The association of oxidative stress and pro-inflammatory cytokines in diabetic patients with hyperglycemic crisis

Li, Juan; Huang, Minglian; Shen, Xingping

doi:10.1016/j.jdiacomp.2014.06.008

Cited by 66 publications

(60 citation statements)

References 29 publications

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“…In addition to insulin resistance, chronic hyperglycemia is one of the main biological features involves in diabetic complications (10,13). Moreover, we have recently reported a more pronounced inflammatory phenotype in OA cartilage from patients with diabetes and enhanced IL-1β-induced inflammation in cultured chondrocytes exposed to excess glucose (36).…”

Section: Discussionmentioning

confidence: 92%

“…However, the mechanisms underlying the connection between both diseases remain unclear. Together, oxidative stress and proinflammatory mediators, particularly interleukin 1 beta (IL-1β), actively induce the changes in articular cartilage that predispose this tissue to the development of OA (5,6), as well as to T2DM and T2DM complications (7)(8)(9)(10). Elevated intracellular glucose levels primarily generate oxidative damage as a consequence of glycolytic pathway saturation in the cell and the subsequent production of advanced glycation end products (AGEs) (11)(12)(13).…”

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confidence: 99%

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The nuclear factor-erythroid 2-related factor/heme oxygenase-1 axis is critical for the inflammatory features of type 2 diabetes–associated osteoarthritis

Vaamonde‐García

Pigenet

Laiguillon

et al. 2017

Journal of Biological Chemistry

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Epidemiological findings support the hypothesis that type 2 diabetes mellitus (T2DM) is a risk factor for osteoarthritis (OA). Moreover, OA cartilage from patients with T2DM exhibits a greater response to inflammatory stress, but the molecular mechanism is unclear. To investigate whether the antioxidant defense system participates in this response, we examined here the expression of nuclear factor-erythroid 2-related factor (Nrf-2), a master antioxidant transcription factor, and of heme oxygenase-1 (HO-1), one of its main target genes, in OA cartilage from T2DM and non-T2DM patients as well as in murine chondrocytes exposed to high glucose (HG). Ex vivo experiments indicated that Nrf-2 and HO-1 expression is reduced in T2DM versus non-T2DM OA cartilage (0.57-fold Nrf-2 and 0.34-fold HO-1), and prostaglandin E 2 (PGE 2 ) release was increased in samples with low HO-1 expression. HG-exposed, IL-1β-stimulated chondrocytes had lower Nrf-2 levels in vitro, particularly in the nuclear fraction, than chondrocytes exposed to normal glucose (NG). Accordingly, HO-1 levels were also decreased (0.49-fold) in these cells. The HO-1 inducer cobalt protoporphyrin IX more efficiently attenuated PGE 2 and IL-6 release in HG+IL-1β-treated cells than in NG+IL-1β-treated cells. Greater reductions in HO-1 expression and increase in PGE 2 /IL-6 production were observed in HG+IL-1β-stimulated chondrocytes from Nrf-2 −/− mice than in chondrocytes from wild-type mice. We conclude that the Nrf-2/HO-1 axis is a critical pathway in the hyperglucidic-mediated dysregulation of chondrocytes. Impairments in this antioxidant system may explain the greater inflammatory responsiveness of OA cartilage from T2DM patients and may inform treatments of such patients.

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Section: Discussionmentioning

confidence: 92%

mentioning

confidence: 99%

The nuclear factor-erythroid 2-related factor/heme oxygenase-1 axis is critical for the inflammatory features of type 2 diabetes–associated osteoarthritis

Vaamonde‐García

Pigenet

Laiguillon

et al. 2017

Journal of Biological Chemistry

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“…It has been documented that chronic hyperglycaemia promotes free radical accumulation that, in turn, results in inflammation and inflammatory-related responses (Li et al 2014b). In fact, increased levels of pro-inflammatory cytokines such as interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-␣), have been reported to play a dual role, i.e., in the development of diabetes as well as depression (Tuttle et al 2004;Luppino et al 2010;Stuart and Baune 2012).…”

Section: Introductionmentioning

confidence: 99%

Anti-depressant effect of hesperidin in diabetic rats

El-Marasy

Abdallah

El‐Shenawy

et al. 2014

Can. J. Physiol. Pharmacol.

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This study aimed to investigate the anti-depressant effect of hesperidin (Hsp) in streptozotocin (STZ)-induced diabetic rats. Additionally, the effect of Hsp on hyperglycaemia, oxidative stress, inflammation, brain-derived neurotrophic factor (BDNF), and brain monoamines in diabetic rats was also assessed. The Wistar rats in the experimental groups were rendered hyperglycaemic with a single dose of STZ (52.5 mg·(kg body mass)(-1), by intraperitoneal injection). The normal group received the vehicle only. Hyperglycaemic rats were treated with Hsp (25.0, 50.0, or 100.0 mg·(kg body mass)(-1)·day(-1), per oral) and fluoxetine (Flu) (5.0 mg·(kg body mass)(-1)·day(-1), per oral) 48 h after the STZ injection, for 21 consecutive days. The normal and STZ control groups received the vehicle (distilled water). Behavioral and biochemical parameters were then assessed. When Hsp was administered to the STZ-treated rats, this reversed the STZ-induced increase in immobility duration in the forced swimming test (FST) and attenuated hyperglycaemia, decreased malondialdehyde (MDA), increased reduced glutathione (GSH) decreased interleukin-6 (IL-6), and increased BDNF levels in the brain. Treatment with Hsp attenuated STZ-induced neurochemical alterations, as indicated by increased levels of monoamines in the brain, namely, norepinephrine (NE), dopamine (DA), and serotonin (5-hydroxytryptamine; 5-HT). All of these effects of Hsp were similar to those observed with the established anti-depressant Flu. This study shows that Hsp exerted anti-depressant effect in diabetic rats, which may have been partly mediated by its amelioration of hyperglycaemia as well as its anti-oxidant and anti-inflammatory activities, the enhancement of neurogenesis, and changes in the levels of monoamines in the brain.

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“…Oxidative stress, hypoxia-inducible factor-1a (HIF-1a), and epigenetic changes induced by hyperglycemia promote tumor progression in pancreatic and breast cancer cell lines [17]. Hyperglycemia can increase the level of serum inflammatory cytokines [18]. These studies suggest that hyperglycemia can potentially promote HCC development.…”

Section: Introductionmentioning

confidence: 99%

Effect of hyperglycemia on hepatocellular carcinoma development in diabetes

Niwa

Ishikawa

Ishigami

et al. 2015

Biochemical and Biophysical Research Communications

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Compared with other cancers, diabetes mellitus is more closely associated with hepatocellular carcinoma (HCC). However, whether hyperglycemia is associated with hepatic carcinogenesis remains uncertain. In this study, we investigate the effect of hyperglycemia on HCC development. Mice pretreated with 7,12-dimethylbenz (a) anthracene were divided into three feeding groups: normal diet (Control), high-starch diet (Starch), and high-fat diet (HFD) groups. In addition, an STZ group containing mice that were fed a normal diet and injected with streptozotosin to induce hyperglycemia was included. The STZ group demonstrated severe hyperglycemia, whereas the Starch group demonstrated mild hyperglycemia and insulin resistance. The HFD group demonstrated mild hyperglycemia and severe insulin resistance. Multiple HCC were macroscopically and histologically observed only in the HFD group. Hepatic steatosis was observed in the Starch and HFD groups, but levels of inflammatory cytokines, interleukin (IL)-6, tumor necrosis factor-α, and IL-1β, were elevated only in the HFD group. The composition of gut microbiota was similar between the Control and STZ groups. A significantly higher number of Clostridium cluster XI was detected in the feces of the HFD group than that of all other groups; it was not detectable in the Starch group. These data suggested that hyperglycemia had no effect on hepatic carcinogenesis. Different incidences of HCC between the Starch and HFD groups may be attributable to degree of insulin resistance, but diet-induced changes in gut microbiota including Clostridium cluster XI may have influenced hepatic carcinogenesis. In conclusion, in addition to the normalization of blood glucose levels, diabetics may need to control insulin resistance and diet contents to prevent HCC development.

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The association of oxidative stress and pro-inflammatory cytokines in diabetic patients with hyperglycemic crisis

Cited by 66 publications

References 29 publications

The nuclear factor-erythroid 2-related factor/heme oxygenase-1 axis is critical for the inflammatory features of type 2 diabetes–associated osteoarthritis

The nuclear factor-erythroid 2-related factor/heme oxygenase-1 axis is critical for the inflammatory features of type 2 diabetes–associated osteoarthritis

Anti-depressant effect of hesperidin in diabetic rats

Effect of hyperglycemia on hepatocellular carcinoma development in diabetes

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