scholarly journals Rice‐derived peptide AAGALPS inhibits TNF‐α‐induced inflammation and oxidative stress in vascular endothelial cells

2019 ◽  
Vol 8 (1) ◽  
pp. 659-667 ◽  
Author(s):  
Li‐Tao Tong ◽  
Zhiyuan Ju ◽  
Liya Liu ◽  
Lili Wang ◽  
Xianrong Zhou ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Endothelial Cells ◽  
Vascular Endothelial Cells ◽  
Vascular Endothelial ◽  
Tnf Α ◽  
And Oxidative Stress

Glutamate induces oxidative stress and apoptosis in cerebral vascular endothelial cells: contributions of HO-1 and HO-2 to cytoprotection

2006 ◽  
Vol 290 (5) ◽  
pp. C1399-C1410 ◽  
Author(s):  
Helena Parfenova ◽  
Shyamali Basuroy ◽  
Sujoy Bhattacharya ◽  
Dilyara Tcheranova ◽  
Yan Qu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Endothelial Cells ◽  
Vascular Endothelium ◽  
Vascular Endothelial Cells ◽  
Glutamate Toxicity ◽  
Vascular Endothelial ◽  
Oxygen Species ◽  
Apoptotic Effects ◽  
Cerebral Vascular

In cerebral circulation, epileptic seizures associated with excessive release of the excitatory neurotransmitter glutamate cause endothelial injury. Heme oxygenase (HO), which metabolizes heme to a vasodilator, carbon monoxide (CO), and antioxidants, biliverdin/bilirubin, is highly expressed in cerebral microvessels as a constitutive isoform, HO-2, whereas the inducible form, HO-1, is not detectable. Using cerebral vascular endothelial cells from newborn pigs and HO-2-knockout mice, we addressed the hypotheses that 1) glutamate induces oxidative stress-related endothelial death by apoptosis, and 2) HO-1 and HO-2 are protective against glutamate cytotoxicity. In cerebral endothelial cells, glutamate (0.1–2.0 mM) increased formation of reactive oxygen species, including superoxide radicals, and induced major keystone events of apoptosis, such as NF-κB nuclear translocation, caspase-3 activation, DNA fragmentation, and cell detachment. Glutamate-induced apoptosis was greatly exacerbated in HO-2 gene-deleted murine cerebrovascular endothelial cells and in porcine cells with pharmacologically inhibited HO-2 activity. Glutamate toxicity was prevented by superoxide dismutase, suggesting apoptotic changes are oxidative stress related. When HO-1 was pharmacologically upregulated by cobalt protoporphyrin, apoptotic effects of glutamate in cerebral endothelial cells were completely prevented. Glutamate-induced reactive oxygen species production and apoptosis were blocked by a CO-releasing compound, CORM-A1 (50 μM), and by bilirubin (1 μM), consistent with the antioxidant and cytoprotective roles of the end products of HO activity. We conclude that both HO-1 and HO-2 have anti-apoptotic effects against oxidative stress-related glutamate toxicity in cerebral vascular endothelium. Although HO-1, when induced, provides powerful protection, HO-2 is an essential endogenous anti-apoptotic factor against glutamate toxicity in the cerebral vascular endothelium.

Hydroxytyrosol NO regulates oxidative stress and NO production through SIRT1 in diabetic mice and vascular endothelial cells

Phytomedicine ◽  
2019 ◽  
Vol 52 ◽  
pp. 206-215 ◽  
Author(s):  
Weirong Wang ◽  
Chenxu Shang ◽  
Wei Zhang ◽  
Zhen Jin ◽  
Feng Yao ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Endothelial Cells ◽  
Vascular Endothelial Cells ◽  
No Production ◽  
Vascular Endothelial ◽  
Diabetic Mice

scholarly journals Protective effect of Melissa officinalis extract against H2O2-induced oxidative stress in human vascular endothelial cells

2016 ◽  
Vol 11 (5) ◽  
pp. 383 ◽  
Author(s):  
Leila Safaeian ◽  
SeyyedEbrahim Sajjadi ◽  
ShaghayeghHaghjooy Javanmard ◽  
Hossein Montazeri ◽  
Fariba Samani
Keyword(s):  
Oxidative Stress ◽  
Endothelial Cells ◽  
Protective Effect ◽  
Vascular Endothelial Cells ◽  
Vascular Endothelial ◽  
Melissa Officinalis
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