scholarly journals Curcumin is a Potential Adjuvant to Alleviates Diabetic Retinal Injury via Reducing Oxidative Stress and Maintaining Nrf2 Pathway Homeostasis

2021 ◽  
Vol 12 ◽  
Author(s):  
Ting Xie ◽  
Xiaodong Chen ◽  
Wenyi Chen ◽  
Sien Huang ◽  
Xinye Peng ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Early Stage ◽  
Therapeutic Option ◽  
Combined Therapy ◽  
Diabetic Rats ◽  
Receptor Interaction ◽  
Therapeutic Effects ◽  
Hydrogen Atoms ◽  
Nrf2 Pathway ◽  
Retinal Injury

Curcumin is a natural polyphenol compound with anti-diabetic, anti-oxidative, and anti-inflammatory effects. Although many studies have reported the protective effect of curcumin in diabetes mellitus or diabetic nephropathy, there is a lack of research on curcumin in diabetic retinopathy. The purpose of this study was to investigate the therapeutic effects of curcumin on the diabetic retinal injury. Streptozotocin (STZ)-induced diabetic rats (60, n = 12 each) were respectively given curcumin orally (200 mg/kg/day), insulin subcutaneously (4–6 IU/day), and combined therapy with curcumin and insulin for 4 weeks. Retinal histopathological changes, oxidative stress markers, and transcriptome profiles from each group were observed. Curcumin, insulin, or combination therapy significantly reduced blood glucose, alleviated oxidative stress, and improved pathological damage in diabetic rats. Curcumin not only significantly reduced retinal edema but also had a better anti-photoreceptor apoptosis effect than insulin. In the early stage of diabetes, the enhancement of oxidative stress in the retina induced the adaptive activation of the nuclear factor E2-associated factor 2 (Nrf2) pathway. Treatment of curcumin alleviated the compensatory activation of the Nrf2 pathway induced by oxidative stress, by virtue of its antioxidant ability to transfer hydrogen atoms to free radicals. When curcumin combined with insulin, the effect of maintaining Nrf2 pathway homeostasis in diabetic rats was better than that of insulin alone. Transcriptomic analyses revealed that curcumin either alone, or combined with insulin, inhibited the AGE-RAGE signaling pathway and the extracellular matrix (ECM)-receptor interaction in the diabetic retina. Thus, at the early stage of diabetes, curcumin can be used to alleviate diabetic retinal injury through its anti-oxidative effect. If taking curcumin as a potential complementary therapeutic option in combination with antihyperglycemic agents, which would lead to more effective therapeutic outcomes against diabetic complications.

scholarly journals TBHQ Regulates the Nrf2/HO-1 Pathway to Enhance Stem Cell Treatment of Diabetic Retinopathy

2021 ◽  
Author(s):  
Ze-Peng XU ◽  
Ni TIAN ◽  
Song-Tiao LI ◽  
Kun-Meng LI ◽  
Xiao-Yu WANG ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Diabetic Retinopathy ◽  
Therapeutic Effect ◽  
Biological Effects ◽  
Combined Therapy ◽  
Diabetic Rats ◽  
Inflammatory Factors ◽  
Diabetic Rat ◽  
Human Umbilical Cord ◽  
Therapeutic Effects

Abstract Objective: To investigate the therapeutic effect of human umbilical cord mesenchymal stem cells (hUCMSCs) on diabetic retinopathy (DR) in diabetic rats, and to study the mechanism of hUCMSCs in treating diabetic retinopathy by tert-butylhydroquinone (tBHQ) regulation of the Nrf2/HO-1 pathway.Methods: The diabetic rat model was induced by intraperitoneal injection of streptozotocin (STZ). The experimental animals were divided into six groups: Normal, diabetes mellitus (DM), hUCMSCs, tBHQ, combined tBHQ-hUCMSCs, and all-trans-retinoid acid (ATRA)-hUCMSCs combined group. Visual function experiments and histological analyses were performed eight weeks post intravitreal injection. Biochemical and molecular analyses were used to assess the hUCMSCs composition and its biological effects.Results: Improvements in systemic oxidative stress and inflammation were found in the tBHQ group. Although hUCMSCs had no significant effect on oxidative stress, retinal structure was improved, visual defects reduced and expression of local retinal inflammatory factors were inhibited following its application. The effect of combined therapy was better than that of single therapy. Inhibition of the Nrf2/HO-1 pathway can promote the expression of systemic inflammatory factors and inhibit the therapeutic effect of hUCMSCs in the retina.Conclusions: Intravitreal administration of hUCMSCs triggers an effective cytoprotective microenvironment in the retina of diabetic mice. Alone, however, it may not significantly improve the systemic inflammatory response of diabetes. In combination with tBHQ it may promote Nrf2expression, systemic antioxidant stress and therapeutic effects of hUCMSCs.

scholarly journals Spirulina maxima and its effect on antioxidant activity in fructose induced oxidative stress with histopathological observations

2015 ◽  
Vol 62 (2) ◽  
pp. 13-19
Author(s):  
Urmila Jarouliya ◽  
Anish Zacharia ◽  
Raj K. Keservani ◽  
Godavarthi B.K.S Prasad
Keyword(s):  
Oxidative Stress ◽  
Antioxidant Activity ◽  
Superoxide Dismutase ◽  
Blood Glucose ◽  
Reduced Glutathione ◽  
Thiobarbituric Acid ◽  
Diabetic Rats ◽  
Therapeutic Effects ◽  
Thiobarbituric Acid Reactive Substances ◽  
Spirulina Maxima

Abstract Diabetes mellitus is a metabolic disorder characterised by hyperglycemia and oxidative stress. The aim of the present study is to explore the antioxidant effect of Spirulina maxima in rat model along with the histopathological observations. Diabetes was induced by feeding 10% fructose solution orally to Wistar rats (n = 6) for 30 days, analysed for plasma blood glucose and the markers of the oxidative stress [catalase (CAT), superoxide dismutase (SOD), reduced glutathione (GSH) and thiobarbituric acid reactive substances (TBARS)]. These biochemical studies were associated with histopathological examination of liver and kidney sections. The microalga Spirulina maxima being rich in proteins and other essential nutrients is widely used as a food supplement. S. maxima at a dose of 5 and 10% per kg and the metformin (500 mg/kg) as reference drug were given orally for 30 days to the diabetic rats. Diabetic rats showed significant (p < 0.001) elevations in plasma blood glucose, thiobarbituric acid-reactive substances and significant reduction in catalase, superoxide dismutase and reduced glutathione activity. Oral administration of 5 and 10% aqueous extract of S. maxima for 30 days restored not only of blood glucose levels but also markers of oxidative stress. Histopathological observations of tissues manifested that the S. maxima administration had the protective and therapeutic effects against fructose-induced abnormalities in diabetic rats. It is concluded that S. maxima is effective in reinstating the antioxidant activity in addition to its antidiabetic effect in type 2 diabetic rats.

scholarly journals Oxidative stress is associated with the aortic change in early stage type II diabetic rats

2000 ◽  
Vol 82 ◽  
pp. 66
Author(s):  
Toshiki Fukui ◽  
Takahisa Noma ◽  
Matlubur Rahman ◽  
Run-Xia Tian ◽  
Yasuharu Aki ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Early Stage ◽  
Diabetic Rats ◽  
Type Ii

Dietary troglitazone decreases oxidative stress in early stage type II diabetic rats

Life Sciences ◽  
2000 ◽  
Vol 66 (21) ◽  
pp. 2043-2049 ◽  
Author(s):  
Toshiki Fukui ◽  
Takahisa Noma ◽  
Katsufumi Mizushige ◽  
Yauharu Aki ◽  
Shoji Kimura ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Early Stage ◽  
Diabetic Rats ◽  
Type Ii

scholarly journals P0991EFFECTS OF TRIGONELLA FOENUM GRAECUM AND SODIUM ORTHOVANADATE ON ALTERED RENAL MEMBRANE FUNCTIONS IN ALLOXAN DIABETIC RATS

2020 ◽  
Vol 35 (Supplement_3) ◽  
Author(s):  
Pardeep Kumar ◽  
Najma Baquer
Keyword(s):  
Oxidative Stress ◽  
Blood Glucose ◽  
Glucose Transporter ◽  
Combined Therapy ◽  
Renin Angiotensin System ◽  
Polyol Pathway ◽  
Diabetic Rats ◽  
Sodium Orthovanadate ◽  
High Blood Glucose ◽  
Trigonella Foenum Graecum

Abstract Background and Aims The present study was carried out to observe, the antihyperglycemic and renoprotective effect of sodium orthovanadate (SOV) and Trigonella foenum graecum seed powder (TSP) administration on blood glucose, renal functions, expression of glucose transporter, DNA fragmentation, inflammatory cytokines and oxidative stress markers in kidney tissues and to see whether the treatment with SOV and TSP was capable of reversing the diabetic effects. Method Diabetes was induced by administration of alloxan monohydrate (15 mg/100 g body weight.) and rats were treated with 2 IU insulin, 0.6mg/ml SOV, 5% TSP in the diet and a combination of 0.2 mg/ml SOV and 5% TSP separately for three weeks. Renal damage was assessed by measuring proteinuria, enzymuria, expression of glucose transporters, renin-angiotensin system, and activities of polyol pathway enzymes. Results Diabetic rats showed hyperglycemia with almost four fold high blood glucose levels. Activity of Na+K+ATPase decreased in diabetic kidney. Diabetic rats exhibited an increased level of lipid peroxidation, intracellular Ca2+ levels, and decreased membrane fluidity. Combined therapy of lower dose of SOV with TSP significantly reduced metabolites of polyol pathway, oxidative stress, nitric oxide, and N-acetyl-β-d-glucosaminidase activity with glucose transporter in kidney of alloxan diabetic rats. Markers of podocyte damage in kidney (nephrin, podocin, and podocalyxin) and their urinary excretion were normalized along with downregulation of the expression of kidney injury molecule-1 by SOV and TSP treatment. TSP treatment alone is partially effective in restoring the above diabetes induced alterations. Dietary combined SOV and TSP effectively countered the diabetes-induced structural abnormalities of renal tissue. Conclusion Our results showed that lower doses of SOV (0.2mg/ml) could be used in combination with TSP to effectively in normalization of altered metabolic parameters and membrane linked enzymes without any harmful side effect and renoprotective actions.

Dimethyl Fumarate is a Potential Therapeutic Option for Alzheimer’s Disease

2021 ◽  
pp. 1-14
Author(s):  
Xiaodi Sun ◽  
Xinjun Suo ◽  
Xianyou Xia ◽  
Chunshui Yu ◽  
Yan Dou
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Antioxidant Enzymes ◽  
Therapeutic Option ◽  
Amyloid Β ◽  
Dimethyl Fumarate ◽  
Therapeutic Effects ◽  
Embryonic Mouse ◽  
Nrf2 Pathway ◽  
Anti Inflammatory

Background: Dimethyl fumarate (DMF) has been approved for clinical treatment of multiple sclerosis based on its antioxidant and anti-inflammatory effects by activating the Nrf2 pathway. Since both oxidative stress and inflammation are involved in Alzheimer’s disease (AD), DMF is a potential therapeutic option for AD. Objective: This study aims to test the therapeutic effects of DMF on AD model mice and to reveal its underlying molecular mechanisms. Methods: Cell viability assay and in vitro immunofluorescence imaging were used to evaluate the antioxidant effect of DMF on embryonic mouse hippocampal neurons. Behavioral test and brain magnetic resonance imaging were used to assess the therapeutic effects of DMF on spatial learning and memory as well as hippocampal volume in AD model mice with and without Nrf2 knockdown. Western blotting was used to analyze the expression of antioxidant enzymes and molecules associated with AD-related pathological pathways. Results: DMF inhibits reactive oxygen species overproduction and protects neurons without Nrf2 knockdown from death. DMF reduces amyloid-β induced memory impairment and hippocampal atrophy in AD model mice rather than in Nrf2 knockdown AD mice. DMF delays the progression of AD by activating the Nrf2 pathway to enhance the expression of downstream antioxidant enzymes and inhibits lipid peroxidation, apoptosis, inflammation, mitochondrial dysfunction and amyloid-β deposition. Conclusion: These results indicate that DMF is a potential therapeutic option for AD through its antioxidant, anti-inflammatory, anti-apoptotic, and other anti-AD effects by activating the Nrf2 pathway.

scholarly journals Consumption of Terpenoids-Rich Padina pavonia Extract Attenuates Hyperglycemia, Insulin Resistance and Oxidative Stress, and Upregulates PPARγ in a Rat Model of Type 2 Diabetes

Antioxidants ◽  
2019 ◽  
Vol 9 (1) ◽  
pp. 22 ◽  
Author(s):  
Mousa O. Germoush ◽  
Hassan A. Elgebaly ◽  
Sherif Hassan ◽  
Emadeldin M. Kamel ◽  
May Bin-Jumah ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Type 2 Diabetes ◽  
Insulin Sensitivity ◽  
Glucose Tolerance ◽  
Diabetic Rats ◽  
Antidiabetic Activity ◽  
Therapeutic Effects ◽  
Peroxisome Proliferator ◽  
Gene And Protein Expression

Seaweeds are rich in structurally diverse bioactive compounds with promising therapeutic effects. This study aimed to isolate and identify terpenes from the brown alga Padina pavonia and to investigate its antidiabetic activity, pointing to the possible involvement of peroxisome proliferator-activated receptor (PPAR)γ. Type 2 diabetes was induced by feeding rats a high fat diet (HFD) for 4 weeks followed by injection of 35 mg/kg streptozotocin (STZ). The diabetic rats received P. pavonia extract (PPE; 50, 100 and 200 mg/kg) for 4 weeks and samples were collected for analyses. HFD/STZ-induced rats showed hyperglycemia, dyslipidemia, impaired glucose tolerance, decreased insulin, and increased HbA1c and HOMA-IR. PPE ameliorated hyperglycemia and dyslipidemia, and improved glucose tolerance and insulin sensitivity in diabetic rats. Treatment with PPE increased hepatic hexokinase activity and glycogen, suppressed glucose-6-phosphatase, fructose-1,6-biphosphatase, and glycogen phosphorylase, and attenuated oxidative stress, inflammation, and liver injury and lipid infiltration in HFD/STZ-induced rats. In addition, PPE boosted antioxidants and upregulated PPARγ gene and protein expression in the liver of diabetic rats. Phytochemical investigation resulted in the isolation of six terpenes from PPE and in silico analysis revealed their binding affinity toward PPARγ. In conclusion, P. pavonia-derived terpenes attenuated hyperglycemia, dyslipidemia, oxidative stress, and inflammation, and improved insulin sensitivity and carbohydrate metabolism in type 2 diabetic rats. These beneficial effects are mediated via PPARγ activation. However, further studies to explore the exact mechanisms underlying the antidiabetic effect of PPE are recommended.

scholarly journals Up-Regulation of Advanced Glycated Products Receptors in the Brain of Diabetic Rats Is Prevented by Antioxidant Treatment

Endocrinology ◽  
2005 ◽  
Vol 146 (12) ◽  
pp. 5561-5567 ◽  
Author(s):  
Manuela Aragno ◽  
Raffaella Mastrocola ◽  
Claudio Medana ◽  
Francesca Restivo ◽  
Maria G. Catalano ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Neuronal Damage ◽  
Antioxidant Properties ◽  
Nuclear Factor Κb ◽  
Diabetic Rats ◽  
Receptor Interaction ◽  
Antioxidant Compounds ◽  
Nuclear Factor ◽  
Wide Range ◽  
S 100

Diabetics have at least twice the risk of stroke and may show performance deficit in a wide range of cognitive domains. The mechanisms underlying this gradually developing end-organ damage may involve both vascular changes and direct damage to neuronal cells as a result of overproduction of superoxide by the respiratory chain and consequent oxidative stress. The study aimed to assess the role of oxidative stress on the aldose reductase-polyol pathway, on advanced glycated end-product (AGE)/AGE-receptor interaction, and on downstream signaling in the hippocampus of streptozotocin-treated rats. Data show that, in diabetic rats, levels of prooxidant compounds increase, whereas levels of antioxidant compounds fall. Receptor for AGE and galectin-3 content and polyol flux increase, whereas glyceraldehyde-3-phosphate dehydrogenase activity is impaired. Moreover, nuclear factor κB (p65) transcription factor levels and S-100 protein are increased in the hippocampus cytosol, suggesting that oxidative stress triggers the cascade of events that finally leads to neuronal damage. Dehydroepiandrosterone, the most abundant hormonal steroid in the blood, has been reported to possess antioxidant properties. When dehydroepiandrosterone was administered to diabetic rats, the improved oxidative imbalance and the marked reduction of AGE receptors paralleled the reduced activation of nuclear factor κB and the reduction of S-100 levels, reinforcing the suggestion that oxidative stress plays a role in diabetes-related neuronal damage.

scholarly journals Quantitative Proteomic Analysis of Bi Zhong Xiao Decoction Against Collagen-induced Arthritis Rats in the Early and Late Stages

2021 ◽  
Author(s):  
Cailin He ◽  
Yang Wang ◽  
Yuqi Wen ◽  
Teng Li ◽  
En Hu ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Proteomic Analysis ◽  
Early Stage ◽  
Receptor Interaction ◽  
Therapeutic Effects ◽  
Sprague Dawley ◽  
Weight Changes ◽  
Collagen Induced Arthritis ◽  
Anti Inflammatory ◽  
Late Stages

Abstract Background: Rheumatoid arthritis (RA) is a chronic, progressive, systemic autoimmune inflammatory disease. Bi Zhong Xiao decoction (BZXD) performs multiple functions for rheumatoid arthritis (RA) treatment for decades. In this study, we aimed to study the protein alterations of BZXD in the early and late stages of RA.Methods: Sprague-Dawley rats were randomly divided into the Control, collagen-induced arthritis (CIA) and BZXD groups. Clinical assessment, paw thickness, weight changes and serum inflammatory cytokine levels were used to evaluate anti-inflammatory effects. Histopathological tests were performed to assess the improvement of inflammation and synovial hyperplasia. Moreover, we analyzed the proteins profiling of synovial tissue samples with different time intervals after BZXD treatment by Isobaric Tag for Relative Absolute (ITRAQ) quantitative proteomics technology. To further explore the interrelationships among differentially expressed proteins (DEPs), we used DAVID Bioinformatics Resources v6.8 and STRING 11.0 for bioinformatics analysis. Besides, western blot was exerted to verify related proteins.Results: In our study, BZXD ameliorated joint inflammation, suppressed the pathological changes in arthrosis of CIA rats. The proteomic analysis demonstrated that CIA rats were mainly involved in two significant pathways (the focal adhesion and the ECM-receptor interaction) in the early stage. BZXD down-regulated the expression of proteins involved in these pathways, such as CAV1, CHAD, COL3A1, COL5A2, COL6A1 and COL6A5. Additionally, BZXD exerts anti-inflammatory effects in the late stage mainly by increasing the expression of FASN, and affecting fatty acid metabolism.Conclusion: BZXD exerts therapeutic effects on RA through multi-pathways in the early and late stages. This work may provide proteomic clues for treating RA by BZXD.

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