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.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117 Front+Physiol
2018 ; 9
(ä): 102
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Neferine Protects Endothelial Glycocalyx via Mitochondrial ROS in
Lipopolysaccharide-Induced Acute Respiratory Distress Syndrome
#MMPMID29520236
Liu XY
; Xu HX
; Li JK
; Zhang D
; Ma XH
; Huang LN
; Lü JH
; Wang XZ
Front Physiol
2018[]; 9
(ä): 102
PMID29520236
show ga
Damage to the endothelial glycocalyx is a critical factor in increased pulmonary
vascular permeability, which is the basic pathological feature of acute
respiratory distress syndrome (ARDS). Neferine (Nef), a bisbenzylisoquinoline
alkaloid isolated from green seed embryos of Nelumbo nucifera Gaertn, has
extensive pharmacological activity. In this study, we showed that Nef reduced
lung-capillary permeability, down-regulated the production of cytokines (IL-1?,
IL-6, TNF-?, and IL-10) and inhibited the activation of the NF-?B signaling
pathway in mice with lipopolysaccharide (LPS)-induced ARDS. Further analysis
indicated that Nef provided protection against endothelial glycocalyx degradation
in LPS-induced ARDS mice (in vivo) and in LPS-stimulated human umbilical vein
endothelial cells (in vitro). The glycocalyx-protective effect of Nef may be
initiated by suppressing the production of mitochondrial ROS (mtROS) and
decreasing oxidative damage. Nef was also found to promote glycocalyx restoration
by accelerating the removal of mtROS in endothelial cells in LPS-induced ARDS.
These results suggested the potential of Nef as a therapeutic agent for ARDS
associated with Gram-negative bacterial infections and elucidated the mechanisms
underlying the protection and restoration of the endothelial glycocalyx.