scholarly journals Yiqihuoxuejiedu Formula Restrains Vascular Remodeling by Reducing the Inflammation Reaction and Cx43 Expression in the Adventitia after Balloon Injury

2015 ◽  
Vol 2015 ◽  
pp. 1-10 ◽  
Author(s):  
Hong Chang ◽  
Huan Lei ◽  
Yizhou Zhao ◽  
Ruixue Yang ◽  
Aiming Wu ◽  
...  
Keyword(s):  
Inflammatory Response ◽  
Vascular Remodeling ◽  
Cx43 Expression ◽  
Vessel Injury ◽  
Injury Model ◽  
Adventitial Fibroblasts ◽  
Intimal Injury ◽  
New Ideas ◽  
Supplementing Qi ◽  
Inflammation Reaction

Vascular remodeling is closely related to hypertension, atherosclerosis, and restenosis after PCI. Considerable evidence indicates that the activation and proliferation of adventitial fibroblasts play key roles in vessel injury. The inflammatory response and high expression of connexins contribute to adventitial remodeling. Therefore, reducing inflammation reaction and connexins expression in adventitia may become a new target to prevent vascular remodeling. Yiqihuoxuejiedu formula, composed of TCM therapeutic principle of supplementing qi, activating blood and detoxification, can inhibit restenosis after intimal injury. To further investigate the effect of Yiqihuoxuejiedu formula on inflammation and connexins, we established a carotid artery injury model. In model rats, hyperplasia in the intima was mild but obvious in the adventitia; CRP heightened; expressions of MCP-1, CD68, and Cx43 increased. Yiqihuoxuejiedu formula relieved intimal hyperplasia and adventitial area, obviously diminished the expressions of CD68 and Cx43 in the adventitia, and reduced CRP but did not lower MCP-1. These results indicated that Yiqihuoxuejiedu formula inhibited vascular remodeling especially adventitial hyperplasia by reducing the inflammation reaction including lowering macrophages infiltration and systemic nonspecific inflammatory response and also restraining gap junction connexins leading to less communication among cells. This study provides new ideas and methods for the prevention and treatment of vascular remodeling.

scholarly journals An Ex Vivo Vessel Injury Model to Study Remodeling

2018 ◽  
Vol 27 (9) ◽  
pp. 1375-1389 ◽  
Author(s):  
Mehmet H. Kural ◽  
Guohao Dai ◽  
Laura E. Niklason ◽  
Liqiong Gui
Keyword(s):  
Shear Stress ◽  
Animal Models ◽  
Intimal Hyperplasia ◽  
Vascular Remodeling ◽  
Ex Vivo ◽  
Vessel Injury ◽  
Injury Model ◽  
Human Arteries

Objective: Invasive coronary interventions can fail due to intimal hyperplasia and restenosis. Endothelial cell (EC) seeding to the vessel lumen, accelerating re-endothelialization, or local release of mTOR pathway inhibitors have helped reduce intimal hyperplasia after vessel injury. While animal models are powerful tools, they are complex and expensive, and not always reflective of human physiology. Therefore, we developed an in vitro 3D vascular model validating previous in vivo animal models and utilizing isolated human arteries to study vascular remodeling after injury. Approach: We utilized a bioreactor that enables the control of intramural pressure and shear stress in vessel conduits to investigate the vascular response in both rat and human arteries to intraluminal injury. Results: Culturing rat aorta segments in vitro, we show that vigorous removal of luminal ECs results in vessel injury, causing medial proliferation by Day-4 and neointima formation, with the observation of SCA1+ cells (stem cell antigen-1) in the intima by Day-7, in the absence of flow. Conversely, when endothelial-denuded rat aortae and human umbilical arteries were subjected to arterial shear stress, pre-seeding with human umbilical ECs decreased the number and proliferation of smooth muscle cell (SMC) significantly in the media of both rat and human vessels. Conclusion: Our bioreactor system provides a novel platform for correlating ex vivo findings with vascular outcomes in vivo. The present in vitro human arterial injury model can be helpful in the study of EC-SMC interactions and vascular remodeling, by allowing for the separation of mechanical, cellular, and soluble factors.

scholarly journals Transplantation of bone marrow-derived mononuclear cells can improve the survival rate and suppress the inflammatory response in a rat crush injury model

Critical Care ◽  
2014 ◽  
Vol 18 (Suppl 1) ◽  
pp. P65
Author(s):  
J Nakagawa ◽  
N Matsumoto ◽  
K Yamakawa ◽  
T Yamada ◽  
H Matsumoto ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Survival Rate ◽  
Inflammatory Response ◽  
Mononuclear Cells ◽  
Crush Injury ◽  
Injury Model

Efficacy and hemodynamic response of pleural carbon dioxide insufflation during thoracoscopic surgery in a swine vessel injury model

Surgery Today ◽  
2016 ◽  
Vol 46 (12) ◽  
pp. 1464-1470 ◽  
Author(s):  
Ryo Okamura ◽  
Yusuke Takahashi ◽  
Hitoshi Dejima ◽  
Takashi Nakayama ◽  
Hirofumi Uehara ◽  
...  
Keyword(s):  
Carbon Dioxide ◽  
Thoracoscopic Surgery ◽  
Hemodynamic Response ◽  
Carbon Dioxide Insufflation ◽  
Vessel Injury ◽  
Injury Model

scholarly journals Activation and Migration of Adventitial Fibroblasts Contributes to Vascular Remodeling

2018 ◽  
Author(s):  
Xiaowan Han ◽  
Aiming Wu ◽  
Jie Wang ◽  
Hong Chang ◽  
Yizhou Zhao ◽  
...  
Keyword(s):  
Vascular Remodeling ◽  
Adventitial Fibroblasts ◽  
And Migration

Trimethylamine N-oxide promotes hyperlipidemia acute pancreatitis via inflammatory response

2021 ◽  
pp. 1-7
Author(s):  
Guodong Yang ◽  
Xiaoying Zhang
Keyword(s):  
Acute Pancreatitis ◽  
Inflammatory Response ◽  
Tissue Injury ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Pancreatic Injury ◽  
Pancreatic Tissue ◽  
Lipoprotein Cholesterol ◽  
Model Group ◽  
New Ideas

Trimethylamine N-oxide (TMAO), a metabolite of gut microbiota, is involved in the regulation of lipid metabolism and inflammatory response; however, the role of TMAO in hyperlipidemia acute pancreatitis (HAP) is not clear. In this study, HAP mice were used as an animal model to explore the effects and possible mechanism of TMAO on HAP, which may provide new ideas for the treatment of HAP. Results found that the levels of triglycerides, total cholesterol, low-density lipoprotein cholesterol, nonestesterified fatty acid, aspartate aminotransferase, alanine aminotransferase, alkaline phosphatase, α-amylase, TMAO, and flavin-containing monooxygenase 3 were significantly increased, the levels of high-density lipoprotein cholesterol and insulin were significantly decreased, and there was an obvious pancreatic injury and inflammatory response in the model group. The choline analogue 3,3-dimethyl-1-butanol (DMB) treatment reversed the changes of serum biochemical parameters, alleviated the pancreatic tissue injury, and reduced the levels of inflammatory cytokines. Further studies of toll-like receptor (TLR)/p-glycoprotein 65 (p65) pathway found that the expressions of TLR2, TLR4, and p-p65/p65 in the model group were significantly increased, which was more obvious after Escherichia coli (Migula) Castellani & Chalmers treatment, while activation of the TLR/p65 pathway was inhibited by DMB. The results indicated that TMAO promotes HAP by promoting inflammatory response through TLR/p65 signaling pathway, suggesting that TMAO may be a potential target of HAP.

Cystathionine-β-synthase gene transfer and 3-deazaadenosine ameliorate inflammatory response in endothelial cells

2007 ◽  
Vol 293 (6) ◽  
pp. C1779-C1787 ◽  
Author(s):  
Utpal Sen ◽  
Neetu Tyagi ◽  
Munish Kumar ◽  
Karni S. Moshal ◽  
Walter E. Rodriguez ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Inflammatory Response ◽  
Protein Expression ◽  
Adhesion Molecules ◽  
Adhesion Molecule ◽  
Vascular Remodeling ◽  
Collagen Type ◽  
Gene Transfection ◽  
Collagen Type 1

Although elevated levels of homocysteine (Hcy) known as hyperhomocysteinemia (HHcy) are associated with increased inflammation and vascular remodeling, the mechanism of Hcy-mediated inflammation and vascular remodeling is unclear. The matrix metalloproteinases (MMPs) and adhesion molecules play an important role in vascular remodeling. We hypothesized that HHcy induces inflammation by increasing adhesion molecules and matrix protein expression. Endothelial cells were supplemented with high methionine, and Hcy accumulation was measured by HPLC. Nitric oxide (NO) bioavailability was detected by a NO probe. The protein expression was measured by Western blot analysis. MMP-9 activity was detected by gelatin-gel zymography. We demonstrated that methionine supplement promoted upregulation of intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) through increased Hcy accumulation. In addition, increased synthesis of collagen type-1 was also observed. MMP-9 gene expression and protein activity were increased in methionine supplement groups. 3-Deazaadenosine (DZA), an adenosine analogue, prevented high methionine-induced ICAM-1 and VCAM-1 expression and collagen type-1 synthesis. Transfection of endothelial cells with cystathionine-β-synthase (CBS) gene construct, which converts Hcy to cystathionine, reduced Hcy accumulation in high methionine-fed cells. CBS gene transfection reduced the inflammatory response, as evident by attenuated ICAM-1 and VCAM-1 expression. Furthermore, collagen type-1 expression and MMP-9 activity were dramatically attenuated with CBS gene transfection. These results suggested that methionine supplement increased Hcy accumulation, which was associated with inflammatory response and matrix remodeling such as collagen type-1 synthesis and MMP-9 activity. However, in vitro DZA and CBS gene therapy successfully treated the HHcy-induced inflammatory reaction in the methionine metabolism pathway.

Effect of xiongshao capsule on vascular remodeling in porcine coronary balloon injury model

2000 ◽  
Vol 6 (4) ◽  
pp. 278-282
Author(s):  
Hao Xu ◽  
Dazhuo Shi ◽  
Keji Chen ◽  
Xiaochang Ma ◽  
Yongli Li ◽  
...  
Keyword(s):  
Vascular Remodeling ◽  
Balloon Injury ◽  
Xiongshao Capsule ◽  
Injury Model

Lung inflammation and vascular remodeling after repeated allergen challenge detected noninvasively by MRI

2007 ◽  
Vol 292 (3) ◽  
pp. L644-L653 ◽  
Author(s):  
Bruno Tigani ◽  
Catherine Cannet ◽  
Harry Karmouty-Quintana ◽  
François-Xavier Blé ◽  
Stefan Zurbruegg ◽  
...  
Keyword(s):  
Inflammatory Response ◽  
Vascular Permeability ◽  
Vascular Remodeling ◽  
Lung Inflammation ◽  
Time Course ◽  
Repeated Administration ◽  
Brown Norway ◽  
Intratracheal Administration ◽  
Dce Mri ◽  
Fluid Analysis

Magnetic resonance imaging (MRI) has been used previously to follow noninvasively inflammatory processes in rat acute models of lung inflammation. Here the technique was applied to a model involving repeated intratracheal administration of ovalbumin (OA). Anatomical MRI was performed at different time points with respect to a single or multiple OA challenges in Brown Norway rats actively sensitized to the allergen. Vascular permeability was assessed using dynamic contrast-enhanced MRI (DCE-MRI). Bronchoalveolar lavage (BAL) fluid analysis and histology were performed to validate the MRI data. The time course of MRI signals after a single OA challenge reached a maximum at 48 h and decreased significantly at 96 h. After the second and subsequent challenges, the maximum signal occurred at 6 h with a time-dependent decline over the remainder of the time course. A reduction of the inflammatory response following repeated administration of OA was also detected by BAL fluid analysis. The decrease in vascular permeability assessed by DCE-MRI in repeatedly OA-challenged rats was consistent with the thickening of the vascular wall for vessels of diameter up to 300 μm revealed by histology. Angiogenesis of vessels smaller than 30 μm was also detected histologically. These results suggest that MRI can be used to detect the inflammatory response and vascular remodeling associated with chronic airway inflammation in rat models involving repeated administration of allergen. As the contrast agent used in the DCE-MRI experiments is approved for clinical use, there is potential to translate the approach to patients.

scholarly journals SIRT1 Regulates the Inflammatory Response of Vascular Adventitial Fibroblasts through Autophagy and Related Signaling Pathway

2017 ◽  
Vol 41 (2) ◽  
pp. 569-582 ◽  
Author(s):  
Wei-Rong Wang ◽  
Ting-Ting Li ◽  
Ting Jing ◽  
Yan-Xiang Li ◽  
Xiao-Feng Yang ◽  
...  
Keyword(s):  
Inflammatory Response ◽  
Signaling Pathway ◽  
Degradation Pathway ◽  
Sirtuin 1 ◽  
Akt Inhibitor ◽  
Cellular Survival ◽  
Akt Phosphorylation ◽  
Transmission Electron ◽  
Tnf Α ◽  
Adventitial Fibroblasts

Background/Aims: Autophagy is a lysosomal degradation pathway that is essential for cellular survival, differentiation, and homeostasis. Sirtuin 1 (SIRT1), a NAD+-dependent deacetylase, plays a pivotal role in modulation of autophagy. Recent studies found that autophagy was involved in the regulation of inflammatory response. In this study, we aimed to determine the effect of SIRT1 on autophagy and inflammation, and whether autophagy can regulate the inflammatory response in vascular adventitial fibroblasts (VAFs). Methods: Cell autophagy was evaluated by fluorescence microscope and transmission electron microscopy. The expression of protein and mRNA were determined by Western blot analysis and real time-PCR. The production of cytokine was detected by ELISA. Results: TNF-α induced autophagy and increased SIRT1 expression in VAFs. SIRT1 activator resveratrol enhanced TNF-α-induced VAF autophagy. In contrast, SIRT1 knockdown attenuated VAF autophagy. Both the Akt inhibitor MK2206 and mTOR inhibitor rapamycin further increased TNF-α-induced VAF autophagy. Furthermore, SIRT1 knockdown increased Akt phosphorylation and inhibited the autophagy in VAFs. However, MK2206 attenuated the effect of SIRT1 knockdown on VAF autophagy. In addition, ingenuity pathway analysis showed that there is a relationship between cell autophagy and inflammation. We found that SIRT1 knockdown increased the expression of NLRP3 and interleukin (IL)-6 and promoted the production of IL-1β in VAFs. Further study showed that autophagy activation decreased the expression of NLRP3 and IL-6 and inhibited the production of IL-1β, whereas autophagy inhibition increased the inflammatory response of VAFs. More importantly, our study showed that autophagy was involved in the degradation of NLRP3 through the autophagy-lysosome pathway. Conclusion: SIRT1 not only regulates VAF autophagy through the Akt/mTOR signaling pathway but also suppresses the inflammatory response of VAFs through autophagy.

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