Buyang Huanwu Decoction promotes angiogenesis in myocardial infarction through suppression of PTEN and activation of the PI3K/Akt signalling pathway

2021 ◽  
pp. 114929
Author(s):  
Xin Han ◽  
Guoyong Zhang ◽  
Guanghong Chen ◽  
Yuting Wu ◽  
Tong Xu ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Signalling Pathway ◽  
Buyang Huanwu Decoction

Rosuvastatin Attenuates Atrial Structural Remodelling in Rats with Myocardial Infarction through the Inhibition of the p38 MAPK Signalling Pathway

2015 ◽  
Vol 24 (4) ◽  
pp. 386-394 ◽  
Author(s):  
Mengzan Wang ◽  
Zhiyuan Li ◽  
Xiaohong Zhang ◽  
Xinxing Xie ◽  
Yujiao Zhang ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
P38 Mapk ◽  
Signalling Pathway ◽  
Mapk Signalling Pathway ◽  
Mapk Signalling

Abstract 117: TWEAK (Tumor Necrosis Factor-Like Weak Inducer of Apoptosis) Impedes Healing After Myocardial Infarction in Mice

2012 ◽  
Vol 111 (suppl_1) ◽  
Author(s):  
Christina Pachel ◽  
Helga Wagner ◽  
Barbara Bayer ◽  
Charlotte Dienesch ◽  
Sandra Umbenhauer ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Wound Healing ◽  
Inflammatory Response ◽  
Mrna Expression ◽  
Left Ventricular ◽  
Signalling Pathway ◽  
Border Zone ◽  
Left Ventricular Dimensions ◽  
Ifn Γ ◽  
Necrosis Factor

Introduction: TNF-related weak inducer of apoptosis (TWEAK) triggers multiple cellular responses involved in left ventricular remodelling after myocardial infarction (MI), including cytokine production, inflammation, and wound healing. We therefore hypothesized that TWEAK-Fn14 interactions improve wound healing after experimental MI. Methods/Results: We investigated the effects of exogenous TWEAK by applying (1) cross-linked TWEAK - activating the classical NF-kB-signalling pathway, (2) TWEAK and (3) human serum albumin-tagged (HSA)-TWEAK - both activating the alternative NFkB-signalling pathway, or (4) placebo after the induction of experimental MI. Treatment with TWEAK and HSA-TWEAK surprisingly resulted in significantly higher mortality after MI (survival, placebo vs. TWEAK vs. HSA-TWEAK, 66.7 (10 of 15) vs. 14.3 (4 of 26) vs. 7.1 % (1 of 19)) due to cardiac ruptures in the TWEAK- and HSA-TWEAK groups. Ruptures were not related to changes in cardiac architecture since left ventricular dimensions as measured by echocardiography were identical between HSA-TWEAK and the placebo group three days after MI, a time point where cardiac ruptures had not taken place yet. We rule out direct remodelling defects, since MMP9 mRNA expression and proteolytic activity (gelatine zymography), and collagen1α1 mRNA expression were not altered between the groups. HSA-TWEAK induced an exaggerated inflammatory response: Infiltration of neutrophils into the border zone was significantly increased as assessed by immunohistochemistry (placebo vs. HSA-TWEAK, 297.91 vs. 455.75 neutrophils/ mm2, p < 0.001). FACS-Analysis showed a significant up-regulation of CD45+-cells in the infarcted area (CD45+-cells, placebo vs. HSA-TWEAK, 4.52 vs. 9.38 %, p < 0.05). This was associated with the up-regulation of genes important for the recruitment (MIP2, MCP-1 and MCP-5) and differentiation (IL5, IL12 and IFN-γ) of leukocytes (pg/ml, placebo vs. HSA-TWEAK: p < 0.05: MIP2, 1.41 vs. 7.83; IL5, 4.13 vs. 18.75; p < 0.001: MCP-1, N.D. vs. 28.72; MCP-5, N.D. vs. 7.36; IL12, 2.07 vs. 44.51; IFN-γ, N.D. vs. 7.47). Conclusion: Treatment with TWEAK reduces survival after experimental MI due to left ventricular rupture. This may be mediated by an exaggerated inflammatory response.

Resveratrol protects against isoproterenol induced myocardial infarction in rats through VEGF-B/AMPK/eNOS/NO signalling pathway

2019 ◽  
Vol 53 (1) ◽  
pp. 82-93 ◽  
Author(s):  
Lifeng Feng ◽  
Jiling Ren ◽  
Yafei Li ◽  
Guifang Yang ◽  
Licheng Kang ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Signalling Pathway

Overexpression of microRNA ‐23a‐5p induces myocardial infarction by promoting cardiomyocyte apoptosis through inhibited of PI3K / AKT signalling pathway

2020 ◽  
Vol 38 (8) ◽  
pp. 1047-1055
Author(s):  
Jiechun Huang ◽  
Rongrong Jiang ◽  
Xianglin Chu ◽  
Fangrui Wang ◽  
Xiaotian Sun ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Signalling Pathway ◽  
Cardiomyocyte Apoptosis

scholarly journals Buyang Huanwu Decoction Exerts Cardioprotective Effects through Targeting Angiogenesis via Caveolin-1/VEGF Signaling Pathway in Mice with Acute Myocardial Infarction

2019 ◽  
Vol 2019 ◽  
pp. 1-15 ◽  
Author(s):  
Jia-Zhen Zhu ◽  
Xiao-Yi Bao ◽  
Qun Zheng ◽  
Qiang Tong ◽  
Peng-Chong Zhu ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Treated Group ◽  
Border Zone ◽  
Vascular Endothelial ◽  
Buyang Huanwu Decoction ◽  
Caveolin 1 ◽  
Vegf Signaling ◽  
Cardioprotective Effects ◽  
Endothelial Growth Factor ◽  
Vegf Signaling Pathway

Background. Acute myocardial infarction (AMI) remains a leading cause of morbidity and mortality worldwide. The idea of therapeutic angiogenesis in ischemic myocardium is a promising strategy for MI patients. Buyang Huanwu decoction (BHD), a famous Chinese herbal prescription, exerted antioxidant, antiapoptotic, and anti-inflammatory effects, which contribute to cardio-/cerebral protection. Here, we aim to investigate the effects of BHD on angiogenesis through the caveolin-1 (Cav-1)/vascular endothelial growth factor (VEGF) pathway in MI model of mice. Materials and Methods. C57BL/6 mice were randomly divided into 3 groups by the table of random number: (1) sham-operated group (sham, n=15), (2) AMI group (AMI+sham, n=20), and (3) BHD-treated group (AMI+BHD, n=20). 2,3,5-Triphenyltetrazolium chloride solution stain was used to determine myocardial infarct size. Myocardial histopathology was tested using Masson staining and hematoxylin-eosin staining. CD31 immunofluorescence staining was used to analyze the angiogenesis in the infarction border zone. Western blot analysis, immunofluorescence staining, and/or real-time quantitative reverse transcription polymerase chain reaction was applied to test the expression of Cav-1, VEGF, vascular endothelial growth factor receptor 2 (VEGFR2), and/or phosphorylated extracellular signal-regulated kinase (p-ERK). All statistical analyses were performed using the SPSS 20.0 software and GraphPad Prism 6.05. Values of P<0.05 were considered as statistically significant. Results and Conclusion. Compared with the AMI group, the BHD-treated group showed a significant improvement in the heart weight/body weight ratio, echocardiography images, cardiac function, infarct size, Mason staining of the collagen deposition area, and density of microvessel in the infarction border zone (P<0.05). Compared with the AMI group, BHD promoted the expression of Cav-1, VEGF, VEGFR2, and p-ERK in the infarction border zone after AMI. BHD could exert cardioprotective effects on the mouse model with AMI through targeting angiogenesis via Cav-1/VEGF signaling pathway.

An electron microscopic study of the intra-myocardial lesions in cases of acute myocardial infarction

1978 ◽  
Vol 36 (2) ◽  
pp. 484-485
Author(s):  
Masahiro Ono ◽  
Kaoru Aihara ◽  
Gompachi Yajima
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Coronary Vessels ◽  
Vascular Wall ◽  
Vascular Changes ◽  
Electron Microscopic ◽  
Main Trunk ◽  
Mechanical Destruction ◽  
Transmission Electron ◽  
Myocardial Lesions

The pathogenesis of the arteriosclerosis in the acute myocardial infarction is the matter of the extensive survey with the transmission electron microscopy in experimental and clinical materials. In the previous communication,the authors have clarified that the two types of the coronary vascular changes could exist. The first category is the case in which we had failed to observe no occlusive changes of the coronary vessels which eventually form the myocardial infarction. The next category is the case in which occlusive -thrombotic changes are observed in which the myocardial infarction will be taken placed as the final event. The authors incline to designate the former category as the non-occlusive-non thrombotic lesions. The most important findings in both cases are the “mechanical destruction of the vascular wall and imbibition of the serous component” which are most frequently observed at the proximal portion of the coronary main trunk.

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