ||
| 500 | |a published: Electronic-eCollection | ||
| 500 | |a Citation Status PubMed-not-MEDLINE | ||
| 520 | |a AJTR Copyright © 2023. | ||
| 520 | |a OBJECTIVE: Forkhead box protein O1 (FOXO1) has been shown to regulate multiple proteins in various cardiovascular disease processes. However, the effect of FOXO1 on lipopolysaccharide (LPS)-induced cardiotoxicity remains unknown. The aim of this study was to explore the impact of FOXO1 on LPS-induced cardiotoxicity | ||
| 520 | |a METHODS: Rat-derived H9c2 cells were subjected to LPS, and the manipulation of FOXO1 was achieved through overexpression and knockdown using the adeno-associated virus system and siRNA, respectively. Western blotting and quantitative real-time polymerase chain reaction were utilized to examine the inhibitory effect of FOXO1. Cell viability was examined utilizing Cell Counting Kit-8 assay. The changes of apoptosis were examined utilizing Annexin V-FITC/PI method. The levels of pro-inflammatory cytokines, including interleukin (IL)-1β, IL-18, and tumor necrosis factor-α in the H9c2 cells were measured using ELISA kits. Reactive oxygen species (ROS) generation was quantified using the 2'-7'dichlorofluorescin diacetate assay kit | ||
| 520 | |a RESULTS: In H9c2 cells treated with LPS, FOXO1 expression was downregulated in a dose-dependent and time-dependent manner. Overexpression of FOXO1 attenuated LPS-induced apoptosis, oxidative stress injury, and cardiomyocyte inflammation, while FOXO1 inhibition aggravated these processes. Additionally, FOXO1 was found to regulate LPS-related myocardial injury by downregulating the expression of NLR family pyrin domain-containing 3 (NLRP3) | ||
| 520 | |a CONCLUSION: FOXO1 overexpression attenuated apoptosis, ROS generation, and inflammation, whereas FOXO1 inhibition aggravated LPS-induced cardiomyocyte injury via the NLRP3 inflammasome signaling pathway | ||
| 650 | 4 | |a Journal Article | |
| 650 | 4 | |a FOXO1 | |
| 650 | 4 | |a H9c2 cells | |
| 650 | 4 | |a Lipopolysaccharide | |
| 650 | 4 | |a NLRP3 | |
| 650 | 4 | |a cardiomyopathy | |
| 650 | 4 | |a inflammation | |
| 700 | 1 | |a Qin, Lingcun |e verfasserin |4 aut | |
| 700 | 1 | |a Wang, Ruyi |e verfasserin |4 aut | |
| 700 | 1 | |a Qu, Dejie |e verfasserin |4 aut | |
| 700 | 1 | |a Li, Suting |e verfasserin |4 aut | |
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