18β-Glycyrrhetinic Acid Alleviates P. multocida-Induced Vascular Endothelial Inflammation by PARP1-Mediated NF-κB and HMGB1 Signalling Suppression in PIEC Cells
© 2023 Lu et al..
Background: At present, the treatment and prevention of Pasteurella multocida infections in pigs mainly rely on antibiotics and vaccines, but inflammatory injury cannot be eliminated. The compound 18β-glycyrrhetinic acid (GA), a pentacyclic triterpenoid extracted from Glycyrrhiza glabra L. root (liquorice) and with a chemical structure similar to that of steroidal hormones, has become a research focus because of its anti-inflammatory, antiulcer, antimicrobial, antioxidant, immunomodulatory, hepatoprotective and neuroprotective effects, but its potential for the treatment of vascular endothelial inflammatory injury by P. multocida infections has not been evaluated. This study aimed to investigate the effects and mechanisms of GA intervention in the treatment of vascular endothelial inflammatory injury by P. multocida infections.
Materials and Methods: Putative targets of GA intervention in the treatment of vascular endothelial inflammatory injury by P. multocida infections were identified using network pharmacological screening and molecular docking simulation. The cell viability of PIEC cells was investigated via the CCK-8 assay. The mechanism of GA intervention in the treatment of vascular endothelial inflammatory injury by P. multocida infections were investigated using cell transfection and western blot.
Results: Through network pharmacological screening and molecular docking simulation, this study found that PARP1 may be a core target for GA to exert anti-inflammatory effects. Mechanistically, GA alleviates P. multocida-induced vascular endothelial inflammation by PARP1-mediated NF-κB and HMGB1 signalling suppression.
Conclusion: These findings, for the first time, demonstrate the potential therapeutic relationship among GA, PARP1 and inflammatory injury, providing a candidate drug, therapeutic targets and explanation for treating vascular endothelial inflammatory injury caused by P. multocida infection.
| Medienart: |
E-Artikel |
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| Erscheinungsjahr: |
2023 |
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| Erschienen: |
2023 |
| Enthalten in: |
Zur Gesamtaufnahme - volume:16 |
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| Enthalten in: |
Infection and drug resistance - 16(2023) vom: 03., Seite 4201-4212 |
| Sprache: |
Englisch |
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| Beteiligte Personen: |
Lu, Qirong [VerfasserIn] |
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| Links: |
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| Themen: |
GA |
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| Anmerkungen: |
Date Revised 18.07.2023 published: Electronic-eCollection Citation Status PubMed-not-MEDLINE |
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| doi: |
10.2147/IDR.S413242 |
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| funding: |
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| Förderinstitution / Projekttitel: |
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| PPN (Katalog-ID): |
NLM359054269 |
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| 245 | 1 | 0 | |a 18β-Glycyrrhetinic Acid Alleviates P. multocida-Induced Vascular Endothelial Inflammation by PARP1-Mediated NF-κB and HMGB1 Signalling Suppression in PIEC Cells |
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| 500 | |a Date Revised 18.07.2023 | ||
| 500 | |a published: Electronic-eCollection | ||
| 500 | |a Citation Status PubMed-not-MEDLINE | ||
| 520 | |a © 2023 Lu et al. | ||
| 520 | |a Background: At present, the treatment and prevention of Pasteurella multocida infections in pigs mainly rely on antibiotics and vaccines, but inflammatory injury cannot be eliminated. The compound 18β-glycyrrhetinic acid (GA), a pentacyclic triterpenoid extracted from Glycyrrhiza glabra L. root (liquorice) and with a chemical structure similar to that of steroidal hormones, has become a research focus because of its anti-inflammatory, antiulcer, antimicrobial, antioxidant, immunomodulatory, hepatoprotective and neuroprotective effects, but its potential for the treatment of vascular endothelial inflammatory injury by P. multocida infections has not been evaluated. This study aimed to investigate the effects and mechanisms of GA intervention in the treatment of vascular endothelial inflammatory injury by P. multocida infections | ||
| 520 | |a Materials and Methods: Putative targets of GA intervention in the treatment of vascular endothelial inflammatory injury by P. multocida infections were identified using network pharmacological screening and molecular docking simulation. The cell viability of PIEC cells was investigated via the CCK-8 assay. The mechanism of GA intervention in the treatment of vascular endothelial inflammatory injury by P. multocida infections were investigated using cell transfection and western blot | ||
| 520 | |a Results: Through network pharmacological screening and molecular docking simulation, this study found that PARP1 may be a core target for GA to exert anti-inflammatory effects. Mechanistically, GA alleviates P. multocida-induced vascular endothelial inflammation by PARP1-mediated NF-κB and HMGB1 signalling suppression | ||
| 520 | |a Conclusion: These findings, for the first time, demonstrate the potential therapeutic relationship among GA, PARP1 and inflammatory injury, providing a candidate drug, therapeutic targets and explanation for treating vascular endothelial inflammatory injury caused by P. multocida infection | ||
| 650 | 4 | |a Journal Article | |
| 650 | 4 | |a GA | |
| 650 | 4 | |a P. multocida infection | |
| 650 | 4 | |a PARP1 | |
| 650 | 4 | |a inflammatory injury | |
| 650 | 4 | |a network pharmacology | |
| 700 | 1 | |a Han, Wantong |e verfasserin |4 aut | |
| 700 | 1 | |a Wen, Defeng |e verfasserin |4 aut | |
| 700 | 1 | |a Guo, Pu |e verfasserin |4 aut | |
| 700 | 1 | |a Liu, Yu |e verfasserin |4 aut | |
| 700 | 1 | |a Wu, Zhongyuan |e verfasserin |4 aut | |
| 700 | 1 | |a Fu, Shulin |e verfasserin |4 aut | |
| 700 | 1 | |a Ye, Chun |e verfasserin |4 aut | |
| 700 | 1 | |a Wang, Xu |e verfasserin |4 aut | |
| 700 | 1 | |a Qiu, Yinsheng |e verfasserin |4 aut | |
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