Oxidative stress in diabetes-induced endothelial dysfunction involvement of nitric oxide and protein kinase C

2003 ◽  
Vol 35 (6) ◽  
pp. 683-694 ◽  
Author(s):  
Flavia Pricci ◽  
Gaetano Leto ◽  
Lorena Amadio ◽  
Carla Iacobini ◽  
Samantha Cordone ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Nitric Oxide ◽  
Protein Kinase C ◽  
Protein Kinase ◽  
Endothelial Dysfunction ◽  
Kinase C

scholarly journals Docetaxel Facilitates Endothelial Dysfunction through Oxidative Stress via Modulation of Protein Kinase C Beta: The Protective Effects of Sotrastaurin

2015 ◽  
Vol 145 (1) ◽  
pp. 59-67 ◽  
Author(s):  
Ching-Hsia Hung ◽  
Shih-Hung Chan ◽  
Pei-Ming Chu ◽  
Kun-Ling Tsai
Keyword(s):  
Oxidative Stress ◽  
Protein Kinase C ◽  
Protein Kinase ◽  
Endothelial Dysfunction ◽  
Protective Effects ◽  
Kinase C ◽  
Protein Kinase C Beta

Gene‐gene interactions in the protein kinase C/endothelial nitric oxide synthase axis impact the hypotensive effects of propofol

2021 ◽  
Author(s):  
Gustavo H. Oliveira‐Paula ◽  
Daniela A. Pereira ◽  
Lucas C. Pinheiro ◽  
Graziele C. Ferreira ◽  
Waynice N. Paula‐Garcia ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Protein Kinase C ◽  
Protein Kinase ◽  
Nitric Oxide Synthase ◽  
Endothelial Nitric Oxide Synthase ◽  
Gene Interactions ◽  
Kinase C ◽  
Oxide Synthase ◽  
Endothelial Nitric Oxide

Mechanism of Hepatic Heme Oxygenase-1 Induction by Isoflurane

2006 ◽  
Vol 104 (1) ◽  
pp. 101-109 ◽  
Author(s):  
Alexander Hoetzel ◽  
Daniel Leitz ◽  
Rene Schmidt ◽  
Eva Tritschler ◽  
Inge Bauer ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Protein Kinase C ◽  
Protein Kinase ◽  
Phospholipase A2 ◽  
Heme Oxygenase ◽  
Kupffer Cell ◽  
Cell Function ◽  
Heme Oxygenase 1 ◽  
Gadolinium Chloride ◽  
Kinase C

Background The heme oxygenase pathway represents a major cell and organ protective system in the liver. The authors recently showed that isoflurane and sevoflurane up-regulate the inducible isoform heme oxygenase 1 (HO-1). Because the activating cascade remained unclear, it was the aim of this study to identify the underlying mechanism of this effect. Methods Rats were anesthetized with pentobarbital intravenously or with isoflurane per inhalation (2.3 vol%). Kupffer cell function was inhibited by dexamethasone or gadolinium chloride. Nitric oxide synthases were inhibited by either N(omega)-nitro-L-arginine methyl ester or S-methyl thiourea. N-acetyl-cysteine served as an antioxidant, and diethyldithiocarbamate served as an inhibitor of cytochrome P450 2E1. Protein kinase C and phospholipase A2 were inhibited by chelerythrine or quinacrine, respectively. HO-1 was analyzed in liver tissue by Northern blot, Western blot, immunostaining, and enzymatic activity assay. Results In contrast to pentobarbital, isoflurane induced HO-1 after 4-6 h in hepatocytes in the pericentral region of the liver. The induction was prevented in the presence of dexamethasone (P < 0.05) and gadolinium chloride (P < 0.05). Inhibition of nitric oxide synthases or reactive oxygen intermediates did not affect isoflurane-mediated HO-1 up-regulation. In contrast, chelerythrine (P < 0.05) and quinacrine (P < 0.05) resulted in a blockade of HO-1 induction. Conclusion The up-regulation of HO-1 by isoflurane in the liver is restricted to parenchymal cells and depends on Kupffer cell function. The induction is independent of nitric oxide or reactive oxygen species but does involve protein kinase C and phospholipase A2.

Relationship between aldose reductase enzyme and the signaling pathway of protein kinase C in an in vitro diabetic retinopathy model

2020 ◽  
Vol 98 (4) ◽  
pp. 243-251
Author(s):  
Mutlu Sarikaya ◽  
Nuray Yazihan ◽  
Net Daş Evcimen
Keyword(s):  
Oxidative Stress ◽  
Protein Kinase C ◽  
Protein Kinase ◽  
Molecular Mechanisms ◽  
Signaling Molecules ◽  
Protein Levels ◽  
Kinase C ◽  
The Relationship ◽  
And Oxidative Stress ◽  
Expression And Activity

Protein kinase C (PKC) and aldose reductase (AR) enzyme activities are increased in diabetes and complications are include retinopathy, nephropathy, and neuropathy. However, the relationship between PKC and AR and the underlying molecular mechanisms is still unclear. We aimed to evaluate the relationship between these two enzymes and clarify the underlying molecular mechanisms by the related signaling molecules. The effects of hyperglycemia and oxidative stress on AR and PKC enzymes and the signaling molecules such as nuclear factor-kappa B (NF-κB), inhibitor kappa B-alpha (IkB-α), total c-Jun, phospho c-Jun, and stress-activated protein kinases (SAPK)/Jun amino-terminal kinases (JNK) were evaluated in human retinal pigment epithelial cells (ARPE-19). AR, PKC protein levels, and related signaling molecules increased with hyperglycemia and oxidative stress. The AR inhibitor sorbinil decreased PKC expression and activity and all signaling molecule protein levels. Increased AR expression during hyperglycemia and oxidative stress was found to be correlated with the increase in PKC expression and activity in both conditions. Decreased expression and activity of PKC and the protein levels of related signaling molecules with the AR inhibitor sorbinil showed that AR enzyme may play a key role in the expression of PKC enzyme and oxidative stress during diabetes.

Protein Kinase C as a Sensor for Oxidative Stress in Tumor Promotion and Chemoprevention

1997 ◽  
pp. 157-180 ◽  
Author(s):  
Rayudu Gopalakrishna ◽  
Zhen-Hai Chen ◽  
Usha Gundimeda
Keyword(s):  
Oxidative Stress ◽  
Protein Kinase C ◽  
Protein Kinase ◽  
Tumor Promotion ◽  
Kinase C
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