The Marine Compound Isaridin E Ameliorates Lipopolysaccharide-Induced Vascular Endothelial Inflammation via the Downregulation of the TLR4/NF-κB Signaling Pathway

Isaridin E, a cyclodepsipeptide derived from the marine fungus <i>Beauveria felina</i> (SYSU-MS7908), has been demonstrated to possess multiple biological properties. In this study, we employed both lipopolysaccharide (LPS)-stimulated human umbilical vein endothelial cells (HUVECs) and a...

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Main Authors: Jing Liu, Xin Zeng, Yu-Quan Lin, Yu-Sheng Peng, Lan Liu, Sen-Hua Chen, Yan-Hua Du
Format: Article
Language:English
Published: MDPI AG 2025-03-01
Series:Marine Drugs
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Online Access:https://www.mdpi.com/1660-3397/23/4/145
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author Jing Liu
Xin Zeng
Yu-Quan Lin
Yu-Sheng Peng
Lan Liu
Sen-Hua Chen
Yan-Hua Du
author_facet Jing Liu
Xin Zeng
Yu-Quan Lin
Yu-Sheng Peng
Lan Liu
Sen-Hua Chen
Yan-Hua Du
author_sort Jing Liu
collection DOAJ
description Isaridin E, a cyclodepsipeptide derived from the marine fungus <i>Beauveria felina</i> (SYSU-MS7908), has been demonstrated to possess multiple biological properties. In this study, we employed both lipopolysaccharide (LPS)-stimulated human umbilical vein endothelial cells (HUVECs) and a LPS-induced murine endotoxemia model to investigate its anti-inflammatory effects. Our results revealed that isaridin E suppressed the expression of pro-inflammatory cytokines and adhesion molecules in a concentration dependent manner, while also reducing monocyte adhesion to endothelial cells. Furthermore, this compound attenuated vascular hyperpermeability and inflammatory cell infiltration in the lungs, as well as preserving the integrity of the aortic and pulmonary tissues. At the molecular level, isaridin E was found to downregulate TLR4 expression, increase IκBα levels, and inhibit the LPS-induced phosphorylation and nuclear translocation of NF-κB p65. In conclusion, our findings indicate that isaridin E exerts robust anti-inflammatory effects in LPS-induced endotoxemia through the suppression of the TLR4/NF-κB signaling axis, positioning it as a promising therapeutic candidate for vascular inflammatory disorders.
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publishDate 2025-03-01
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series Marine Drugs
spelling doaj-art-61ca6862d34e45f98d7e0ba5afaf9f622025-08-20T02:18:19ZengMDPI AGMarine Drugs1660-33972025-03-0123414510.3390/md23040145The Marine Compound Isaridin E Ameliorates Lipopolysaccharide-Induced Vascular Endothelial Inflammation via the Downregulation of the TLR4/NF-κB Signaling PathwayJing Liu0Xin Zeng1Yu-Quan Lin2Yu-Sheng Peng3Lan Liu4Sen-Hua Chen5Yan-Hua Du6Department of Pharmacology, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou 510080, ChinaDepartment of Pharmacology, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou 510080, ChinaDepartment of Pharmacology, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou 510080, ChinaDepartment of Pharmacology, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou 510080, ChinaSchool of Marine Sciences, Sun Yat-sen University, Guangzhou 510275, ChinaSchool of Marine Sciences, Sun Yat-sen University, Guangzhou 510275, ChinaDepartment of Pharmacology, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou 510080, ChinaIsaridin E, a cyclodepsipeptide derived from the marine fungus <i>Beauveria felina</i> (SYSU-MS7908), has been demonstrated to possess multiple biological properties. In this study, we employed both lipopolysaccharide (LPS)-stimulated human umbilical vein endothelial cells (HUVECs) and a LPS-induced murine endotoxemia model to investigate its anti-inflammatory effects. Our results revealed that isaridin E suppressed the expression of pro-inflammatory cytokines and adhesion molecules in a concentration dependent manner, while also reducing monocyte adhesion to endothelial cells. Furthermore, this compound attenuated vascular hyperpermeability and inflammatory cell infiltration in the lungs, as well as preserving the integrity of the aortic and pulmonary tissues. At the molecular level, isaridin E was found to downregulate TLR4 expression, increase IκBα levels, and inhibit the LPS-induced phosphorylation and nuclear translocation of NF-κB p65. In conclusion, our findings indicate that isaridin E exerts robust anti-inflammatory effects in LPS-induced endotoxemia through the suppression of the TLR4/NF-κB signaling axis, positioning it as a promising therapeutic candidate for vascular inflammatory disorders.https://www.mdpi.com/1660-3397/23/4/145isaridin Emarine natural productsendothelial inflammationTLR4NF-κB
spellingShingle Jing Liu
Xin Zeng
Yu-Quan Lin
Yu-Sheng Peng
Lan Liu
Sen-Hua Chen
Yan-Hua Du
The Marine Compound Isaridin E Ameliorates Lipopolysaccharide-Induced Vascular Endothelial Inflammation via the Downregulation of the TLR4/NF-κB Signaling Pathway
Marine Drugs
isaridin E
marine natural products
endothelial inflammation
TLR4
NF-κB
title The Marine Compound Isaridin E Ameliorates Lipopolysaccharide-Induced Vascular Endothelial Inflammation via the Downregulation of the TLR4/NF-κB Signaling Pathway
title_full The Marine Compound Isaridin E Ameliorates Lipopolysaccharide-Induced Vascular Endothelial Inflammation via the Downregulation of the TLR4/NF-κB Signaling Pathway
title_fullStr The Marine Compound Isaridin E Ameliorates Lipopolysaccharide-Induced Vascular Endothelial Inflammation via the Downregulation of the TLR4/NF-κB Signaling Pathway
title_full_unstemmed The Marine Compound Isaridin E Ameliorates Lipopolysaccharide-Induced Vascular Endothelial Inflammation via the Downregulation of the TLR4/NF-κB Signaling Pathway
title_short The Marine Compound Isaridin E Ameliorates Lipopolysaccharide-Induced Vascular Endothelial Inflammation via the Downregulation of the TLR4/NF-κB Signaling Pathway
title_sort marine compound isaridin e ameliorates lipopolysaccharide induced vascular endothelial inflammation via the downregulation of the tlr4 nf κb signaling pathway
topic isaridin E
marine natural products
endothelial inflammation
TLR4
NF-κB
url https://www.mdpi.com/1660-3397/23/4/145
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