Dexamethasone reduces bilirubin-induced toxicity and IL-8 and MCP-1 release in human NT2-N neurons

Almaas, Runar; Hankø, Erik; Mollnes, Tom Eirik; Rootwelt, Terje

doi:10.1016/j.brainres.2012.04.007

Cited by 5 publications

(6 citation statements)

References 29 publications

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“…In NT2-N neurons Almaas et al (21) found increased CXCL10 after oxidative stress, and we have earlier reported increased CXCL10 after hypoxia, but with no augmented response after hyperoxic reoxygenation (22). In concordance with our study, increased expression of Il1b has been found after hyperoxic reoxygenation in fetal sheep (23), and after hyperoxia alone in neonatal rats (10).…”

Section: Igf1rsupporting

confidence: 93%

Increased expression of inflammatory genes in the neonatal mouse brain after hyperoxic reoxygenation

et al. 2014

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Background: Hyperoxic reoxygenation following hypoxia increases the expression of inflammatory genes in the neonatal mouse brain. We have therefore compared the temporal profile of 44 a priori selected genes after hypoxia and hyperoxic or normoxic reoxygenation. Methods: Postnatal day 7 mice were subjected to 2 h of hypoxia (8% O 2 ) and 30 min reoxygenation with 60% or 21% O 2 . After 0 to 72 h observation, mRNA and protein were examined in the hippocampus and striatum. results: There were significantly higher gene expression changes in six genes after hyperoxic compared to normoxic reoxygenation. Three genes had a generally higher expression throughout the observation period: the inflammatory genes Hmox1 (mean difference: 0.52, 95% confidence interval (CI): 0.15-1.01) and Tgfb1 (mean difference: 0.099, CI: 0.003-0.194), and the transcription factor Nfkb1 (mean difference: 0.049, CI: 0.011-0.087). The inflammatory genes Cxcl10 and Il1b, and the DNA repair gene Neil3, had a higher gene expression change after hyperoxic reoxygenation at one time point only. Nineteen genes involved in inflammation, transcription regulation, apoptosis, angiogenesis, and glucose transport had significantly different gene expression changes with time in all intervention animals. conclusion: We confirm that hyperoxic reoxygenation induces a stronger inflammatory gene response than reoxygenation with air.

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Section: Igf1rsupporting

confidence: 93%

Increased expression of inflammatory genes in the neonatal mouse brain after hyperoxic reoxygenation

et al. 2014

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“…The effect of DEX on CCL2 has been found in other diseases and tissues by several studies (25)(26)(27). These studies showed that DEX inhibited both increases of CCL2 and CXCL10 which could induced by hydrogen peroxide in neurons (25) or by IFN-γ in endothelial cells (26).…”

Section: Discussionmentioning

confidence: 83%

Intrathyroid injection of dexamethasone inhibits Th2 cells in Graves’ disease

Peng²,

Liu³

et al. 2020

Archives of Endocrinology and Metabolism

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Objective: Intrathyroid injection of dexamethasone (IID) was used for decrease the relapse rate of hyperthyroidism in the treatment of Graves' disease (GD), but the mechanism is still unclear. We aimed to explore the effect of IID on T help (Th)1/Th2 cells and their chemokine in patients with GD. Subjects and methods: A total of 42 patients with GD who were euthyroidism by methimazole were randomly divided into IID group (n = 20) and control group (n = 22). Thyroid function and associated antibody, Th1/Th2 cells proportion, serum CXCL10 and CCL2 levels, and CXCR3/CCR2 mRNA expression in peripheral blood mononuclear cells before and after 3-month IID treatment were tested by chemiluminescence assay, Flow cytometry, ELISA, and real-time PCR, respectively. Thyroid follicular cells were stimulated by IFN-γ and TNF-α and treated with dexamethasone in vitro. CXCL10 and CCL2 levels in supernatant were determined. Results: After 3-month therapy, the proportion of Th2 cells and serum CCL2 levels, as well as TPOAb, TRAb levels and thyroid volume decreased in IID group (p < 0.05). However, the proportion of Th1 and CXCL10 levels had no change in IID group and control (p > 0.05). The CXCR3/CCR2 ratio had no change in both groups (p > 0.05). Conclusion: IID therapy could inhibit peripheral Th2 cells via decreasing CCL2 level in peripheral blood, and this result partly explain the effects of IID therapy on prevention of relapse of GD.

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“…MMP-3, 9 activation and iron toxicity played a deleterious role in acute neuron degeneration after ICH (Wang and Tsirka, 2005, Caliaperumal et al, 2012). Increased unconjugated bilirubin in ICH brain after ICH caused neuronal death (Clark et al, 2008, Almaas et al, 2012). Treatment with a nNOS inhibitor or knocking out nNOS can protect neurons against glutamate and ischemic injury, NMDA toxicity and improve functional recovery (Huang et al, 1994, Dawson et al, 1996, Coert et al, 2003).…”

Section: Discussionmentioning

confidence: 99%

Administration of S-methyl-l-thiocitrulline protects against brain injuries after intracerebral hemorrhage

Wagner

Broderick

et al. 2014

Neuroscience

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Although intracerebral hemorrhage (ICH) increases the level of glutamate in the perihematomal area and cerebral spinal fluid (CSF) in the ICH acute phase, it is unclear whether elevated glutamate activates neuronal nitric oxide synthase (nNOS) in the ICH brain and whether nNOS is an important target for ICH treatment. Here, we assessed the role of the nNOS inhibitor S-methyl-L-thiocitrulline (SMTC) in the activity of nicotinamide adenine dinucleotide phosphate-diaphorase (NADPH-d) and ICH-induced brain injuries. An autologous blood intracerebral infusion model in male rats was used. All of the rats were sacrificed 24 hours after ICH. ICH increased NADPH-d activity in the striatum. Administering SMTC 3 h after ICH decreased the activity of NADH-d (p < 0.05 vs. the ICH group). The activation of gelatinolytic enzymes in the perihematomal region of the striatum was reduced by SMTC treatment (p < 0.01, vs. the ICH group). The loss of laminin- and occludin-stained vessels was significant in perihematomal regions after 24 h of ICH and was significantly attenuated by the administration of SMTC (p < 0.01 for laminin, p < 0.05 for occluding, compared with the ICH group). Neuronal death and neurological deficits after ICH were also decreased in SMTC treatment rats (p < 0.01, vs. the ICH group). The results suggest that the administration of the nNOS inhibitor SMTC after ICH protects against ICH-induced brain injuries and improves neurological function.

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Dexamethasone reduces bilirubin-induced toxicity and IL-8 and MCP-1 release in human NT2-N neurons

Cited by 5 publications

References 29 publications

Increased expression of inflammatory genes in the neonatal mouse brain after hyperoxic reoxygenation

Increased expression of inflammatory genes in the neonatal mouse brain after hyperoxic reoxygenation

Intrathyroid injection of dexamethasone inhibits Th2 cells in Graves’ disease

Administration of S-methyl-l-thiocitrulline protects against brain injuries after intracerebral hemorrhage

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