scholarly journals The H2S-Donor Erucin Exhibits Protective Effects against Vascular Inflammation in Human Endothelial and Smooth Muscle Cells

Antioxidants ◽  
2021 ◽  
Vol 10 (6) ◽  
pp. 961
Author(s):  
Alma Martelli ◽  
Eugenia Piragine ◽  
Era Gorica ◽  
Valentina Citi ◽  
Lara Testai ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Cell Viability ◽  
Caspase 3 ◽  
Metabolic Diseases ◽  
Vascular Inflammation ◽  
Endothelial Permeability ◽  
Muscle Cells ◽  
Significant Inhibition ◽  
Protective Effects

Preservation of vascular wall integrity against degenerative processes associated with ageing, fat-rich diet and metabolic diseases is a timely therapeutical challenge. The loss of endothelial function and integrity leads to cardiovascular diseases and multiorgan inflammation. The protective effects of the H2S-donor erucin, an isothiocyanate purified by Eruca sativa Mill. seeds, were evaluated on human endothelial and vascular smooth muscle cells. In particular, erucin actions were evaluated on cell viability, ROS, caspase 3/7, inflammatory markers levels and the endothelial hyperpermeability in an inflammatory model associated with high glucose concentrations (25 mM, HG). Erucin significantly prevented the HG-induced decrease in cell viability as well as the increase in ROS, caspase 3/7 activation, and TNF-α and IL-6 levels. Similarly, erucin suppressed COX-2 and NF-κB upregulation associated with HG exposure. Erucin also caused a significant inhibition of p22phox subunit expression in endothelial cells. In addition, erucin significantly prevented the HG-induced increase in endothelial permeability as also confirmed by the quantification of the specific markers VE-Cadherin and ZO-1. In conclusion, our results assess anti-inflammatory and antioxidant effects by erucin in vascular cells undergoing HG-induced inflammation and this protection parallels the preservation of endothelial barrier properties.

Sorghum Fermented by Aspergillus oryzae NK Enhances Inhibition of Vascular Inflammation in TNF-α-stimulated Human Aortic Smooth Muscle Cells

2018 ◽  
Vol 88 (5-6) ◽  
pp. 309-318
Author(s):  
Hae Seong Song ◽  
Jung-Eun Kwon ◽  
Hyun Jin Baek ◽  
Chang Won Kim ◽  
Hyelin Jeon ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Inflammatory Response ◽  
Smooth Muscle Cells ◽  
Adhesion Molecule ◽  
Vascular Inflammation ◽  
Muscle Cells ◽  
Aortic Smooth Muscle Cells ◽  
Aortic Smooth Muscle ◽  
Tnf Α ◽  
Cox 2

Abstract. Sorghum bicolor L. Moench is widely grown all over the world for food and feed. The effects of sorghum extracts on general inflammation have been previously studied, but its anti-vascular inflammatory effects are unknown. Therefore, this study investigated the anti-vascular inflammation effects of sorghum extract (SBE) and fermented extract of sorghum (fSBE) on human aortic smooth muscle cells (HASMCs). After the cytotoxicity test of the sorghum extract, a series of experiments were conducted. The inhibition effects of SBE and fSBE on the inflammatory response and adhesion molecule expression were measured using treatment with tumor necrosis factor-α (TNF-α), a crucial promoter for the development of atherosclerotic lesions, on HASMCs. After TNF-α (10 ng/mL) treatment for 2 h, then SBE and fSBE (100 and 200 μg/mL) were applied for 12h. Western blotting analysis showed that the expression of vascular cell adhesion molecule-1 (VCAM-1) (2.4-fold) and cyclooxygenase-2 (COX-2) (6.7-fold) decreased, and heme oxygenase-1 (HO-1) (3.5-fold) increased compared to the TNF-α control when treated with 200 μg/mL fSBE (P<0.05). In addition, the fSBE significantly increased the expression of HO-1 and significantly decreased the expression of VCAM-1 and COX-2 compared to the TNF-α control in mRNA level (P<0.05). These reasons of results might be due to the increased concentrations of procyanidin B1 (about 6-fold) and C1 (about 30-fold) produced through fermentation with Aspergillus oryzae NK for 48 h, at 37 °C. Overall, the results demonstrated that fSBE enhanced the inhibition of the inflammatory response and adherent molecule expression in HASMCs.

Enhance Smooth Muscle Cells Apoptosis Associated With Pulmonary Arterial Remodeling in Dogs Affected With Pulmonary Hypertension Secondary to Degenerative Mitral Valve Disease

2021 ◽  
Author(s):  
Siriwan Sakarin ◽  
Anudep Rungsipipat ◽  
Sirilak Disatian Surachetpong
Keyword(s):  
Pulmonary Hypertension ◽  
Smooth Muscle ◽  
Mitral Valve ◽  
Pulmonary Artery ◽  
Smooth Muscle Cells ◽  
Mitral Valve Disease ◽  
Caspase 3 ◽  
Muscle Cells ◽  
Pulmonary Arterial ◽  
Medial Thickening

Abstract Background: Degenerative mitral valve disease (DMVD) is the most common cause of pulmonary hypertension (PH) in dogs. Medial thickening of the pulmonary artery is a major histopathological change in PH. A decrease in apoptosis of pulmonary arterial smooth muscle cells (SMCs) may be the cause of medial thickening. This study aimed to demonstrate the expression of apoptosis molecules in the pulmonary artery of dogs affected with PH secondary to DMVD (DMVD+PH) compared to DMVD without PH (DMVD) and healthy dogs (control). Lung samples were collected from three groups including control (n=5), DMVD (n=7) and DMVD+PH (n=7) groups. Masson trichrome and apoptotic proteins including Bax, Bcl2 and caspase-3 and -8, were stained. Results: The medial thickness in the DMVD and DMVD+PH groups was greater than in the control group and it was greatest in the DMVD+PH group. Bax, Bcl2 and caspase-3 and -8 were expressed mainly in the medial layer of the pulmonary artery. The percentages of Bax and caspase-3 and -8 positive cells were higher in the DMVD group compared to the DMVD+PH group, whereas the percentage of Bcl2-positive cells was increased in the DMVD and DMVD+PH groups. These findings suggested that apoptosis of pulmonary arterial SMCs occurred mainly in the DMVD group and decreased dramatically in the DMVD+PH group. Conclusions: An increase in the medial thickness in dogs affected with PH secondary to DMVD may occur due to a decrease in apoptosis of pulmonary arterial SMCs.

Quinic acid inhibits vascular inflammation in TNF-α-stimulated vascular smooth muscle cells

2017 ◽  
Vol 96 ◽  
pp. 563-571 ◽  
Author(s):  
Seon-A Jang ◽  
Dae Won Park ◽  
Jeong Eun Kwon ◽  
Hae Seong Song ◽  
Bongkyun Park ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Vascular Inflammation ◽  
Quinic Acid ◽  
Muscle Cells ◽  
Tnf Α

scholarly journals Intravascular Glucocorticoid Metabolism during Inflammation and Injury in Mice

Endocrinology ◽  
2007 ◽  
Vol 148 (1) ◽  
pp. 166-172 ◽  
Author(s):  
Anna R. Dover ◽  
Patrick W. F. Hadoke ◽  
Linsay J. Macdonald ◽  
Eileen Miller ◽  
David E. Newby ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Tissue ◽  
Reductase Activity ◽  
Vascular Inflammation ◽  
Feedback Regulation ◽  
Muscle Cells ◽  
Femoral Arteries

11β-Hydroxysteroid dehydrogenases (11βHSDs) catalyze interconversion of 11-hydroxy-glucocorticoids with inactive 11-keto metabolites. In blood vessel walls, loss of 11βHSD1 is thought to reduce local glucocorticoid concentrations, reducing the progression of atheroma and enhancing angiogenesis. Conversely, on the basis that 11βHSD1 is up-regulated approximately 5-fold by inflammatory cytokines in cultured human vascular smooth muscle cells, it has been proposed that increased 11βHSD1 during vascular inflammation provides negative feedback suppression of inflammation. We aimed to determine whether inflammation and injury selectively up-regulate 11βHSD1 reductase activity in vitro and in vivo in intact vascular tissue in mice. In isolated mouse aortae and femoral arteries, reductase activity (converting 11-dehydrocorticosterone to corticosterone) was approximately 10-fold higher than dehydrogenase activity and was entirely accounted for by 11βHSD1 because it was abolished in vessels from 11βHSD1−/− mice. Although 11βHSD1 activity was up-regulated by proinflammatory cytokines in cultured murine aortic smooth muscle cells, no such effect was evident in intact aortic rings in vitro. Moreover, after systemic inflammation induced by ip lipopolysaccharide injection, there was only a modest (18%) increase in 11β-reductase activity in the aorta and no increase in the perfused hindlimb. Furthermore, in femoral arteries in which neointimal proliferation was induced by intraluminal injury, there was no change in basal 11βHSD1 activity or the sensitivity of 11βHSD1 to cytokine up-regulation. We conclude that increased generation of glucocorticoids by 11βHSD1 in the murine vessel wall is unlikely to contribute to feedback regulation of inflammation.

scholarly journals Activation of cAMP signaling transiently inhibits apoptosis in vascular smooth muscle cells in a site upstream of caspase-3

1999 ◽  
Vol 6 (7) ◽  
pp. 661-672 ◽  
Author(s):  
Sergei N Orlov ◽  
Nathalie Thorin-Trescases ◽  
Nickolai O Dulin ◽  
Than-Vinh Dam ◽  
Maria A Fortuno ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Caspase 3 ◽  
Muscle Cells ◽  
Camp Signaling ◽  
A Site

scholarly journals Involvement of p53, p21, and Caspase-3 in Apoptosis of Coronary Artery Smooth Muscle Cells in a Kawasaki Vasculitis Mouse Model

2020 ◽  
Vol 26 ◽  
Author(s):  
Minghong Deng ◽  
Chunwang Lin ◽  
Xianglin Zeng ◽  
Jianping Zhang ◽  
Fang Wen ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Coronary Artery ◽  
Mouse Model ◽  
Smooth Muscle Cells ◽  
Caspase 3 ◽  
Muscle Cells

scholarly journals Carrot Genotypes Contrasted by Root Color and Grown under Different Conditions Displayed Differential Pharmacological Profiles in Vascular and Metabolic Cells

Nutrients ◽  
2020 ◽  
Vol 12 (2) ◽  
pp. 337
Author(s):  
Raffaella Soleti ◽  
Patricia Mallegol ◽  
Grégory Hilairet ◽  
Mehdi Frifra ◽  
Florent Perrin ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Biotic Stress ◽  
Lipid Accumulation ◽  
Metabolic Diseases ◽  
Muscle Cells ◽  
Combined Stress ◽  
Beneficial Effects ◽  
Growing Conditions

Carrots’ genotype and growing conditions influence their potential properties to fight against cardiovascular and metabolic diseases. The present study evaluated the influence of carrot genotypes contrasted by root color (Bolero, Presto, Karotan, Deep Purple, Kintoki and Blanche des Vosges) growing under standard, water-restricted, biotic stress (Alternaria dauci inoculation), and combined stress conditions (water restriction and A. dauci inoculation). The effect of carrots’ polyphenol and carotenoid content was assessed on endothelial and smooth muscle cells, hepatocytes, adipocytes and macrophages functions (oxidative stress, apoptosis, proliferation, lipid accumulation and inflammation). Independently of varieties or growing conditions, all carrot extracts affected vascular cells’ oxidative stress and apoptosis, and metabolic cells’ oxidative stress and lipid accumulation. Three clusters were revealed and displayed beneficial properties mostly for adipocytes function, smooth muscle cells and hepatocytes, and endothelial cells and hepatocytes, respectively. Karotan and Presto varieties exhibited endothelial tropism while Blanche des Vosges targeted adipocytes. Carrots under biotic stress are more efficient in inducing beneficial effects, with the Bolero variety being the most effective. However, extracts from carrots which grew under combined stress conditions had limited beneficial effects. This report underscores the use of certain carrot extracts as potential effective nutraceutical supplements for metabolic diseases.

scholarly journals Protective Effects of Adiponectin against Cobalt Chloride-Induced Apoptosis of Smooth Muscle Cells via cAMP/PKA Pathway

2020 ◽  
Vol 2020 ◽  
pp. 1-11
Author(s):  
Jingjie Xiao ◽  
Yingying Zhang ◽  
Wei Zhang ◽  
Liang Zhang ◽  
Li Li ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Cell Viability ◽  
Cobalt Chloride ◽  
Muscle Cells ◽  
Camp Level ◽  
Control Group ◽  
Dependent Manner ◽  
Sod Activity

Adiponectin (APN) is an adipokine secreted from adipose tissue and exhibits biological functions such as microcirculation-regulating, hearing-protective, and antiapoptotic. However, the effect of APN on the apoptosis of spiral arterial smooth muscle cells (SMCs) under hypoxic conditions in vitro is not clear. We used cobalt chloride (CoCl2) to simulate chemical hypoxia in vitro, and the SMCs were pretreated with APN and then stimulated with CoCl2. The viability of cells and apoptosis were assessed by CCK-8 and flow cytometry, respectively. Superoxide dismutase (SOD) activity, malondialdehyde (MDA) levels, cAMP level, and the activity of PKA were detected by ELISA. Protein expression and localization were studied by Western blot and immunofluorescence analysis. In the present study, we found that APN exhibits antiapoptosis effects. CoCl2 exhibited decreased cell viability, increased apoptosis and MDA levels, and decreased SOD activity in a concentration-dependent manner, compared with the control group. Moreover, CoCl2 upregulated the expression levels of Bax and cleaved caspase-3 and then downregulated Bcl-2 levels in a time-dependent manner. Compared with the CoCl2 group, the group pretreated with APN had increased cell viability, SOD activity, PKA activity, cAMP level, and PKA expression, but decreased MDA levels and apoptosis. Lastly, the protective effect of APN was blocked by cAMP inhibitor SQ22536 and PKA inhibitor H 89. These results showed that APN protected SMCs against CoCl2-induced hypoxic injury via the cAMP/PKA signaling pathway.

SET8，a novel regulator to ameliorate vascular calcification via activating PI3K/Akt mediated anti-apoptotic effects.

2021 ◽  
Author(s):  
Ya Ling Bai ◽  
Mei Juan Cheng ◽  
Jing Jing Jin ◽  
Hui Ran Zhang ◽  
Lei He ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Calcification ◽  
Vascular Smooth Muscle Cells ◽  
Caspase 3 ◽  
Muscle Cells ◽  
Akt Phosphorylation ◽  
High Phosphorus ◽  
Apoptotic Effects

Previous studies have showed that the apoptosis of vascular smooth muscle cells (VSMCs) underlies the mechanism of pathological calcifications in patients with chronic kidney disease (CKD). SET domain-containing protein 8 (SET8), as an efficient protein has been reported to modulate cell apoptosis in hepatocellular carcinoma cell, esophageal squamous cell and neuronal cell through regulating pathological processes, such as cell-cycle progression and transcription regulation. However, whether SET8 is involved in high phosphorus induced vascular calcification by mediating apoptosis remains undefined. Here, we reported that SET8 was located both in nucleus and cytoplasm, and significantly downregulated in calcification models. SET8 deficiency promoted the apoptosis of VSMCs, which was indicated by the increased Bax/Bcl-2 and cleaved caspase-3/total caspase-3 ratios. Mechanistically, PI3K/Akt pathway was mediated by SET8 and inhibition of PI3K/Akt signaling pathway by giving LY294002 or transfecting Akt phosphorylation inactivated mutation plasmid increased apoptosis and calcification. Akt phosphorylation constitutively activated mutation could reduce apoptosis and calcification of VSMCs. Furthermore, exogenous overexpression of SET8 could reverse the effect of PI3K/Akt inhibition on the apoptosis and calcification of VSMCs. In summary, our researches suggested that SET8 overexpression ameliorated high phosphorus induced calcification of vascular smooth muscle cells via activating PI3K/Akt mediated anti-apoptotic effects.

Sign in / Sign up

Export Citation Format

Share Document