scholarly journals Antioxidants: Pharmacothearapeutic Boon for Diabetes

2021 ◽  
Author(s):  
Varuna Suresh ◽  
Amala Reddy ◽  
Pavithra Muthukumar ◽  
Thendarl Selvam
Keyword(s):  
Oxidative Stress ◽  
Defense Mechanisms ◽  
Cellular Response ◽  
Cell Function ◽  
Glucose Variability ◽  
Diabetic Rats ◽  
Long Term Effects ◽  
Free Radical Damage ◽  
Cellular Defense ◽  
Elevated Glucose

Glucose-induced oxidative stress can be found related to “glucose variability” and “glucose memory”. The irregular low and elevated glucose conditions cause damage to endothelial cell function than a steady, constant rise in level of glucose. Activation of PKC, NADPH oxidases, and mitochondrial oxidants are some of the pathways exhibited as a result of this aggravated cellular response. Regarding glucose memory, long after the normalization elevated level of glucose in the endothelial cells of diabetic rats and culture, a existance or ‘memory’ of induced basement membrane mRNA is expressed. This demonstrates that glucose causes dangerous long-term effects beyond the hyperglycemia period. Oxidative stress give rise to glucotoxicity and lipotoxicity which are phenomena’s related to diabetes. Following the pathogenesis of diabetes, hyperglycemia and hyperlipidemia exerts a supplementary toxic effect on the beta-cells. So, hyperglycemia can be considered as a requirement for the destructive effects of lipotoxicity. Thus glucolipotoxicity can be considered as a substitute for lipotoxicity which relates the detrimental correlation between lipids and beta-cell function. Generally, the antioxidant pharmacotherapy can be coupled with drugs to boost the natural cellular defense mechanisms as the naturally existing antioxidant components, which neutralizes free radical damage. This considers antioxidant a boon tool for pharmacotherapeutic agent.

The role of corneal crystallins in the cellular defense mechanisms against oxidative stress

2008 ◽  
Vol 19 (2) ◽  
pp. 100-112 ◽  
Author(s):  
Natalie Lassen ◽  
William J. Black ◽  
Tia Estey ◽  
Vasilis Vasiliou
Keyword(s):  
Oxidative Stress ◽  
Defense Mechanisms ◽  
Cellular Defense

scholarly journals Effects of Fermented Houttuynia cordata Thunb. on Diabetic Rats Induced by a High-Fat Diet with Streptozotocin and on Insulin Resistance in 3T3-L1 Adipocytes

2021 ◽  
Vol 2021 ◽  
pp. 1-15
Author(s):  
Wannachai Sakuludomkan ◽  
Ranchana Yeewa ◽  
Subhawat Subhawa ◽  
Chakkrit Khanaree ◽  
Arisa Imsumran Bonness ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Insulin Resistance ◽  
Cell Function ◽  
Pancreatic Beta Cell ◽  
Biological Properties ◽  
Diabetic Rats ◽  
Human Consumption ◽  
High Fat ◽  
Houttuynia Cordata ◽  
Houttuynia Cordata Thunb

Houttuynia cordata Thunb. (plukaow in Thai language) exhibits several biological properties, and many products of H. cordata are therefore commercially available for human consumption, such as fermented juice or tablets as food supplements. This study aimed to investigate the antidiabetic effects of fermented H. cordata (HC) in high-fat diets and streptozotocin-induced diabetic rats. Oral administration of HC at a dose of 100 mg/kg.bw not only maintained bodyweight, food intake, and water consumption but also reduced blood glucose levels and improved glucose tolerance ability in the diabetic rats. Moreover, HC also decreased oxidative stress markers in serum and inflammatory-related mediators in pancreas tissues, indicating the improvement of pancreatic beta-cell function in the diabetic rats. In order to clarify the mechanism of HC, the effects of ethanolic extract of HC (HCE) on insulin resistance were determined in 3T3-L1 adipocytes. FHE could recover glucose uptake and decrease lipolysis in palmitate-treated 3T3-L1 adipocytes. Taken together, these results demonstrate that HC can improve diabetic symptoms by enhancing insulin sensitivity, reducing oxidative stress, and suppressing inflammation.

scholarly journals Quantification and Mechanisms of Oxidative Stress in Chronic Disease

Proceedings ◽  
2019 ◽  
Vol 11 (1) ◽  
pp. 18 ◽  
Author(s):  
Davies
Keyword(s):  
Oxidative Stress ◽  
Chronic Disease ◽  
Defense Mechanisms ◽  
Antioxidant Defense ◽  
Cell Function ◽  
Critical Role ◽  
Extracellular Proteins ◽  
Oxidation Chemistry ◽  
Redox Equilibria

There is now strong evidence that the redox environment inside cells is very different to that outside the cell, and that many extracellular environments are both more oxidizing and also subject to extensive oxidation. This difference in redox environments results in significant changes in oxidation chemistry and biology, altered redox equilibria, and antioxidant defense mechanisms. It is also increasingly apparent that oxidation events both inside and outside cells (extracellular oxidation) play a critical role in driving many diseases. Many extracellular proteins are highly abundant, long-lived and relatively poorly protected against damage. They can therefore accumulate high levels of modification during ageing and chronic disease, resulting in their use as biomarkers of long-term oxidative stress. Furthermore, increasing evidence supports the hypothesis that oxidized extracellular matrix materials play a key role in determining cell function and fate.

scholarly journals The role of oxidative stress during inflammatory processes

2014 ◽  
Vol 395 (2) ◽  
pp. 203-230 ◽  
Author(s):  
Jérôme Lugrin ◽  
Nathalie Rosenblatt-Velin ◽  
Roumen Parapanov ◽  
Lucas Liaudet
Keyword(s):  
Oxidative Stress ◽  
Defense Mechanisms ◽  
Cellular Response ◽  
Current Knowledge ◽  
High Mobility ◽  
Nuclear Factor Κb ◽  
Redox Biology ◽  
Inflammatory Processes ◽  
Reactive Oxidant ◽  
Endogenous Antioxidant

Abstract The production of various reactive oxidant species in excess of endogenous antioxidant defense mechanisms promotes the development of a state of oxidative stress, with significant biological consequences. In recent years, evidence has emerged that oxidative stress plays a crucial role in the development and perpetuation of inflammation, and thus contributes to the pathophysiology of a number of debilitating illnesses, such as cardiovascular diseases, diabetes, cancer, or neurodegenerative processes. Oxidants affect all stages of the inflammatory response, including the release by damaged tissues of molecules acting as endogenous danger signals, their sensing by innate immune receptors from the Toll-like (TLRs) and the NOD-like (NLRs) families, and the activation of signaling pathways initiating the adaptive cellular response to such signals. In this article, after summarizing the basic aspects of redox biology and inflammation, we review in detail the current knowledge on the fundamental connections between oxidative stress and inflammatory processes, with a special emphasis on the danger molecule high-mobility group box-1, the TLRs, the NLRP-3 receptor, and the inflammasome, as well as the transcription factor nuclear factor-κB.

scholarly journals The Role of Oxidative Stress in Pancreatic β Cell Dysfunction in Diabetes

2021 ◽  
Vol 22 (4) ◽  
pp. 1509
Author(s):  
Natsuki Eguchi ◽  
Nosratola D. Vaziri ◽  
Donald C. Dafoe ◽  
Hirohito Ichii
Keyword(s):  
Oxidative Stress ◽  
Cell Function ◽  
Pancreatic Β Cell ◽  
Antioxidative Capacity ◽  
Β Cells ◽  
Β Cell ◽  
Glucose Levels ◽  
Cell Dysfunction ◽  
Elevated Glucose ◽  
Β Cell Function

Diabetes is a chronic metabolic disorder characterized by inappropriately elevated glucose levels as a result of impaired pancreatic β cell function and insulin resistance. Extensive studies have been conducted to elucidate the mechanism involved in the development of β cell failure and death under diabetic conditions such as hyperglycemia, hyperlipidemia, and inflammation. Of the plethora of proposed mechanisms, endoplasmic reticulum (ER) stress, mitochondrial dysfunction, and oxidative stress have been shown to play a central role in promoting β cell dysfunction. It has become more evident in recent years that these 3 factors are closely interrelated and importantly aggravate each other. Oxidative stress in particular is of great interest to β cell health and survival as it has been shown that β cells exhibit lower antioxidative capacity. Therefore, this review will focus on discussing factors that contribute to the development of oxidative stress in pancreatic β cells and explore the downstream effects of oxidative stress on β cell function and health. Furthermore, antioxidative capacity of β cells to counteract these effects will be discussed along with new approaches focused on preserving β cells under oxidative conditions.

scholarly journals TXNIP Links Innate Host Defense Mechanisms to Oxidative Stress and Inflammation in Retinal Muller Glia under Chronic Hyperglycemia: Implications for Diabetic Retinopathy

2012 ◽  
Vol 2012 ◽  
pp. 1-19 ◽  
Author(s):  
Takhellambam S. Devi ◽  
Icksoo Lee ◽  
Maik Hüttemann ◽  
Ashok Kumar ◽  
Kwaku D. Nantwi ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Diabetic Retinopathy ◽  
Er Stress ◽  
Host Defense ◽  
Defense Mechanisms ◽  
Immune Response Gene ◽  
Ros Generation ◽  
Muller Glia ◽  
Müller Glia ◽  
Cellular Defense

Thioredoxin Interacting Protein (TXNIP) mediates retinal inflammation, gliosis, and apoptosis in experimental diabetes. Here, we investigate the temporal response of Muller glia to high glucose (HG) and TXNIP expression using a rat Muller cell line (rMC1) in culture. We examined if HG-induced TXNIP expression evokes host defense mechanisms in rMC1 in response to metabolic abnormalities. HG causes sustained up-regulation of TXNIP (2 h to 5 days), ROS generation, ATP depletion, ER stress, and inflammation. Various cellular defense mechanisms are activated by HG: (i) NLRP3 inflammasome, (ii) ER stress response (sXBP1), (iii) hypoxic-like HIF-1αinduction, (iv) autophagy/mitophagy, and (v) apoptosis. We also foundin vivothat streptozocin-induced diabetic rats have higher retinal TXNIP and innate immune response gene expression than normal rats. Knock down of TXNIP by intravitreal siRNA reduces inflammation (IL-1β) and gliosis (GFAP) in the diabetic retina. TXNIP ablationin vitroprevents ROS generation, restores ATP level and autophagic LC3B induction in rMC1. Thus, our results show that HG sustains TXNIP up-regulation in Muller glia and evokes a program of cellular defense/survival mechanisms that ultimately lead to oxidative stress, ER stress/inflammation, autophagy and apoptosis. TXNIP is a potential target to ameliorate blinding ocular complications of diabetic retinopathy.

scholarly journals In vivo Assessment of Combined Effects of Glibenclamide and Losartan in Diabetic Rats

2018 ◽  
Vol 28 (2) ◽  
pp. 178-185 ◽  
Author(s):  
Moureq R. Alotaibi ◽  
Amal J. Fatani ◽  
Ahmed T. Almnaizel ◽  
Mohammed M. Ahmed ◽  
Hatem M. Abuohashish ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Defense Mechanisms ◽  
Antihypertensive Agents ◽  
Thiobarbituric Acid ◽  
Diabetic Rats ◽  
Histological Structure ◽  
Antioxidant Enzyme Activities ◽  
Necrosis Factor Alpha ◽  
Liver And Kidney

Objective: Diabetic complications involve multiple pathological pathways, including hyperglycemia-induced oxidative stress and inflammation. Combination therapy is usually employed to improve treatment outcomes and to lower potential adverse effects. In this study, we evaluated the effects of antidiabetic and antihypertensive agents, glibenclamide (GLI) and losartan (LT), on diabetes mellitus (DM)-associated metabolic changes in rats. Materials and Methods: Streptozotocin-induced diabetic animals were orally treated with GLI 5 mg/kg and/or LT 25 mg/kg for 4 weeks. Blood glucose, insulin, aspartate aminotransferase, alanine aminotransferase, urinary creatinine, and urea levels were measured. Serum, liver, and kidney values of inflammatory markers, such as interleukin-1β, tumor necrosis factor alpha, and interleukin-6 were assessed, along with lipid peroxidation products (e.g., thiobarbituric acid reactive substances), endogenous antioxidants (e.g., glutathione), as well as antioxidant enzyme activities (e.g., catalase, superoxide dismutase, and glutathione peroxidase). Finally, histological changes in liver and kidney tissues were evaluated. Results: DM markedly induced systemic, hepatic, and renal inflammation and lowered antioxidant defense mechanisms. Treatment of diabetic rats with either GLI or LT significantly improved liver and kidney functions and histological structure. Moreover, both medications reduced signs of oxidative stress and inflammation in blood, liver, and kidney samples. Combining GLI and LT showed similar protective potential against systemic, hepatic, and renal oxidative stress and inflammation. Conclusion: Adding LT to GLI therapy revealed prospective antioxidant and anti-inflammatory action, while no synergistic or additive effects were observed.

scholarly journals Kluyveromyces lactis: A Suitable Yeast Model to Study Cellular Defense Mechanisms against Hypoxia-Induced Oxidative Stress

2012 ◽  
Vol 2012 ◽  
pp. 1-14 ◽  
Author(s):  
M. Isabel González Siso ◽  
M. Esperanza Cerdán
Keyword(s):  
Oxidative Stress ◽  
Defense Mechanisms ◽  
Molecular Mechanisms ◽  
Kluyveromyces Lactis ◽  
Oxidative Stress Response ◽  
Unicellular Eukaryote ◽  
Extended Model ◽  
Cellular Defense ◽  
Health Disorders ◽  
Fermentative Yeast

Studies about hypoxia-induced oxidative stress in human health disorders take advantage from the use of unicellular eukaryote models. A widely extended model is the fermentative yeastSaccharomyces cerevisiae. In this paper, we describe an overview of the molecular mechanisms induced by a decrease in oxygen availability and their interrelationship with the oxidative stress response in yeast. We focus on the differential characteristics betweenS. cerevisiaeand the respiratory yeastKluyveromyces lactis, a complementary emerging model, in reference to multicellular eukaryotes.

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