当前位置： SCI文献检索 > JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY期刊下所有文献 > Cinnamaldehyde ameliorates LPS-induced cardiac dysfunction via TLR4-NOX4 pathway: The regulation of autophagy and ROS production.

Cinnamaldehyde ameliorates LPS-induced cardiac dysfunction via TLR4-NOX4 pathway: The regulation of autophagy and ROS production.

Abstract：

:Cinnamaldehyde (CA), a major bioactive compound extracted from the essential oil of Cortex Cinnamomi, exhibits anti-inflammatory activity on endotoxemia. Accumulating evidence indicates reactive oxygen species (ROS) and autophagy play a vital role in the cardiac dysfunction during endotoxemia. The aim of this study was to unveil the mechanism of CA on ROS production and autophagy during endotoxemia. Male Sprague-Dawley rats were stimulated by LPS (20mg/kg i.v.) with or without treatment of CA. Cardiac function and histopathological staining were preformed 4h after LPS stimulation. The levels of TNF-α, IL-1β and IL-6 were detected by ELISA. The expression of p-JNK, p-ERK, p-p38, TLR4, NOX4, NOX2, ATG5 and LC3 proteins were determined by Western blot. The results showed that CA inhibited cardiac dysfunction, inflammatory infiltration and the levels of TNF-α, IL-1β and IL-6 in LPS stimulated rats by blocking the TLR4, NOX4, MAPK and autophagy signalings. In order to obtain further confirmation of the mechanism of CA on endotoxemia in vitro, a limited time-course study was firstly performed by Western blot. TLR4, NOX4 and LC3 were significantly increased after 4h LPS stimulation. CA reversed the intracellular ROS production and MAPK signaling activation induced by LPS. Electron microscopy, mRFP-GFP-LC3 transfection and western blot results revealed autophagic flux were attenuated after CA treatment. The siRNA and molecular docking results suggest that CA can suppress both TLR4 and NOX4 during endotoxemia. Our data revealed that CA ameliorated LPS-induced cardiac dysfunction by inhibiting ROS production and autophagy through TLR4-NOX4 pathway.

journal_name

J Mol Cell Cardiol

journal_title

Journal of molecular and cellular cardiology

authors

Zhao H,Zhang M,Zhou F,Cao W,Bi L,Xie Y,Yang Q,Wang S

doi

10.1016/j.yjmcc.2016.10.017

subject

Has Abstract

pub_date

2016-12-01 00:00:00

pages

11-24

eissn

0022-2828

issn

1095-8584

pii

S0022-2828(16)30391-1

journal_volume

101

pub_type

杂志文章

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