Effect of redox status of peripheral blood on immune signature of circulating regulatory and cytotoxic T cells in streptozotocin induced rodent model of type I diabetes

Anupam, Kumari; Kaushal, Jyotsana; Prabhakar, Nirmal; Bhatnagar, Archana

doi:10.1016/j.imbio.2018.07.004

Cited by 24 publications

(22 citation statements)

References 49 publications

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“…Our model predicts that high ROS will increase cytosolic calcium, leading to the activation of NFAT and thus a preferential expression of IL-4 over that of pro-inflammatory cytokines [36]. This is in agreement with high IL-4 expression in neonatal cells and other conditions in which high ROS induces the expression of IL-4 [37, 38].…”

Section: Discussionsupporting

confidence: 79%

Contribution of ROS and metabolic status to neonatal and adult CD8+ T cell activation

et al. 2019

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In neonatal T cells, a low response to infection contributes to a high incidence of morbidity and mortality of neonates. Here we have evaluated the impact of the cytoplasmic and mitochondrial levels of Reactive Oxygen Species of adult and neonatal CD8+ T cells on their activation potential. We have also constructed a logical model connecting metabolism and ROS with T cell signaling. Our model indicates the interplay between antigen recognition, ROS and metabolic status in T cell responses. This model displays alternative stable states corresponding to different cell fates, i.e. quiescent, activated and anergic states, depending on ROS levels. Stochastic simulations with this model further indicate that differences in ROS status at the cell population level contribute to the lower activation rate of neonatal, compared to adult, CD8+ T cells upon TCR engagement. These results are relevant for neonatal health care. Our model can serve to analyze the impact of metabolic shift during cancer in which, similar to neonatal cells, a high glycolytic rate and low concentrations of glutamine and arginine promote tumor tolerance.

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Section: Discussionsupporting

confidence: 79%

Contribution of ROS and metabolic status to neonatal and adult CD8+ T cell activation

et al. 2019

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“…induced type 1 DM exhibit changed immune responses [41][42][43]. However, the immune responses of STZ-induced type 1 DM in neonatal rats were undetermined in our study.…”

Section: Discussioncontrasting

confidence: 56%

Bilobalide Enhances AMPK Activity to Improve Liver Injury and Metabolic Disorders in STZ-Induced Diabetes in Immature Rats via Regulating HMGB1/TLR4/NF-κB Signaling Pathway

Zhao

Qin

Shen

et al. 2021

BioMed Research International

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This study was aimed at examining the effect and underlying mechanisms of bilobalide (BB) on hepatic injury in streptozotocin- (STZ-) induced diabetes mellitus (DM) in immature rats. Immature rats (one day old) were randomly divided into five groups: group I, control nondiabetic rats; group II, STZ-induced, untreated diabetic rats; groups III/IV/V, STZ-induced and BB-treated diabetic rats, which were intraperitoneally injected with BB (2.5 mg/kg, 5 mg/kg, or 10 mg/kg) after 3 days followed by STZ treatment. We observed that BB improved the histopathological changes and maintained normal glucose metabolism, blood lipid, and liver function indicators, such as fasting blood glucose, obesity index, HbA1c, HOMA-IR, fast serum insulin, adiponectin, total cholesterol (TC), triglyceride (TG), high-density lipoprotein (HDL), low-density lipoprotein (LDL), aspartate transaminase (AST), and alanine transaminase (ALT) in STZ-induced DM in immature rats by a biochemical analyzer or ELISA. Meanwhile, Western blot analysis showed that in STZ-induced DM immature rats, BB decreased the expression of apoptosis-related proteins Bax, cleaved caspase-3, and cleaved caspase-9 while enhancing the Bcl-2 expression; BB downregulated the expression of ACC related to fat anabolism, while upregulating the expression of CPT-1 related to fat catabolism. Strikingly, treatment with BB significantly increased the expression of AMPKα1 as well as inhibited HMGB1, TLR4, and p-P65 expression in hepatic tissues of immature DM rats. AMPK inhibitor (compound C, CC) cotreated with BB undermined the protective effect of BB on the liver injury. The results of the present study suggested BB may have a significant role in alleviating liver damage in the STZ-induced immature DM rats.

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“…Previous studies have revealed that diabetes mellitus and atherosclerosis share the same oxidative stress and mitochondrial pathologies [18] . Hyperglycemia increases ROS production by driving mitochondria toward increased oxygen use and increased redox potential [19] and by shifting O 2 transport toward the respiratory chain complex II [7] . The conversion of ADP to ATP reduces membrane potential, and hyperglycemia increases ADP regeneration and consumption rates, resulting in decreased ATP formation, a continuing increase in membrane potential, and augmentation of ROS production [20] .…”

Section: Hyperglycemia-induced Excessive Ros Production and Acceleratmentioning

confidence: 99%

New insights into oxidative stress and inflammation during diabetes mellitus-accelerated atherosclerosis

et al. 2019

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Oxidative stress and inflammation interact in the development of diabetic atherosclerosis. Intracellular hyperglycemia promotes production of mitochondrial reactive oxygen species (ROS), increased formation of intracellular advanced glycation end-products, activation of protein kinase C, and increased polyol pathway flux. ROS directly increase the expression of inflammatory and adhesion factors, formation of oxidized-low density lipoprotein, and insulin resistance. They activate the ubiquitin pathway, inhibit the activation of AMP-protein kinase and adiponectin, decrease endothelial nitric oxide synthase activity, all of which accelerate atherosclerosis. Changes in the composition of the gut microbiota and changes in microRNA expression that influence the regulation of target genes that occur in diabetes interact with increased ROS and inflammation to promote atherosclerosis. This review highlights the consequences of the sustained increase of ROS production and inflammation that influence the acceleration of atherosclerosis by diabetes. The potential contributions of changes in the gut microbiota and microRNA expression are discussed.

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Effect of redox status of peripheral blood on immune signature of circulating regulatory and cytotoxic T cells in streptozotocin induced rodent model of type I diabetes

Cited by 24 publications

References 49 publications

Contribution of ROS and metabolic status to neonatal and adult CD8+ T cell activation

Contribution of ROS and metabolic status to neonatal and adult CD8+ T cell activation

Bilobalide Enhances AMPK Activity to Improve Liver Injury and Metabolic Disorders in STZ-Induced Diabetes in Immature Rats via Regulating HMGB1/TLR4/NF-κB Signaling Pathway

New insights into oxidative stress and inflammation during diabetes mellitus-accelerated atherosclerosis

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