Article ; Online: Emodin Blocks mPTP Opening and Improves LPS-Induced HMEC-1 Cell Injury by Upregulation of ATP5A1.
2024 Volume 21, Issue 5, Page(s) e202301916
Abstract: Background: Emodin has been shown to exert anti-inflammatory and cytoprotective effects. Our study aimed to identify a novel anti-inflammatory mechanism of emodin.: Methods: An LPS-induced model of microvascular endothelial cell (HMEC-1) injury was ... ...
Abstract | Background: Emodin has been shown to exert anti-inflammatory and cytoprotective effects. Our study aimed to identify a novel anti-inflammatory mechanism of emodin. Methods: An LPS-induced model of microvascular endothelial cell (HMEC-1) injury was constructed. Cell proliferation was examined using a CCK-8 assay. The effects of emodin on reactive oxygen species (ROS), cell migration, the mitochondrial membrane potential (MMP), and the opening of the mitochondrial permeability transition pore (mPTP) were evaluated. Actin-Tracker Green was used to examine the relationship between cell microfilament reconstruction and ATP5A1 expression. The effects of emodin on the expression of ATP5A1, NALP3, and TNF-α were determined. After treatment with emodin, ATP5A1 and inflammatory factors (TNF-α, IL-1, IL-6, IL-13 and IL-18) were examined by Western blotting. Results: Emodin significantly increased HMEC-1 cell proliferation and migration, inhibited the production of ROS, increased the mitochondrial membrane potential, and blocked the opening of the mPTP. Moreover, emodin could increase ATP5A1 expression, ameliorate cell microfilament remodeling, and decrease the expression of inflammatory factors. In addition, when ATP5A1 was overexpressed, the regulatory effect of emodin on inflammatory factors was not significant. Conclusion: Our findings suggest that emodin can protect HMEC-1 cells against inflammatory injury. This process is modulated by the expression of ATP5A1. |
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MeSH term(s) | Emodin/pharmacology ; Emodin/chemistry ; Lipopolysaccharides/pharmacology ; Humans ; Cell Proliferation/drug effects ; Up-Regulation/drug effects ; Membrane Potential, Mitochondrial/drug effects ; Cell Movement/drug effects ; Reactive Oxygen Species/metabolism ; Mitochondrial Proton-Translocating ATPases/metabolism ; Mitochondrial Permeability Transition Pore/metabolism ; Mitochondrial Membrane Transport Proteins/metabolism ; Mitochondrial Membrane Transport Proteins/drug effects ; Endothelial Cells/drug effects ; Endothelial Cells/metabolism ; Cell Line ; Anti-Inflammatory Agents/pharmacology ; Anti-Inflammatory Agents/chemistry |
Language | English |
Publishing date | 2024-04-17 |
Publishing country | Switzerland |
Document type | Journal Article |
ZDB-ID | 2139001-0 |
ISSN | 1612-1880 ; 1612-1872 |
ISSN (online) | 1612-1880 |
ISSN | 1612-1872 |
DOI | 10.1002/cbdv.202301916 |
Database | MEDical Literature Analysis and Retrieval System OnLINE |
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