scholarly journals The Potency of Trigona’s Propolis Extract as Reactive Oxygen Species Inhibitor in Diabetic Mice

2015 ◽  
Vol 47 (3) ◽  
pp. 261-268
Author(s):  
Ahmad Ridwan ◽  
Ayu Nirmala Sari ◽  
Ramadhani Eka Putra
Keyword(s):  
Reactive Oxygen Species ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Diabetic Mice ◽  
Propolis Extract ◽  
Reactive Oxygen Species Inhibitor

Abstract 070: Canonical Wnt Signaling Mediates Enhanced Renal Afferent Arteriolar Reactive Oxygen Species and Contractility in Diabetic Mice

Hypertension ◽  
2017 ◽  
Vol 70 (suppl_1) ◽  
Author(s):  
En Yin Lai ◽  
Suping Zhang ◽  
Qian Huang ◽  
Qiaoling Wang ◽  
Liang Zhao ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Wnt Signaling ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Diabetic Mice ◽  
Canonical Wnt Signaling ◽  
Protein Expressions ◽  
Afferent Arterioles ◽  
Gsk 3Β ◽  
Canonical Wnt

Background: Canonical Wnt signaling is involved in oxidative stress and diabetes but its role in diabetic renal microvascular dysfunction is unclear. We tested the hypothesis that enhanced canonical Wnt signaling in renal afferent arterioles from diabetic mice increases reactive oxygen species (ROS) and contractions to endothelin-1 (ET-1). Methods: Diabetic or control C57Bl/6 mice received vehicle or sulindac (40 mg·kg -1 ·day -1 ) to block canonical Wnt signaling for 4 weeks. ET-1 contractions were measured in diameter changes and H 2 O 2 and O 2 .- by fluorescence microscopy. Arteriolar protein expression and enzymatic activity were examined by standard methods. Results: Compared to control, diabetic mouse afferent arteriole had significantly increased O 2 .- (+84%) and H 2 O 2 (+91%) and enhanced sensitivity to ET-1 at 10 -8 mol·l -1 (-72±4% versus -43±4%, P<0.05) accompanied by significantly (P<0.005) reduced protein expressions and activities for catalase and superoxide dismutase 2 (SOD2). Incubation of afferent arterioles from normal or diabetic mice with PEG-SOD reduced responses to ET-1 whereas incubation with PEG-catalase reduced sensitivity to ET-1 selectively in arterioles from diabetic mice. The arteriolar protein expressions for canonical Wnt signaling indicated overactivation of this pathway in diabetic mice (2.6-fold increase in p-GSK-3β/GSK-3β and 3.3-fold decrease in p-β-catenin/β-catenin). Sulindac given to diabetic mice normalized the canonical Wnt signaling protein and arteriolar O 2 .- , H 2 O 2 and ET-1 contractions while doubling (P<0.05) microvascular catalase and SOD2. Conclusions: Increased ROS, notably H 2 O 2 , mediated by canonical Wnt signaling contributes to enhanced afferent arteriolar sensitivity to ET-1 in diabetes. Thus, antioxidant pharmacological strategies targeting canonical Wnt signaling may improve vascular function in diabetic nephropathy.

scholarly journals Mitochondria-Targeted Antioxidant SkQ1 Improves Dermal Wound Healing in Genetically Diabetic Mice

2017 ◽  
Vol 2017 ◽  
pp. 1-10 ◽  
Author(s):  
Ilya A. Demyanenko ◽  
Vlada V. Zakharova ◽  
Olga P. Ilyinskaya ◽  
Tamara V. Vasilieva ◽  
Artem V. Fedorov ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Wound Healing ◽  
Smooth Muscle Actin ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Diabetic Mice ◽  
Mitochondrial Reactive Oxygen Species ◽  
Genetically Diabetic Mice

Oxidative stress is widely recognized as an important factor in the delayed wound healing in diabetes. However, the role of mitochondrial reactive oxygen species in this process is unknown. It was assumed that mitochondrial reactive oxygen species are involved in many wound-healing processes in both diabetic humans and animals. We have applied the mitochondria-targeted antioxidant 10-(6′-plastoquinonyl)decyltriphenylphosphonium (SkQ1) to explore the role of mitochondrial reactive oxygen species in the wound healing of genetically diabetic mice. Healing of full-thickness excisional dermal wounds in diabetic C57BL/KsJ-db−/db− mice was significantly enhanced after long-term (12 weeks) administration of SkQ1. SkQ1 accelerated wound closure and stimulated epithelization, granulation tissue formation, and vascularization. On the 7th day after wounding, SkQ1 treatment increased the number of α-smooth muscle actin-positive cells (myofibroblasts), reduced the number of neutrophils, and increased macrophage infiltration. SkQ1 lowered lipid peroxidation level but did not change the level of the circulatory IL-6 and TNF. SkQ1 pretreatment also stimulated cell migration in a scratch-wound assay in vitro under hyperglycemic condition. Thus, a mitochondria-targeted antioxidant normalized both inflammatory and regenerative phases of wound healing in diabetic mice. Our results pointed to nearly all the major steps of wound healing as the target of excessive mitochondrial reactive oxygen species production in type II diabetes.

Ameliorative effect of quercetin nanorods on diabetic mice: mechanistic and therapeutic strategies

RSC Advances ◽  
2016 ◽  
Vol 6 (60) ◽  
pp. 55092-55103 ◽  
Author(s):  
Md. Maroof Alam ◽  
K. M. Abdullah ◽  
Braj Raj Singh ◽  
Alim Hussain Naqvi ◽  
Imrana Naseem
Keyword(s):  
Reactive Oxygen Species ◽  
Reactive Oxygen ◽  
Therapeutic Strategies ◽  
Oxygen Species ◽  
Diabetic Mice ◽  
Polyphenolic Compound ◽  
Chemical Action ◽  
Ameliorative Effect

Quercetin is a natural polyphenolic compound that acts as a strong antioxidant for reactive oxygen species (ROS) generated by any physical or chemical action.

scholarly journals Nicotine worsens the severity of nephropathy in diabetic mice: implications for the progression of kidney disease in smokers

2010 ◽  
Vol 299 (4) ◽  
pp. F732-F739 ◽  
Author(s):  
Ping Hua ◽  
Wenguang Feng ◽  
Shaonin Ji ◽  
Leopoldo Raij ◽  
Edgar A. Jaimes
Keyword(s):  
Blood Pressure ◽  
Reactive Oxygen Species ◽  
Diabetic Nephropathy ◽  
Kidney Disease ◽  
Renal Injury ◽  
Reactive Oxygen ◽  
Acute Glomerulonephritis ◽  
Oxygen Species ◽  
Diabetic Mice ◽  
Mesangial Area

Epidemiological studies have established the role of cigarette smoking as a risk factor in the progression of chronic kidney disease, including diabetic nephropathy. We have previously reported that nicotine promotes mesangial cell proliferation and hypertrophy via activation of nonneuronal nicotinic acetylcholine receptors and that nicotine worsens renal injury in a model of acute glomerulonephritis (Jaimes E, Tian RX, Raij L. Am J Physiol Heart Circ Physiol 292: H76–H82, 2007; Jaimes EA, Tian RX, Joshi M, Raij L. Am J Nephrol 29: 319–326, 2009). These studies were designed to test the hypothesis that nicotine worsens renal injury in db/db mice, a well-established model of diabetic nephropathy, and that reactive oxygen species play an important as mediators of these effects. For these studies, nicotine (100 μg/ml) was administered in the drinking water to control and db/db mice for 10 wk. Blood pressure was measured by the tail-cuff method, and urine was collected for proteinuria. At death, kidneys were collected for histology and molecular biology. The administration of nicotine did not result in significant changes in blood pressure or blood glucose and resulted in cotinine levels similar to those found in the plasma of smokers. In diabetic mice, the administration of nicotine significantly increased urinary protein excretion (1-fold), glomerular hypertrophy, and mesangial area (∼20%). These changes were accompanied by significant increases in NADPH oxidase 4 (∼30%) and increased nitrotyrosine and Akt expression. In vitro, we determined that nicotine has additive effects to high glucose on reactive oxygen species generation and Akt phosphorylation in human mesangial cells. These findings unveil novel mechanisms that may result in the development of novel strategies in the treatment and prevention of diabetic nephropathy in smokers.

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