scholarly journals Effect of Quamoclit angulata Extract Supplementation on Oxidative Stress and Inflammation on Hyperglycemia-Induced Renal Damage in Type 2 Diabetic Mice

Antioxidants ◽  
2020 ◽  
Vol 9 (6) ◽  
pp. 459 ◽  
Author(s):  
Ji Eun Park ◽  
Heaji Lee ◽  
Hyunkyung Rho ◽  
Seong Min Hong ◽  
Sun Yeou Kim ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Nlrp3 Inflammasome ◽  
High Fat Diet ◽  
Renal Damage ◽  
Model Assessment ◽  
Diabetic Mice ◽  
Homeostasis Model Assessment ◽  
And Oxidative Stress ◽  
Type 2 Diabetic

Type 2 diabetes mellitus (T2DM) is caused by abnormalities of controlling blood glucose and insulin homeostasis. Especially, hyperglycemia causes hyper-inflammation through activation of NLRP3 inflammasome, which can lead to cell apoptosis, hypertrophy, and fibrosis. Quamoclit angulata (QA), one of the annual winders, has been shown ameliorative effects on diabetes. The current study investigated whether the QA extract (QAE) attenuated hyperglycemia-induced renal inflammation related to NLRP inflammasome and oxidative stress in high fat diet (HFD)-induced diabetic mice. After T2DM was induced, the mice were treated with QAE (5 or 10 mg/kg/day) by gavage for 12 weeks. The QAE supplementation reduced homeostasis model assessment insulin resistance (HOMA-IR), kidney malfunction, and glomerular hypertrophy in T2DM. Moreover, the QAE treatment significantly attenuated renal NLRP3 inflammasome dependent hyper-inflammation and consequential renal damage caused by oxidative stress, apoptosis, and fibrosis in T2DM. Furthermore, QAE normalized aberrant energy metabolism (downregulation of p-AMPK, sirtuin (SIRT)-1, and PPARγ-coactivator α (PGC-1 α)) in T2DM mice. Taken together, the results suggested that QAE as a natural product has ameliorative effects on renal damage by regulation of oxidative stress and inflammation in T2DM.

scholarly journals Effect of endurance exercise on oxidative stress marker malondialdehyde in type 2 diabetic mice.

2020 ◽  
Vol 27 (07) ◽  
pp. 1493-1498
Author(s):  
Sana Akram ◽  
Maimona Tabssum ◽  
Maryam Rao ◽  
Hamid Javaid Qureshi
Keyword(s):  
Oxidative Stress ◽  
Body Weight ◽  
Endurance Exercise ◽  
High Fat Diet ◽  
Exercise Program ◽  
Oxidative Stress Marker ◽  
Diabetic Mice ◽  
High Fat ◽  
Type 2 Diabetic

Diabetes is associated with oxidative stress and has a significant role in the pathophysiology of the disease and its complications. Exercise training is a powerful therapeutic approach in diabetes and has protective effects against the progress of its complications. Objectives: The aim of this study was to investigate the effect of an endurance exercise program on the oxidative stress marker malondialdehyde (MDA) in high fat diet-low dose streptozotocin induced type 2 diabetic mouse model. Study Design: Randomized Control trial. Setting: Department of Physiology, Akhtar Saeed Medical and Dental College, Lahore. Period: August 2017 to August 2018. Material & Methods: 60 male albino mice were fed a high fat diet containing 60% kCal as fat for 4 weeks. This was followed by intra peritoneal injection of 40mg/kg body weight streptozotocin, given on three consecutive days. Mice with fasting blood glucose more than 250mg/dl after a week were considered diabetic. Half the mice underwent an exercise program which comprised of a 20 minute swimming session per day, with a 6% body weight load attached to the tail of mice, 3 days a week, for 4 weeks. The level of MDA was estimated in both groups using TBARs method. Results: Mean malondialdehyde level was significantly (p˂0.05) reduced in diabetic mice that underwent endurance exercise training. Conclusion: This study highlights the important role of endurance exercise in reducing oxidative stress in diabetes.

scholarly journals Aqueous Blackcurrant Extract Improves Insulin Sensitivity and Secretion and Modulates the Gut Microbiome in Non-Obese Type 2 Diabetic Rats

Antioxidants ◽  
2021 ◽  
Vol 10 (5) ◽  
pp. 756
Author(s):  
Hye-Jeong Yang ◽  
Ting Zhang ◽  
Xuan-Gao Wu ◽  
Min-Jung Kim ◽  
Young-Ho Kim ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Insulin Sensitivity ◽  
High Fat Diet ◽  
Control Group ◽  
High Fat ◽  
Β Cell ◽  
Α Diversity ◽  
And Oxidative Stress ◽  
Type 2 Diabetic

This study was undertaken to determine whether aqueous blackcurrant extracts (BC) improve glucose metabolism and gut microbiomes in non-obese type 2 diabetic animals fed a high-fat diet and to identify the mechanism involved. Partially pancreatectomized male Sprague–Dawley rats were provided a high-fat diet containing 0% (control), 0.2% (L-BC; low dosage), 0.6% (M-BC; medium dosage), and 1.8% (H-BC; high dosage) blackcurrant extracts; 0.2% metformin (positive-C); plus 1.8%, 1.6%, 1.2%, 0%, and 1.6% dextrin, specifically indigestible dextrin, daily for 8 weeks. Daily blackcurrant extract intakes were equivalent to 100, 300, and 900 mg/kg body weight (bw). After a 2 g glucose or maltose/kg bw challenge, serum glucose and insulin concentrations during peak and final states were obviously lower in the M-BC and H-BC groups than in the control group (p < 0.05). Intraperitoneal insulin tolerance testing showed that M-BC and H-BC improved insulin resistance. Hepatic triglyceride deposition, TNF-α expression, and malondialdehyde contents were lower in the M-BC and H-BC groups than in the control group. Improvements in insulin resistance in the M-BC and H-BC groups were associated with reduced inflammation and oxidative stress (p < 0.05). Hyperglycemic clamp testing showed that insulin secretion capacity increased in the acute phase (2 to 10 min) in the M-BC and H-BC groups and that insulin sensitivity in the hyperglycemic state was greater in these groups than in the control group (p < 0.05). Pancreatic β-cell mass was greater in the M-BC, H-BC, and positive-C groups than in the control group. Furthermore, β-cell proliferation appeared to be elevated and apoptosis was suppressed in these three groups (p < 0.05). Serum propionate and butyrate concentrations were higher in the M-BC and H-BC groups than in the control group. BC dose-dependently increased α-diversity of the gut microbiota and predicted the enhancement of oxidative phosphorylation-related microbiome genes and downregulation of carbohydrate digestion and absorption-related genes, as determined by PICRUSt2 analysis. In conclusion, BC enhanced insulin sensitivity and glucose-stimulated insulin secretion, which improved glucose homeostasis, and these improvements were associated with an incremental increase of the α-diversity of gut microbiota and suppressed inflammation and oxidative stress.

scholarly journals Exercise training improves endothelial function via adiponectin-dependent and independent pathways in type 2 diabetic mice

2011 ◽  
Vol 301 (2) ◽  
pp. H306-H314 ◽  
Author(s):  
Sewon Lee ◽  
Yoonjung Park ◽  
Kevin C. Dellsperger ◽  
Cuihua Zhang
Keyword(s):  
Oxidative Stress ◽  
Endothelial Dysfunction ◽  
Exercise Training ◽  
Endothelial Function ◽  
Protein Expression ◽  
Diabetic Mice ◽  
Ifn Γ ◽  
And Oxidative Stress ◽  
Type 2 Diabetic

Type 2 diabetes (T2D) is a leading risk factor for a variety of cardiovascular diseases including coronary heart disease and atherosclerosis. Exercise training (ET) has a beneficial effect on these disorders, but the basis for this effect is not fully understood. This study was designed to investigate whether the ET abates endothelial dysfunction in the aorta in T2D. Heterozygous controls (m Lepr db) and type 2 diabetic mice ( db/db; Lepr db) were either exercise entrained by forced treadmill exercise or remained sedentary for 10 wk. Ex vivo functional assessment of aortic rings showed that ET restored acetylcholine-induced endothelial-dependent vasodilation of diabetic mice. Although the protein expression of endothelial nitric oxide synthase did not increase, ET reduced both IFN-γ and superoxide production by inhibiting gp91phox protein levels. In addition, ET increased the expression of adiponectin (APN) and the antioxidant enzyme, SOD-1. To investigate whether these beneficial effects of ET are APN dependent, we used adiponectin knockout (APNKO) mice. Indeed, impaired endothelial-dependent vasodilation occurred in APNKO mice, suggesting that APN plays a central role in prevention of endothelial dysfunction. APNKO mice also showed increased protein expression of IFN-γ, gp91phox, and nitrotyrosine but protein expression of SOD-1 and -3 were comparable between wild-type and APNKO. These findings in the aorta imply that APN suppresses inflammation and oxidative stress in the aorta, but not SOD-1 and -3. Thus ET improves endothelial function in the aorta in T2D via both APN-dependent and independent pathways. This improvement is due to the effects of ET in inhibiting inflammation and oxidative stress (APN-dependent) as well as in improving antioxidant enzyme (APN-independent) performance in T2D.

scholarly journals Sporidiobolus pararoseuswall-broken powder ameliorates oxidative stress in diabetic nephropathy in type-2 diabetic mice by activating the Nrf2/ARE pathway

RSC Advances ◽  
2019 ◽  
Vol 9 (15) ◽  
pp. 8394-8403 ◽  
Author(s):  
Yuliang Cheng ◽  
Chang Liu ◽  
Yan Cui ◽  
Tianqi Lv ◽  
Yahui Guo ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Diabetic Nephropathy ◽  
High Fat Diet ◽  
Rich Source ◽  
Diabetic Mice ◽  
High Fat ◽  
Type 2 Diabetic ◽  
Β Carotene

STZ-induced diabetic mice are given a high-fat diet and SPP, which is a rich source of β-carotene, γ-carotene, torulene and torularhodin. The result indicated SPP can ameliorate diabetic nephropathyviaactivating Nrf2/ARE pathway.

scholarly journals Effect of Pterostilbene on cardiac oxidative stress on high-fat diet-fed and Streptozotocin-induced type 2 diabetic mice

2019 ◽  
Vol 5 (4) ◽  
pp. 827-833
Author(s):  
Gunaseelan Thangasamy ◽  
Leelavinothan Pari ◽  
Paari Ellappan ◽  
Kannan Duraisamy
Keyword(s):  
Oxidative Stress ◽  
High Fat Diet ◽  
Diabetic Mice ◽  
High Fat ◽  
Type 2 Diabetic

scholarly journals Rap1a Overlaps the AGE/RAGE Signaling Cascade to Alter Expression of α-SMA, p-NF-κB, and p-PKC-ζ in Cardiac Fibroblasts Isolated from Type 2 Diabetic Mice

Cells ◽  
2021 ◽  
Vol 10 (3) ◽  
pp. 557
Author(s):  
Stephanie D. Burr ◽  
James A. Stewart
Keyword(s):  
Oxidative Stress ◽  
Heart Failure ◽  
Hydrogen Peroxide ◽  
Cardiac Fibroblasts ◽  
The Body ◽  
Signaling Cascade ◽  
Diabetic Mice ◽  
Pkc Ζ ◽  
Type 2 Diabetic

Cardiovascular disease, specifically heart failure, is a common complication for individuals with type 2 diabetes mellitus. Heart failure can arise with stiffening of the left ventricle, which can be caused by “active” cardiac fibroblasts (i.e., myofibroblasts) remodeling the extracellular matrix (ECM). Differentiation of fibroblasts to myofibroblasts has been demonstrated to be an outcome of AGE/RAGE signaling. Hyperglycemia causes advanced glycated end products (AGEs) to accumulate within the body, and this process is greatly accelerated under chronic diabetic conditions. AGEs can bind and activate their receptor (RAGE) to trigger multiple downstream outcomes, such as altering ECM remodeling, inflammation, and oxidative stress. Previously, our lab has identified a small GTPase, Rap1a, that possibly overlaps the AGE/RAGE signaling cascade to affect the downstream outcomes. Rap1a acts as a molecular switch connecting extracellular signals to intracellular responses. Therefore, we hypothesized that Rap1a crosses the AGE/RAGE cascade to alter the expression of AGE/RAGE associated signaling proteins in cardiac fibroblasts in type 2 diabetic mice. To delineate this cascade, we used genetically different cardiac fibroblasts from non-diabetic, diabetic, non-diabetic RAGE knockout, diabetic RAGE knockout, and Rap1a knockout mice and treated them with pharmacological modifiers (exogenous AGEs, EPAC, Rap1a siRNA, and pseudosubstrate PKC-ζ). We examined changes in expression of proteins implicated as markers for myofibroblasts (α-SMA) and inflammation/oxidative stress (NF-κB and SOD-1). In addition, oxidative stress was also assessed by measuring hydrogen peroxide concentration. Our results indicated that Rap1a connects to the AGE/RAGE cascade to promote and maintain α-SMA expression in cardiac fibroblasts. Moreover, Rap1a, in conjunction with activation of the AGE/RAGE cascade, increased NF-κB expression as well as hydrogen peroxide concentration, indicating a possible oxidative stress response. Additionally, knocking down Rap1a expression resulted in an increase in SOD-1 expression suggesting that Rap1a can affect oxidative stress markers independently of the AGE/RAGE signaling cascade. These results demonstrated that Rap1a contributes to the myofibroblast population within the heart via AGE/RAGE signaling as well as promotes possible oxidative stress. This study offers a new potential therapeutic target that could possibly reduce the risk for developing diabetic cardiovascular complications attributed to AGE/RAGE signaling.

scholarly journals Soy Milk Consumption, Inflammation, Coagulation, and Oxidative Stress Among Type 2 Diabetic Patients With Nephropathy

Diabetes Care ◽  
2012 ◽  
Vol 35 (10) ◽  
pp. 1981-1985 ◽  
Author(s):  
M. S. Miraghajani ◽  
A. Esmaillzadeh ◽  
M. M. Najafabadi ◽  
M. Mirlohi ◽  
L. Azadbakht
Keyword(s):  
Oxidative Stress ◽  
Diabetic Patients ◽  
Milk Consumption ◽  
Soy Milk ◽  
Type 2 Diabetic Patients ◽  
And Oxidative Stress ◽  
Type 2 Diabetic
Sign in / Sign up

Export Citation Format

Share Document