title: [Cinnamaldehyde attenuates pressure overload-induced cardiac fibrosis via inhibition of endothelial mesenchymal transition].
abstract: Objective:The aim of this study is to investigate the underlying mechanism of cinnamaldehyde attenuating pressure overload-induced cardiac fibrosis.Methods:The mice were randomly divided into control group, model group and treatment group by random number table and each group had 8 mice.Cardiac hypertrophy was induced by aortic banding. Heart vascular density was detected by immunohistochemical staining of CD31.The expression level of stromal cells marker α-smooth muscle actin (α-SMA) was detected by immunofluorescence staining in different groups.The expression levels of endothelial cell associated markers and stromal cell associated markers were detected by using Western blotting.The possible molecular pathway was also screened by using Western blotting. Human umbilical vein endothelial cell (HUVECs) were stimulated with TGFβ1 and cultured with 10 nmol/L cinnamomum for 24 hour to further confirm the mechanism.Results:Eight weeks after operation, the vascular density was significantly decreased in model group mice heart.The expressions of stromal cells markers were increased (α-SMA: 2.57±0.38; Vimentin: 0.58±0.02) and endothelial cell markers were reduced (CD31: 0.58±0.29; CD34: 0.62±0.21). While cinnamicaldehyde treatment significantly increased the mouse heart vascular density, increased endothelial cell markers expression (CD31: 1.51±0.11; CD34: 2.37±0.44;P<0.05), and reduced stromal cells marker expression (α-SMA: 1.22±0.14; Vimentin: 0.35±0.03;P<0.05). Further studies showed that the anti-fibrosis effect of cinnamicaldehyde was mainly through the TGFβ /smad signaling pathway.10 nmol/L cinnamomum attenuated TGFβ1 induced endothelial mesenchymal transition in HUVECs.Conclusion:Cinnamaldehyde may be able to retard the progression of cardiac fibrosis, via blocking endothelial to mesenchymal transition, which, in verse, is through regulating TGFβ /smad signaling pathway.
authors.affiliation: Department of Cardiology, Renmin Hospital of Wuhan University; Cardiovascular Research Institute, Wuhan University; Hubei Key Laboratory of Cardiology, Wuhan 430060, China.
authors.forename: Y
authors.initials: Y
authors.lastname: Xiao
authors.forename: Q Q
authors.initials: QQ
authors.lastname: Wu
authors.forename: X H
authors.initials: XH
authors.lastname: Jiang
authors.forename: Q Z
authors.initials: QZ
authors.lastname: Tang
mesh_terms: D000171:Acrolein / Q000031:analogs & derivatives* / Q000494:pharmacology; D000199:Actins; D000818:Animals; D042783:Endothelial Cells; D058750:Epithelial-Mesenchymal Transition; D005355:Fibrosis; D006321:Heart; D006801:Humans; D051379:Mice; D053773:Transforming Growth Factor beta1; D014746:Vimentin
chemical_list: C541116:ACTA2 protein, human; D000199:Actins; C508960:TGFB1 protein, human; D053773:Transforming Growth Factor beta1; D014746:Vimentin; D000171:Acrolein; C012843:cinnamaldehyde
keywords: Cinnamaldehyde; Endothelial to mesenchymal transition; Myocardial fibrosis; Pressure overload; Transforming growth factor-β1