scholarly journals Anti‐angiogenic effect of quercetin and its 8‐methyl pentamethyl ether derivative in human microvascular endothelial cells

2019 ◽  
Vol 23 (10) ◽  
pp. 6565-6577 ◽  
Author(s):  
Gabriella Lupo ◽  
Maria Teresa Cambria ◽  
Melania Olivieri ◽  
Concetta Rocco ◽  
Nunzia Caporarello ◽  
...  
2020 ◽  
Vol 26 ◽  
Author(s):  
Yanyan Wang ◽  
Jingjing Zhang ◽  
Mingqiang Fu ◽  
Jingfeng Wang ◽  
Xiaotong Cui ◽  
...  

Background and Objective: Angiogenesis is the most important repair process of tissues subjected to ischemic injury. The present study aims to investigate whether the pro-angiogenic effect of Qiliqiangxin prescription (QL) is mediated through miR-21 signaling. Methods: Cardiac microvascular endothelial cells (CMECs) were isolated and cultured from 2-3 weeks old SD rats by the method of planting myocardium tissues, the purity was identified by CD31 immunofluorescence staining. CMECs were then cultured under 1% O2 hypoxia or normoxia condition for 24h in the presence or absence of QL pretreatment (QL, 0.5mg/ml, 24h). The mimics and inhibitors of miR-21 were transfected into CMECs. miR-21, HIF-1α and VEGF expressions of CMECs were then detected by qRT-PCR and/or Western blot. The proliferation, migration and tube formation functions of CMECs were assessed using the BrdU assay, wound healing test and tube formation assay, respectively. Results: The results showed that compared with control group, hypoxia significantly upregulated the expression of miR-21 and impaired CMECs proliferation, migration and tube formation functions. Compared with hypoxia group, QL further upregulated miR-21, HIF-1α and VEGF expressions, and improved cell proliferation, migration and tube formation of hypoxic CMECs, these effects of QL were abolished by knockdown of miR-21. Conversely, treatment with miR-21 mimics further enhanced QL induced changes in hypoxic CMECs. Conclusions: Our results indicate that the pro-angiogenesis effects of QL on hypoxic CMECs are mediated by activating miR-21, and its downstream HIF-1α/VEGF pathway possibly.


2012 ◽  
Vol 82 (4) ◽  
pp. 267-274 ◽  
Author(s):  
Zahide Cavdar ◽  
Mehtap Y. Egrilmez ◽  
Zekiye S. Altun ◽  
Nur Arslan ◽  
Nilgun Yener ◽  
...  

The main pathophysiology in cerebral ischemia is the structural alteration in the neurovascular unit, coinciding with neurovascular matrix degradation. Among the human matrix metalloproteinases (MMPs), MMP-2 and -9, known as gelatinases, are the key enzymes for degrading type IV collagen, which is the major component of the basal membrane that surrounds the cerebral blood vessel. In the present study, we investigated the effects of resveratrol on cytotoxicity, reactive oxygen species (ROS), and gelatinases (MMP-2 and -9) in human cerebral microvascular endothelial cells exposed to 6 hours of oxygen-glucose deprivation and a subsequent 24 hours of reoxygenation with glucose (OGD/R), to mimic ischemia/reperfusion in vivo. Lactate dehydrogenase increased significantly, in comparison to that in the normoxia group. ROS was markedly increased in the OGD/R group, compared to normoxia. Correspondingly, ROS was significantly reduced with 50 μM of resveratrol. The proMMP-2 activity in the OGD/R group showed a statistically significant increase from the control cells. Resveratrol preconditioning decreased significantly the proMMP-2 in the cells exposed to OGD/R in comparison to that in the OGD/R group. Our results indicate that resveratrol regulates MMP-2 activity induced by OGD/R via its antioxidant effect, implying a possible mechanism related to the neuroprotective effect of resveratrol.


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