High Glucose and Ketosis (Acetoacetate) Increases, and Chromium Niacinate Decreases, IL-6, IL-8, and MCP-1 Secretion and Oxidative Stress in U937 Monocytes

2007 ◽  
Vol 9 (10) ◽  
pp. 1581-1590 ◽  
Author(s):  
Sushil K. Jain ◽  
Justin L. Rains ◽  
Jennifer L. Croad
Keyword(s):  
Oxidative Stress ◽  
High Glucose ◽  
And Oxidative Stress

Role of vasoactive peptides in high glucose-induced increased expression of Gαq/11 proteins and associated signaling in vascular smooth muscle cellsThis review is one of a selection of papers published in a Special Issue on Oxidative Stress in Health and Disease.

2010 ◽  
Vol 88 (3) ◽  
pp. 331-340 ◽  
Author(s):  
Magda Descorbeth ◽  
Madhu B. Anand-Srivastava
Keyword(s):  
Oxidative Stress ◽  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
High Glucose ◽  
Ang Ii ◽  
Vasoactive Peptides ◽  
Enhanced Production ◽  
Enhanced Expression ◽  
Health And Disease ◽  
And Oxidative Stress

We have recently shown that A10 vascular smooth muscle cells (VSMCs) exposed to high glucose exhibited enhanced expression of Gαq and PLCβ proteins. Since high glucose has been reported to increase the levels of vasoactive peptides and oxidative stress, the present study was undertaken to investigate the implication of angiotensin II (Ang II), endothelin (ET)-1, and oxidative stress in the high glucose-induced enhanced expression of Gαq/11 and PLCβ proteins and associated signaling in A10 VSMCs. The levels of Gαq, Gα11, PLCβ-1, and PLCβ-2 proteins, as determined by Western blotting, were significantly higher in A10 VSMCs exposed to high glucose than in control cells. The elevated levels were restored to control values by the antioxidant diphenyleneiodonium (DPI), as well as by the antagonist of Ang II AT1 receptor losartan and the antagonists of ETA and ETB receptors BQ123 and BQ788, respectively. In addition, ET-1-stimulated production of inositol trisphosphate (IP3), which was enhanced by high glucose, was also restored toward control levels by DPI. Furthermore, the enhanced production of superoxide anion (O2–), increased NADPH oxidase activity, and enhanced expression of p22phox and p47phox proteins induced by high glucose were restored to control levels by losartan, BQ123, and BQ788. These results suggest that through increased oxidative stress, high glucose-induced enhanced levels of endogenous Ang II and ET-1 may contribute to the increased levels of Gαq/11 and mediated signaling in A10 VSMCs.

An analysis of high glucose and glucosamine-induced gene expression and oxidative stress in renal mesangial cells

2006 ◽  
Vol 112 (4-5) ◽  
pp. 189-218 ◽  
Author(s):  
Davis W. Cheng ◽  
Yan Jiang ◽  
Anath Shalev ◽  
Renu Kowluru ◽  
Errol D. Crook ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Gene Expression ◽  
High Glucose ◽  
Mesangial Cells ◽  
And Oxidative Stress

Berberine inhibits aldose reductase and oxidative stress in rat mesangial cells cultured under high glucose

2008 ◽  
Vol 475 (2) ◽  
pp. 128-134 ◽  
Author(s):  
Weihua Liu ◽  
Peiqinq Liu ◽  
Sha Tao ◽  
Yanhui Deng ◽  
Xuejuan Li ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Aldose Reductase ◽  
High Glucose ◽  
Mesangial Cells ◽  
And Oxidative Stress ◽  
Cells Cultured

scholarly journals Decorin inhibits glucose-induced lens epithelial cell apoptosis via suppressing p22phox-p38 MAPK signaling pathway

2019 ◽  
Author(s):  
Shanshan Du ◽  
Jingzhi Shao ◽  
Dandan Xie ◽  
Fengyan Zhang
Keyword(s):  
Oxidative Stress ◽  
Epithelial Cell ◽  
P38 Mapk ◽  
Stress Level ◽  
High Glucose ◽  
Lens Epithelial Cell ◽  
Human Lens ◽  
Oxidative Stress Level ◽  
And Oxidative Stress ◽  
Cataract Patients

AbstractPurposeTo determine the effect of decorin on oxidative stress and apoptosis of human lens epithelial (HLE) cells under high glucose condition.MethodsHLE cell line (HLEB3) was incubated in normal glucose (5.5 mM) or high glucose (60 mM) medium. Decorin (50 nM) was applied 2 hours before high glucose medium was added. Apoptosis detection was executed by flow cytometry and western blotting (analysis of bcl-2 and bax). Oxidative stress level was measured by the generation of reactive oxygen species (ROS), glutathione peroxidase (GSH) and superoxide dismutase (SOD). P38 mitogen-activated protein kinase (MAPK) phosphorylation, the expression of p22phox of HLE cells and human lens anterior capsules were detected by western blotting. Small interfering RNA transfection to p22phox and p38 MAPK was also carried out on HLEB3.ResultsHigh glucose caused HLE cells oxidative stress and apoptosis exhibiting the increase of apoptotic cells and ROS production and decrease of bcl-2/bax ratio, GSH/GSSG ration and SOD activity. P22phox and phospho-p38 MAPK were upregulated in high glucose treated HLEB3 cells. Knocking down p22phox or p38 by siRNAs can reduce high glucose induced cell apoptosis and oxidative stress level. Silencing p22phox by siRNA can downregulate p38 MAPK activation. Decorin can inhibit the apoptosis, oxidative stress level and the induction of p22phox and p-p38 of HLEB3 induced by high glucose. Furthermore, the expression of p22phox and p38 were found significantly increased in lens anterior capsules of diabetic cataract patients compared to that of normal age-related cataract patients.ConclusionsResults showed that p22phox-p38 pathway may be particepated in high glucose induced lens epithelial cell injury, decorin may inhibit the high glucose induced apoptosis and oxidative stress injury by suppressing this pathway in part.

scholarly journals Inactivation of TOPK Caused by Hyperglycemia Blocks Diabetic Heart Sensitivity to Sevoflurane Postconditioning by Impairing the PTEN/PI3K/Akt Signaling

2021 ◽  
Vol 2021 ◽  
pp. 1-18
Author(s):  
Sumin Gao ◽  
Rong Wang ◽  
Siwei Dong ◽  
Jing Wu ◽  
Bartłomiej Perek ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Protein Kinase ◽  
High Glucose ◽  
Ischemia Reperfusion ◽  
Akt Signaling ◽  
Cardioprotective Effect ◽  
Diabetic Heart ◽  
H9c2 Cells ◽  
Sevoflurane Postconditioning ◽  
And Oxidative Stress

The cardioprotective effect of sevoflurane postconditioning (SPostC) is lost in diabetes that is associated with cardiac phosphatase and tensin homologue on chromosome 10 (PTEN) activation and phosphoinositide 3-kinase (PI3K)/Akt inactivation. T-LAK cell-originated protein kinase (TOPK), a mitogen-activated protein kinase- (MAPKK-) like serine/threonine kinase, has been shown to inactivate PTEN (phosphorylated status), which in turn activates the PI3K/Akt signaling (phosphorylated status). However, the functions of TOPK and molecular mechanism underlying SPostC cardioprotection in nondiabetes but not in diabetes remain unknown. We presumed that SPostC exerts cardioprotective effects by activating PTEN/PI3K/Akt through TOPK in nondiabetes and that impairment of TOPK/PTEN/Akt blocks diabetic heart sensitivity to SPostC. We found that in the nondiabetic C57BL/6 mice, SPostC significantly attenuated postischemic infarct size, oxidative stress, and myocardial apoptosis that was accompanied with enhanced p-TOPK, p-PTEN, and p-Akt. These beneficial effects of SPostC were abolished by either TOPK kinase inhibitor HI-TOPK-032 or PI3K/Akt inhibitor LY294002. Similarly, SPostC remarkably attenuated hypoxia/reoxygenation-induced cardiomyocyte damage and oxidative stress accompanied with increased p-TOPK, p-PTEN, and p-Akt in H9c2 cells exposed to normal glucose, which were canceled by either TOPK inhibition or Akt inhibition. However, either in streptozotocin-induced diabetic mice or in H9c2 cells exposed to high glucose, the cardioprotective effect of SPostC was canceled, accompanied by increased oxidative stress, decreased TOPK phosphorylation, and impaired PTEN/PI3K/Akt signaling. In addition, TOPK overexpression restored posthypoxic p-PTEN and p-Akt and decreased cell death and oxidative stress in H9c2 cells exposed to high glucose, which was blocked by PI3K/Akt inhibition. In summary, SPostC prevented myocardial ischemia/reperfusion injury possibly through TOPK-mediated PTEN/PI3K/Akt activation and impaired activation of this signaling pathway may be responsible for the loss of SPostC cardioprotection by SPostC in diabetes.

scholarly journals Activation of TGR5 Partially Alleviates High Glucose-Induced Cardiomyocyte Injury by Inhibition of Inflammatory Responses and Oxidative Stress

2019 ◽  
Vol 2019 ◽  
pp. 1-11 ◽  
Author(s):  
Li Deng ◽  
Xuxin Chen ◽  
Yi Zhong ◽  
Xing Wen ◽  
Ying Cai ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Diabetic Cardiomyopathy ◽  
High Glucose ◽  
Inflammatory Responses ◽  
Inhibitory Effects ◽  
Rt Pcr ◽  
Hoechst 33342 ◽  
Selective Agonist ◽  
Cardioprotective Effects ◽  
And Oxidative Stress

High glucose- (HG-) induced cardiomyocyte injury is the leading cause of diabetic cardiomyopathy, which is associated with the induction of inflammatory responses and oxidative stress. TGR5 plays an important role in the regulation of glucose metabolism. However, whether TGR5 has cardioprotective effects against HG-induced cardiomyocyte injury is unknown. Neonatal mouse cardiomyocytes were isolated and incubated in a HG medium. Protein and mRNA expression was detected by western blotting and RT-PCR, respectively. Cell apoptosis was determined by Hoechst 33342 staining and flow cytometry. After treatment of cells with HG, TGR5-selective agonist INT-777 reduced the increase in expression of proinflammatory cytokines and NF-κB, whereas pretreatment of cells with TGR5 shRNA significantly reduced the inhibitory effects of INT-777. We also found that INT-777 increased the protein expression of Nrf2 and HO-1. In the presence of TGR5 shRNA, the expression of Nrf2 and HO-1 was reduced, indicating that TGR5 may exert an antioxidant effect partially through the Nrf2/HO-1 pathway. Furthermore, INT-777 treatment inhibited HG-induced ROS production and apoptosis that were attenuated in the presence of TGR5 shRNA or ZnPP (HO-1 inhibitor). Activation of TGR5 has cardioprotective effects against HG-induced cardiomyocyte injury and could be a pharmacological target for the treatment of diabetic cardiomyopathy.

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