scholarly journals Proanthocyanidin Attenuation of Oxidative Stress and NF-κB Protects Apolipoprotein E-Deficient Mice against Diabetic Nephropathy

2013 ◽  
Vol 2013 ◽  
pp. 1-8 ◽  
Author(s):  
Abdulrahman L. Al-Malki ◽  
Ahmed Amir Radwan Sayed ◽  
Haddad A. El Rabey
Keyword(s):  
Oxidative Stress ◽  
Diabetic Nephropathy ◽  
Apolipoprotein E ◽  
High Fat Diet ◽  
Diabetic Mice ◽  
High Cholesterol ◽  
Beneficial Effects ◽  
Cholesterol Levels ◽  
Reduced Activity ◽  
Deficient Mice

Hyperlipidemia and hyperglycemia result in oxidative stress and play a major role in the development of diabetic nephropathy (DN). We explored the effects of proanthocyanidin (PA) on the induction and progression of DN in apolipoprotein E-deficient mice. Diabetes Mellitus was induced in ten-week-old male apoE−/−mice using streptozotocin (STZ). Mice were fed with a high-fat diet in presence or absence of PA. PA treatment significantly reduced the high cholesterol levels, restored renal functions, and reduced albuminuria in the PA-treated diabetic mice compared with the diabetic untreated mice. In addition, the glomerular mesangial expansion in the diabetic mice was attenuated as a result of PA supplementation. Moreover, PA treatment restored the elevated levels of MDA and CML and the reduced activity of SOD and GSH in the diabetic mice. Furthermore, PA feeding reduced the activation and translocation of NF-κB to the nucleus compared with the diabetic untreated animals. Reduction of NF-κB activation resulted in the attenuation of the expression of IL-6, TGFβ, and RAGE which protected PA-treated mice against DN. The renoprotective effects of PA were found to be time independent regardless of whether the dietary feeding with PA was started pre-, co-, or post-STZ injection. In conclusion, part of the beneficial effects of PA includes the disruption of the detrimental AGE-RAGE-NFκB pathways.

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.

Anti-atherosclerotic effect of housefly (Musca domestica) maggot-derived protein-enriched extracts by dampened oxidative stress in apolipoprotein E-deficient mice

RSC Advances ◽  
2016 ◽  
Vol 6 (107) ◽  
pp. 105363-105370 ◽  
Author(s):  
Xiao Mingzhu ◽  
Jin Xiaobao ◽  
Tang Futian ◽  
Wang Lijing ◽  
Mao Jianwen ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Apolipoprotein E ◽  
Musca Domestica ◽  
Developed Countries ◽  
Morbidity And Mortality ◽  
Deficient Mice

Despitemany therapeutic advances, atherosclerosis remains the leading cause of morbidity and mortality in developed countries.

scholarly journals Effects of atorvastatin and/or probucol on recovery of atherosclerosis in high-fat-diet-fed apolipoprotein E–deficient mice

2019 ◽  
Vol 109 ◽  
pp. 1445-1453 ◽  
Author(s):  
Xiaokun Guo ◽  
Lin Wang ◽  
Xiaoshuang Xia ◽  
Peilu Wang ◽  
Xin Li
Keyword(s):  
Apolipoprotein E ◽  
High Fat Diet ◽  
High Fat ◽  
Deficient Mice

scholarly journals Absence of 12/15 Lipoxygenase Reduces Brain Oxidative Stress in Apolipoprotein E-Deficient Mice

2005 ◽  
Vol 167 (5) ◽  
pp. 1371-1377 ◽  
Author(s):  
Cinzia M. Chinnici ◽  
Yuemang Yao ◽  
Tao Ding ◽  
Colin D. Funk ◽  
Domenico Praticò
Keyword(s):  
Oxidative Stress ◽  
Apolipoprotein E ◽  
Brain Oxidative Stress ◽  
Deficient Mice

scholarly journals Chronic iron overload intensifies atherosclerosis in apolipoprotein E deficient mice: Role of oxidative stress and endothelial dysfunction

Life Sciences ◽  
2019 ◽  
Vol 233 ◽  
pp. 116702 ◽  
Author(s):  
Vinícius Bermond Marques ◽  
Marcos André Soares Leal ◽  
Jandinay Gonzaga Alexandre Mageski ◽  
Helbert Gabriel Fidelis ◽  
Breno Valentim Nogueira ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Endothelial Dysfunction ◽  
Iron Overload ◽  
Apolipoprotein E ◽  
Deficient Mice

P0983INHIBITION OF ATF3 BY RAF INHIBITOR GW5074 ON DIABETIC NEPHROPATHY

2020 ◽  
Vol 35 (Supplement_3) ◽  
Author(s):  
Jee Young Han ◽  
Jin Joo Cha ◽  
Young Sun Kang ◽  
Jung Yeon Ghee ◽  
Ji Ae Yoo ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Transcription Factor ◽  
Diabetic Nephropathy ◽  
High Glucose ◽  
Kinase Inhibitor ◽  
Protective Role ◽  
Activating Transcription Factor 3 ◽  
Diabetic Mice ◽  
Mice Model ◽  
Gene Expressions

Abstract Background and Aims Activating Transcription Factor 3 (ATF3) is a stress-adaptive transcription factor, which has been suggested to be involved in maintaining glucose homeostasis. ATF3 respond rapidly to various stimuli like high glucose, fatty acids and oxidative stress, and is observed to either protective or detrimental effects in diabetic condition. Therefore to elucidate the exact role in diabetic nephropathy of ATF3, we investigated the role of ATF3 by inhibition with Raf-inhibitor GW5047 on diabetic mice model. Method ATF3 level was examined in the mouse podocytes and NRK cells with either overexpression or downregulation with ATF3. 8 week db/m and db/db mice as the model of diabetic mice were examined for the expression of ATF3 and were treated with GW5074, a Raf1 kinase inhibitor targeting the ATF3 intraperitoneally with a dose of 0.5mg/kg for 12 weeks. Results In cultured mouse podocytes and NRK cells, high glucose and angiotensin II markedly increased ATF3 expression. Gene Expressions of NOX4, MCP-1 and NF-kB were augmented by ATF3, and were attenuated by ATF3 siRNA. In db/db mice, plasma ATF3 level was not different from control db/m, however the urinary ATF3 excretion was significantly higher. Treatment of GW5074 decreased urinary ATF3 excretion. After 12 week treatment, serum creatinine level was significantly lower in the treatment db/db group, with less systemic oxidative stress. There were no significant differences in body weight, whereas the food intake was decreased in GW5047 group. Overall lipid profile or HOMA-IR, HbA1c level was not different from each group. Serum adiponectin were otherwise increased in GW5074 group. Urinary excretion of albumin at 2 month of treatment decreased with urinary nephrin excretion. Trend of increased gene expression of JNK, p-38, smad2, ERK which was downregulated by GW5074 was noted. Conclusion These findings suggest that in diabetic condition, the activation of ATF3 is associated pathogenesis of diabetic nephropathy and targeting ATF3 may have a protective role in the disease progression.

scholarly journals The Endogenous Estradiol Metabolite 2-Methoxyestradiol Reduces Atherosclerotic Lesion Formation in Female Apolipoprotein E-Deficient Mice

Endocrinology ◽  
2007 ◽  
Vol 148 (9) ◽  
pp. 4128-4132 ◽  
Author(s):  
Johan Bourghardt ◽  
Göran Bergström ◽  
Alexandra Krettek ◽  
Sara Sjöberg ◽  
Jan Borén ◽  
...  
Keyword(s):  
Apolipoprotein E ◽  
Low Dose ◽  
Hormone Replacement ◽  
Atherosclerotic Lesion ◽  
Total Serum ◽  
High Dose ◽  
Lesion Formation ◽  
Cholesterol Levels ◽  
Deficient Mice ◽  
Atherosclerotic Lesion Formation

Estradiol, the major endogenous estrogen, reduces experimental atherosclerosis and metabolizes to 2-methoxyestradiol in vascular cells. Currently undergoing evaluation in clinical cancer trials, 2-methoxyestradiol potently inhibits cell proliferation independently of the classical estrogen receptors. This study examined whether 2-methoxyestradiol affects atherosclerosis development in female mice. Apolipoprotein E-deficient mice, a well-established mouse model of atherosclerosis, were ovariectomized and treated through slow-release pellets with placebo, 17β-estradiol (6 μg/d), or 2-methoxyestradiol [6.66 μg/d (low-dose) or 66.6 μg/d (high-dose)]. After 90 d, body weight gain decreased and uterine weight increased in the high-dose but not low-dose 2-methoxyestradiol group. En face analysis showed that the fractional area of the aorta covered by atherosclerotic lesions decreased in the high-dose 2-methoxyestradiol (52%) but not in the low-dose 2-methoxyestradiol group. Total serum cholesterol levels decreased in the high- and low-dose 2-methoxyestradiol groups (19%, P < 0.05 and 21%, P = 0.062, respectively). Estradiol treatment reduced the fractional atherosclerotic lesion area (85%) and decreased cholesterol levels (42%). In conclusion, our study shows for the first time that 2-methoxyestradiol reduces atherosclerotic lesion formation in vivo. The antiatherogenic activity of an estradiol metabolite lacking estrogen receptor activating capacity may argue that trials on cardiovascular effects of hormone replacement therapy should use estradiol rather than other estrogens. Future research should define the role of 2-methoxyestradiol as a mediator of the antiatherosclerotic actions of estradiol. Furthermore, evaluation of the effects of 2-methoxyestradiol on cardiovascular disease endpoints in ongoing clinical trials is of great interest.

scholarly journals Pycnogenol® Induces Browning of White Adipose Tissue through the PKA Signaling Pathway in Apolipoprotein E-Deficient Mice

2018 ◽  
Vol 2018 ◽  
pp. 1-11 ◽  
Author(s):  
Huiying Cong ◽  
Wenxia Zhong ◽  
Yiying Wang ◽  
Shoichiro Ikuyama ◽  
Bin Fan ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Apolipoprotein E ◽  
Signaling Pathway ◽  
White Adipose Tissue ◽  
High Fat Diet ◽  
Mrna Level ◽  
Antioxidant Properties ◽  
Expression Of Genes ◽  
Beige Adipocytes ◽  
Deficient Mice

Beige adipocytes in white adipose tissue (WAT) have received considerable recognition because of their potential protective effect against obesity. Pycnogenol (PYC), extracted from French maritime pine bark, has anti-inflammatory and antioxidant properties and can improve lipid profiles. However, the effect of PYC on obesity has never been explored. In this study, we investigated the effects of PYC on obesity and WAT browning in apolipoprotein E- (ApoE-) deficient mice. The results showed that PYC treatment clearly reversed body weight and the mass of eWAT gain resulting from a high-cholesterol and high-fat diet (HCD), but no difference in food intake. The morphology results showed that the size of the adipocytes in the PYC-treated mice was obviously smaller than that in the HCD-fed mice. Next, we found that PYC upregulated the expression of genes related to lipolysis (ATGL and HSL), while it decreased the mRNA level of PLIN1. PYC significantly increased the expression of UCP1 and other genes related to beige adipogenesis. Additionally, PYC increased the expression of proteins related to the protein kinase A (PKA) signaling pathway. The findings suggested that PYC decreased obesity by promoting lipolysis and WAT browning. Thus, PYC may be a novel therapeutic target for obesity.

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