scholarly journals Naringin protects endothelial cells from apoptosis and inflammation by regulating the Hippo-YAP Pathway

2020 ◽  
Vol 40 (3) ◽  
Author(s):  
Hui Zhao ◽  
Meirong Liu ◽  
Hui Liu ◽  
Rong Suo ◽  
Chengzhi Lu
Keyword(s):  
Endothelial Cells ◽  
Endothelial Cell ◽  
Cardiovascular Diseases ◽  
Cell Injury ◽  
Umbilical Vein ◽  
Density Lipoprotein ◽  
Underlying Mechanism ◽  
Inflammatory Factors ◽  
Protective Effects ◽  
Mesenchymal Transition

Abstract Atherosclerosis is the primary cause of several cardiovascular diseases. Oxidized low-density lipoprotein (ox-LDL)-induced apoptosis, endothelial–mesenchymal transition (EndMT), and inflammation are crucial for the progression of cardiovascular diseases, including atherosclerosis. Naringin, a major compound from tomatoes, grapefruits, and related citrus, reportedly exhibits potential protective effects during atherosclerosis development; however, its effect on ox-LDL-induced human umbilical vein endothelial cell (HUVEC) damage remains unknown. In the present study, we investigated the anti-apoptotic and anti-inflammatory activities of naringin against ox-LDL-induced endothelial cells, and the underlying mechanism. Naringin pretreatment significantly and concentration-dependently inhibited ox-LDL-induced cell injury and apoptosis. Additionally, naringin restored endothelial barrier integrity by preventing VE-cadherin disassembly and F-actin remodeling, and down-regulated pro-inflammatory factors like IL-1β, IL-6, and IL-18, in the HUVECs. We also demonstrated that naringin treatment restored ox-LDL-induced YAP (yes-associated protein) down-regulation, given the YAP-shRNA attenuated cytoprotective effect of naringin on ox-LDL-induced endothelial cell injury and apoptosis. Collectively, our data indicate that naringin reversed ox-LDL-triggered HUVEC apoptosis, EndMT, and inflammation by inhibiting the YAP pathway. Therefore, naringin may have a therapeutic effect on endothelial injury-related disorders.

Panax Quinquefolium L. Inhibits Thrombin-Induced Endothelin Release In Vitro

1999 ◽  
Vol 27 (03n04) ◽  
pp. 331-338 ◽  
Author(s):  
Chun-Su Yuan ◽  
Anoja S. Attele ◽  
Ji An Wu ◽  
Tasha K. Lowell ◽  
Zhenlun Gu ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Endothelial Cell ◽  
Cell Injury ◽  
Vascular Endothelial Cells ◽  
Cell Damage ◽  
Umbilical Vein ◽  
American Ginseng ◽  
Protective Effects ◽  
Panax Quinquefolium

Endothelial cell damage is considered to be the initial step in the genesis of thrombosis and arteriosclerosis, the common precursors of cardiovascular disorders. In this study, we evaluated the protective effects of American ginseng or Panax quinquefolium L. extracts on endothelial cell injury, and investigated effects of ginseng extracts on thrombin-induced endothelin release using cultured human umbilical vein endothelial cells. We observed that when endothelial cells pretreated with 1, 10, and 100 μg/ml of Panax quinquefolium L. extracts were incubated for 4 and 24 hr with thrombin, the concentration of endothelin was significantly decreased in a concentration dependent, time related manner (at 4 hr, IC50 = 5.1 μg/ml; at 24 hr, IC50 = 6.2 μg/ml). We further evaluated the effects of NG-nitro-L-arginine (NLA), a nitric oxide (NO) synthetase inhibitor, on the activity of Panax quinquefolium L. extracts. Following pretreatment of cultured endothelial cells with NLA, the inhibition of thrombin-induced endothelin release by Panax quinquefolium L. was significantly reduced (P < 0.05). This result suggests that the pharmacological action of Panax quinquefolium L. is, at least partially, due to NO release. Our data demonstrate that American ginseng may play a therapeutic role in facilitating the hemodynamic balance of vascular endothelial cells.

scholarly journals Colchicine Alleviates Cholesterol Crystal-Induced Endothelial Cell Pyroptosis through Activating AMPK/SIRT1 Pathway

2020 ◽  
Vol 2020 ◽  
pp. 1-18 ◽  
Author(s):  
Mengyue Yang ◽  
Hang Lv ◽  
Qi Liu ◽  
Lu Zhang ◽  
Ruoxi Zhang ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Endothelial Cell ◽  
Cardiovascular Diseases ◽  
Nlrp3 Inflammasome ◽  
Cell Injury ◽  
Inflammatory Factors ◽  
Acute Gout ◽  
Cholesterol Crystal ◽  
Cholesterol Crystals ◽  
Related Proteins

Cholesterol crystal- (CC-) induced endothelial cell inflammation and pyroptosis play an important role in the development of cardiovascular diseases, especially in atherosclerosis (AS). Increasing evidence suggests that cholesterol crystals are known to be a pivotal pathological marker of atherosclerotic plaque vulnerability. As a classical nonspecific anti-inflammatory drug, colchicine has been widely used in the treatment of acute gout. However, whether colchicine could alleviate CC-induced endothelial cell injury and the related mechanisms remains to be addressed. In this study, the protective effect of colchicine on human umbilical vein endothelial cells (HUVECs) was confirmed. Our results revealed that after cotreatment with colchicine and cholesterol crystals in endothelial cells, the uptake of cholesterol crystals was significantly decreased, the cell viability was obviously increased, and the release of lactate dehydrogenase (LDH) and the number of pyroptotic cells decreased significantly; then, the expression of NLRP3 inflammasome-related proteins and various inflammatory factors was also visibly suppressed; moreover, as a potent activator of NLRP3 inflammasome, the intracellular ROS level was clearly reduced, while mitochondrial membrane potential improved significantly. In addition, the expression levels of AMP-dependent kinase (AMPK) pathway-related proteins as well as various antioxidant enzymes were elevated notably in varying degrees. However, the above effects of colchicine were completely offset by the treatment of siRNA targeting AMPKα and Sirtuin1 (SIRT1). Therefore, we conclude that colchicine plays a crucial role in alleviating the intracellular inflammatory response and NLRP3 inflammation activation, attenuating the levels of cellular oxidative stress and pyroptosis in endothelial cells via regulating AMPK/SIRT1 signaling, which may be a concrete mechanism for the secondary prevention of cardiovascular diseases.

scholarly journals Alpha-Asarone Protects Endothelial Cells from Injury by Angiotensin II

2014 ◽  
Vol 2014 ◽  
pp. 1-7 ◽  
Author(s):  
Hai-Xia Shi ◽  
Jiajun Yang ◽  
Tao Yang ◽  
Yong-Liang Xue ◽  
Jun Liu ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Endothelial Cells ◽  
Angiotensin Ii ◽  
Cell Injury ◽  
Fluorescent Dyes ◽  
Umbilical Vein ◽  
Protective Effects ◽  
Ang Ii ◽  
Versus Model

α-Asarone is the major therapeutical constituent ofAcorus tatarinowiiSchott. In this study, the potential protective effects ofα-asarone against endothelial cell injury induced by angiotensin II were investigatedin vitro. The EA.hy926 cell line derived from human umbilical vein endothelial cells was pretreated withα-asarone (10, 50, 100 µmol/L) for 1 h, followed by coincubation with Ang II (0.1 µmol/L) for 24 h. Intracellular nitric oxide (NO) and reactive oxygen species (ROS) were detected by fluorescent dyes, and phosphorylation of endothelial nitric oxide synthase (eNOS) atSer1177was determined by Western blotting.α-Asarone dose-dependently mitigated the Ang II-induced intracellular NO reduction (P<0.01versus model) and ROS production (P<0.01versus model). Furthermore, eNOS phosphorylation (Ser1177) by acetylcholine was significantly inhibited by Ang II, while pretreatment for 1 h withα-asarone partially prevented this effect (P<0.05versus model). Additionally, cell viability determined by the MTT [3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide] assay (105~114.5% versus control,P>0.05) was not affected after 24 h of incubation withα-asarone at 1–100 µmol/L. Therefore,α-asarone protects against Ang II-mediated damage of endothelial cells and may be developed to prevent injury to cardiovascular tissues.

scholarly journals hnRNPA2/B1 Ameliorates LPS-Induced Endothelial Injury through NF-κB Pathway and VE-Cadherin/β-Catenin Signaling Modulation In Vitro

2020 ◽  
Vol 2020 ◽  
pp. 1-11
Author(s):  
Yi Chen ◽  
Dan Tang ◽  
Linjie Zhu ◽  
Tianjie Yuan ◽  
Yingfu Jiao ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Inflammatory Responses ◽  
Umbilical Vein ◽  
Cell Metabolism ◽  
Endothelial Permeability ◽  
Underlying Mechanism ◽  
Endothelial Injury ◽  
Inflammatory Factors ◽  
Barrier Dysfunction

Heterogeneous nuclear ribonucleoprotein A2/B1 (hnRNPA2/B1) is a protein involved in the regulation of RNA processing, cell metabolism, migration, proliferation, and apoptosis. However, the effect of hnRNPA2/B1 on injured endothelial cells (ECs) remains unclear. We investigated the effect of hnRNPA2/B1 on lipopolysaccharide- (LPS-) induced vascular endothelial injury in human umbilical vein endothelial cells (HUVECs) and the underlying mechanisms. LPS was used to induce EC injury, and the roles of hnRNPA2/B1 in EC barrier dysfunction and inflammatory responses were measured by testing endothelial permeability and the expression of inflammatory factors after the suppression and overexpression of hnRNPA2/B1. To explore the underlying mechanism by which hnRNPA2/B1 regulates endothelial injury, we studied the VE-cadherin/β-catenin pathway and NF-κB activation in HUVECs. The results showed that hnRNPA2/B1 was elevated in LPS-stimulated HUVECs. Moreover, knockdown of hnRNPA2/B1 aggravated endothelial injury by increasing EC permeability and promoting the secretion of the inflammatory cytokines TNF-α, IL-1β, and IL-6. Overexpression of hnRNPA2/B1 can reduce the permeability and inflammatory response of HUVEC stimulated by LPS in vitro, while increasing the expression of VE-Cadherin and β-catenin. Furthermore, the suppression of hnRNPA2/B1 increased the LPS-induced NF-κB activation and reduced the VE-cadherin/β-catenin pathway. Taken together, these results suggest that hnRNPA2/B1 can regulate LPS-induced EC damage through regulating the NF-κB and VE-cadherin/β-catenin pathways.

scholarly journals Omentin-1 Ameliorated Free Fatty Acid-Induced Impairment in Proliferation, Migration, and Inflammatory States of HUVECs

2020 ◽  
Vol 2020 ◽  
pp. 1-9
Author(s):  
Yubin Chen ◽  
Fen Liu ◽  
Fei Han ◽  
Lizhi Lv ◽  
Can-e Tang ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Fatty Acid ◽  
Endothelial Cell ◽  
Free Fatty Acid ◽  
Cell Injury ◽  
Umbilical Vein ◽  
Quantitative Polymerase Chain Reaction ◽  
Cell Counting ◽  
Endothelial Cell Injury ◽  
Umbilical Vein Endothelial Cells

Objectives. Endothelial cell injury is a critical pathological change during the development of atherosclerosis. Here, we explored the effect of omentin-1 on free fatty acid- (FFA-) induced endothelial cell injury. Methods. An FFA-induced endothelial cell injury model was established to investigate the role of omentin-1 in this process. Cell proliferation was analyzed with the Cell Counting Kit assay and flow cytometry. Scratch and transwell assays were used to evaluate cell migration. Factors secreted by endothelial cells after injury were detected by western blotting, reverse-transcription quantitative polymerase chain reaction, and cellular fluorescence assay. Results. Omentin-1 rescued the FFA-induced impaired proliferation and migration capabilities of human umbilical vein endothelial cells (HUVECs). It decreased the number of THP-1 cells attached to HUVECs in response to injury and inhibited the FFA-induced proinflammatory state of HUVECs. Conclusion. Omentin-1 could partly ameliorate FFA-induced endothelial cell injury.

scholarly journals CTRP3 Protects against High Glucose-Induced Cell Injury in Human Umbilical Vein Endothelial Cells

2019 ◽  
Vol 2019 ◽  
pp. 1-7 ◽  
Author(s):  
Fang Wang ◽  
Linlin Zhao ◽  
Yingguang Shan ◽  
Ran Li ◽  
Guijun Qin
Keyword(s):  
Endothelial Cells ◽  
Endothelial Dysfunction ◽  
High Glucose ◽  
Cell Injury ◽  
Umbilical Vein ◽  
Cell Loss ◽  
Inflammatory Factors ◽  
Therapeutic Drug ◽  
Human Umbilical Vein ◽  
Umbilical Vein Endothelial Cells

Aims. Inflammation was closely associated with diabetes-related endothelial dysfunction. C1q/tumor necrosis factor-related protein 3 (CTRP3) is a member of the CTRP family and can provide cardioprotection in many cardiovascular diseases via suppressing the production of inflammatory factors. However, the role of CTRP3 in high glucose- (HG-) related endothelial dysfunction remains unclear. This study evaluates the effects of CTRP3 on HG-induced cell inflammation and apoptosis. Materials and Methods. To prevent high glucose-induced cell injury, human umbilical vein endothelial cells (HUVECs) were pretreated with recombinant CTRP3 for 1 hour followed by normal glucose (5.5 mmol/l) or high glucose (33 mmol/l) treatment. After that, cell apoptosis and inflammatory factors were determined. Results. Our results demonstrated that CTRP3 mRNA and protein expression were significantly decreased after HG exposure in HUVECs. Recombinant human CTRP3 inhibited HG-induced accumulation of inflammatory factors and cell loss in HUVECs. CTRP3 treatment also increased the phosphorylation levels of protein kinase B (AKT/PKB) and the mammalian target of rapamycin (mTOR) in HUVECs. CTRP3 lost its inhibitory effects on HG-induced cell inflammation and apoptosis after AKT inhibition. Knockdown of endogenous CTRP3 in HUVECs resulted in increased inflammation and decreased cell viability in vitro. Conclusions. Taken together, these findings indicated that CTRP3 treatment blocked the accumulation of inflammatory factors and cell loss in HUVECs after HG exposure through the activation of AKT-mTOR signaling pathway. Thus, CTRP3 may be a potential therapeutic drug for the prevention of diabetes-related endothelial dysfunction.

scholarly journals Ruscogenin alleviates palmitic acid-induced endothelial cell inflammation by suppressing TXNIP/NLRP3 pathway

2020 ◽  
Vol 19 (8) ◽  
pp. 1605-1610
Author(s):  
Hongtao Liu ◽  
Simin Zheng ◽  
Hongfei Xiong ◽  
Xiaoli Niu
Keyword(s):  
Endothelial Cells ◽  
Endothelial Cell ◽  
Cardiovascular Diseases ◽  
Palmitic Acid ◽  
Umbilical Vein ◽  
Intercellular Adhesion Molecule ◽  
Enzyme Linked Immunosorbent Assay ◽  
Dependent Manner ◽  
Intercellular Adhesion Molecule 1 ◽  
Tnf Α

Purpose: To investigate the involvement of ruscogenin in palmitic acid (PA)-induced endothelial cell inflammation. Method: Cultured human umbilical vein endothelial cells (HUVECs) were divided into five groups: control (normal untreated cells), PA (cell treated with palmitic acid), and PA + ruscogenin (1, 10, or 30 μM). Cell viability and apoptosis rate were determined using MTT (3-(4,5)-dimethylthiahiazo(-z-y1)-3,5- di-phenytetrazolium bromide) and flow cytometry assays, respectively. The levels of cytokines, including interleukin-1β (IL-1β), tumor necrosis factor-α (TNF-α), intercellular adhesion molecule-1 (ICAM-1), and monocyte chemo-attractant protein-1 (MCP-1) were determined by an enzyme-linked immunosorbent assay. Western blotting and real-time polymerase chain reaction (RT-PCR) were used to evaluate the underlying mechanisms of action. Results: PA treatment decreased the viability of HUVECs and induced apoptosis (p < 0.05). Ruscogenin attenuated PA-induced cell death in a dose-dependent manner (p < 0.05). On the other hand, PA induced an increase in IL-1β, TNF-α, ICAM-1, MCP-1, TXNIP (thioredoxin-interacting protein),as well as NLRP3 (nucleotide oligomerization domain-, leucine-rich repeat- and pyrin domain-containing protein 3), all of which were attenuated by ruscogenin (p < 0.05). Conclusion: Ruscogenin alleviates PA-induced endothelial cell inflammation via TXNIP/NLRP3 pathway, thereby providing an insight into new therapeutic strategies to treat cardiovascular diseases. Keywords: Ruscogenin, Palmitic acid, Endothelial cells, Inflammation, TXNIP, NLRP3, Cardiovascular diseases

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