Ameliorative effect of riboflavin on hyperglycemia, oxidative stress and DNA damage in type-2 diabetic mice: Mechanistic and therapeutic strategies

Alam, Mohammad Zubair; Iqbal, Saba; Naseem, Imrana

doi:10.1016/j.abb.2015.08.013

Cited by 80 publications

(64 citation statements)

References 37 publications

(30 reference statements)

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“…Therefore, RF‐induced reduction in neutrophil recruitment into the colon may also be related to the attenuation of oxidative stress. Additionally, RF has been shown to protect tissues from oxidative damage, most probably through its ability to scavenge free radicals . Using the luminol‐ and lucigenin‐enhanced CL method, which is a simple and a reproducible technique, allowed us to quantitate the ROS generation in the present study.…”

Section: Discussionmentioning

confidence: 99%

“…Recently, it was shown that RF treatment prevented abdominal aortic aneurysm formation in a rat model through endogenous superoxide dismutase (SOD) activation . In a diabetic murine model, ameliorative effect of RF on oxidative stress and DNA damage was also demonstrated . RF has been found to reduce mortality and decrease production of several proinflammatory cytokines [e.g.…”

Section: Introductionmentioning

confidence: 99%

“…17 In a diabetic murine model, ameliorative effect of RF on oxidative stress and DNA damage was also demonstrated. 11 RF has been found to reduce mortality and decrease production of several proinflammatory cytokines [e.g. tumor necrosis factor (TNF)α, interleukin (IL)-1β, IL-6, interferon (IFN)γ, monocyte chemotactic protein-1 and nitric oxide] in a murine model of sepsis and septic shock.…”

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confidence: 99%

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Ameliorative effects of riboflavin on acetic acid‐induced colonic injury in rats

Karakoyun

Ertaş

Yüksel

et al. 2017

Clin Exp Pharma Physio

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Riboflavin (RF) has been found to be a promising antioxidant and/or anti-inflammatory agent in several studies. However, the effect of RF against acetic acid (AA)-induced colonic injury is currently unknown. This study aimed to investigate the potential antioxidant and protective effects of RF in a rat model of ulcerative colitis. Starting immediately after the colitis induction (AA+RF group) or 1 week before the colitis induction (RF+AA+RF group), the rats were treated with RF (25 mg/kg per day; p.o.) for 3 days. The control and AA groups received saline (1 mL; p.o.) whereas AA+SS group (positive control) received sulfasalazine (100 mg/kg per day; p.o.) for 3 days. Colonic samples were taken for the biochemical and histological assessments on the third day. High damage scores, elevated tissue wet weight index (WI), tissue myeloperoxidase (MPO) activity, 8-hydroxy-2'-deoxyguanosine levels and chemiluminescence values, and a pronounced decrease in antioxidant glutathione (GSH) levels of the AA group were all reversed by RF pretreatment (RF+AA+RF group) and SS treatment (AA+SS group) (P < .05-.001). Tissue WI, MPO activity and GSH levels were not statistically changed in the AA+RF group. Western blot analysis revealed that the decreased protein expressions of tissue collagen (COL) 1A1, COL3A1 and transforming growth factor-β1 in the AA group were elevated in all the treatment groups (P < .05-.001). In conclusion, RF exerts both the antioxidant and anti-inflammatory effects against AA-induced colonic inflammation by suppressing neutrophil accumulation, inhibiting reactive oxidant generation, preserving endogenous glutathione, improving oxidative DNA damage and regulating inflammatory mediators, suggesting a future potential role in the treatment and prevention of ulcerative colitis.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

mentioning

confidence: 99%

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Ameliorative effects of riboflavin on acetic acid‐induced colonic injury in rats

Karakoyun

Ertaş

Yüksel

et al. 2017

Clin Exp Pharma Physio

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“…The up regulation of atpA, atpH and ppaC stimulated energy metabolism for protein, AA, and nucleic acid catabolism; carbohydrate catabolism; and other kinds of cellular metabolisms. The up-regulation of pfkA, eno, pckA, mqo and sucC regulates glycolysis, the pentose phosphate pathway, and the citrate cycle as well as protects cells from oxidative stress and DNA damage 21 .…”

Section: Resultsmentioning

confidence: 99%

Triphenyltin recognition by primary structures of effector proteins and the protein network of Bacillus thuringiensis during the triphenyltin degradation process

Wang

et al. 2017

Sci Rep

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Herein, triphenyltin (TPT) biodegradation efficiency and its transformation pathway have been elucidated. To better understand the molecular mechanism of TPT degradation, the interactions between amino acids, primary structures, and quaternary conformations of effector proteins and TPT were studied. The results verified that TPT recognition and binding depended on amino acid sequences but not on secondary, tertiary or quaternary protein structure. During this process, TPT could change the molecular weight and isoelectric point of effector proteins, induce their methylation or demethylation, and alter their conformation. The effector proteins, alkyl hydroperoxide reductase and acetyl-CoA acetyltransferase, recognizing TPT were crucial to TPT degradation. Electron transfer flavoprotein subunit alpha, phosphoenolpyruvate carboxykinase, aconitate hydratase, branched-chain alpha-keto acid dehydrogenase E1 component, biotin carboxylase and superoxide dismutase were related to energy and carbon metabolism, which was consistent with the results in vivo. The current findings develop a new approach for investigating the interactions between proteins and target compounds.

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“…Despite their antioxidant properties and effects in the reduction of diabetic complications in diabetic mice models [109], supplementation of B vitamins in general has not been proposed for the primary prevention of T2DM. In fact, recent studies have suggested that long-term exposure to high levels of the B vitamins niacin, thiamin and riboflavin may correlate with prevalence of obesity and diabetes.…”

Section: Effects Of Nutrients On Gene Expression In the Pathogenesmentioning

confidence: 99%

Gene-Diet Interactions in Type 2 Diabetes: The Chicken and Egg Debate

Ortega

Berná

Rojas

et al. 2017

IJMS

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Consistent evidence from both experimental and human studies indicates that Type 2 diabetes mellitus (T2DM) is a complex disease resulting from the interaction of genetic, epigenetic, environmental, and lifestyle factors. Nutrients and dietary patterns are important environmental factors to consider in the prevention, development and treatment of this disease. Nutritional genomics focuses on the interaction between bioactive food components and the genome and includes studies of nutrigenetics, nutrigenomics and epigenetic modifications caused by nutrients. There is evidence supporting the existence of nutrient-gene and T2DM interactions coming from animal studies and family-based intervention studies. Moreover, many case-control, cohort, cross-sectional cohort studies and clinical trials have identified relationships between individual genetic load, diet and T2DM. Some of these studies were on a large scale. In addition, studies with animal models and human observational studies, in different countries over periods of time, support a causative relationship between adverse nutritional conditions during in utero development, persistent epigenetic changes and T2DM. This review provides comprehensive information on the current state of nutrient-gene interactions and their role in T2DM pathogenesis, the relationship between individual genetic load and diet, and the importance of epigenetic factors in influencing gene expression and defining the individual risk of T2DM.

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Ameliorative effect of riboflavin on hyperglycemia, oxidative stress and DNA damage in type-2 diabetic mice: Mechanistic and therapeutic strategies

Cited by 80 publications

References 37 publications

Ameliorative effects of riboflavin on acetic acid‐induced colonic injury in rats

Ameliorative effects of riboflavin on acetic acid‐induced colonic injury in rats

Triphenyltin recognition by primary structures of effector proteins and the protein network of Bacillus thuringiensis during the triphenyltin degradation process

Gene-Diet Interactions in Type 2 Diabetes: The Chicken and Egg Debate

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