Increased expression of immune-related genes in leukocytes of patients with diagnosed gestational diabetes mellitus (GDM)

Wójcik, Marzena; Zieleniak, Andrzej; Źurawska-Kliś, Monika; Cypryk, Katarzyna; Woźniak, Lucyna A.

doi:10.1177/1535370215615699

Cited by 26 publications

(23 citation statements)

References 60 publications

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“…The current study demonstrated that glycyrrhizic acid significantly downregulates the protein expression levels of p38MAPK in MTX-induced enteritis. Additionally, several other previous studies demonstrated that glycyrrhizic acid attenuates glycative stress in the kidneys of diabetic mice through suppression of NF-κB and p-p38MAPK (21,43). These data support the hypothesis that the anti-inflammatory effects of glycyrrhizic acid may be associated with p38MAPK signaling.…”

Section: A B C D a Bsupporting

confidence: 84%

Glycyrrhizic acid prevents enteritis through reduction of NF-κB p65 and p38MAPK expression in rat

Wang

2016

Molecular Medicine Reports

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Glycyrrhizic acid has a variety of biological properties, including a protective function in the liver, and anti‑inflammatory, anti‑ulcer, anti‑anaphylaxis, anti‑oxidant, immunoregulatory, antiviral and anticancer activities. The efficacy of glycyrrhizic acid can be increased when combined with other medicines. In the present study, the potential protective effects of glycyrrhizic acid against enteritis in rats, and its role in regulating anti‑inflammation, anti‑oxidation, angiogenic and apoptotic mechanisms were investigated using enzyme‑linked immunosorbent and bicinchoninic acid assays, and reverse transcription‑quantitative polymerase chain reaction and western blotting analyses. Adult male Sprague‑Dawley rats were injected with 20 mg/kg methotrexate (MTX) to establish enteritis. Additionally, rats with MTX‑induced enteritis were peritoneally injected with 200 mg glycyrrhizic acid for 9 weeks. The current study demonstrated that glycyrrhizic acid could alleviate MTX‑induced increases of tumor necrosis factor‑α, interleukin (IL)‑1β and IL‑6 levels, and raise IL‑10 levels, in rats with enteritis. Treatment with glycyrrhizic acid significantly reduced D‑lactate and intercellular adhesion molecule‑1 gene expression (P<0.01), but did not inhibit diamine oxidase activity in MTX‑induced enteritis. Pretreatment with glycyrrhizic acid significantly suppressed the promotion of p38 mitogen‑activated protein kinase (p38MAPK), nuclear factor‑κB p65 (NF‑κB p65) protein expression, interferon‑γ protein concentration, and caspase‑3 and cycloxygenase‑2 activity in MTX‑induced enteritis (P<0.01). The findings of the current study suggest that glycyrrhizic acid may prevent enteritis by reducing NF‑κB p65 and p38MAPK expression levels, which may inform future therapeutic strategies for the treatment of enteritis.

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Section: A B C D a Bsupporting

confidence: 84%

Glycyrrhizic acid prevents enteritis through reduction of NF-κB p65 and p38MAPK expression in rat

Wang

2016

Molecular Medicine Reports

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“…Therefore, the primary goal for successful medical management of GDM is to maintain the concentration of maternal blood glucose, particularly postprandial blood glucose levels, within the ideal range (10). It has been hypothesized that the mechanism of GDM involves an increase in the hormones produced by the placenta known to resist insulin, which results in a decreased sensitivity to insulin in pregnant women (11,12). This consolidates the scientific basis of medical nutrition therapy for the treatment of GDM (13).…”

Section: Introductionmentioning

confidence: 97%

Effect of various doses of vitamin D supplementation on pregnant women with gestational diabetes mellitus: A randomized controlled trial

Zhang

Chen

et al. 2016

Experimental and Therapeutic Medicine

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It has previously been reported that the influence of vitamin D on the metabolism of calcium and phosphorus is associated with diabetes, cardiovascular disease, Alzheimer's disease, cancer and other systemic diseases, and is considered an important indicator of general health. The present study was conducted to determine the effect of various doses of vitamin D supplementation on glucose metabolism, lipid concentrations, inflammation and the levels of oxidative stress of pregnant women with gestational diabetes mellitus (GDM). The present randomized, double-blind placebo-controlled clinical trial was conducted on 133 pregnant women with GDM during weeks 24-28 of pregnancy. The patients were randomly divided into four groups. The control group (n=20) received a placebo (sucrose; one granule/day), the low dosage group (n=38) received the daily recommended intake of 200 IU vitamin D (calciferol) daily, the medium dosage group (n=38) received 50,000 IU monthly (2,000 IU daily for 25 days) and the high dosage group (n=37) received 50,000 IU every 2 weeks (4,000 IU daily for 12.5 days). The general characteristics and dietary intakes of the patients with GDM were similar between each group. Using ELISA kits, it was determined that insulin, homeostatic model assessment-insulin resistance and total cholesterol were significantly reduced by high dosage vitamin D supplementation (P<0.05). Total antioxidant capacity and total glutathione levels were significantly elevated as a result of high dosage vitamin D supplementation (P<0.01). In conclusion, high-dose vitamin D supplementation (50,000 IU every 2 weeks) significantly improved insulin resistance in pregnant women with GDM.

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“…Our findings show that progeny of experimental gestational diabetes mellitus (EGD) rats have such immune violations of immunological tolerance as AIRE gene repression, reduced mRNA levels of Deaf1, transcription factor Foxp3, the latter being confirmed by decrease in Тreg cells [1] and inhibition of gene expression suppressor cytokine IL-10 and negative costimulatory molecules Ctla4 [2]. However, gestational diabetes (GD) increases the genes expression of immune response in pregnant [3] and leads to violations of innate and adaptive components of immune system in progeny. Thus, Li Q. et al (2016) showed that gestational diabetes mellitus increased interleukin-1β in progeny spleen cells [4].…”

Section: ключові словаmentioning

confidence: 99%

Effect of experimental gestational diabetes and administration of glibenclamide on mRNA level of NLRP3-inflammasome and distribution of NLRP3+-cells in mesenteric lymph nodes in progeny

2017

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A number of dysfunctions of congenital and adaptive components of the immune system are observed in progeny of rats with experimental gestational diabetes (EGD). The key link in pathogenesis of EGD and other diseases is the activation of NLRP3-inflammasome. Therefore, it is an attractive target for pharmaceutical effects. Among the numerous inhibitors of the inflammasome, glibenclamide is the most promising drug, which can effectively correct hyperglycemia in pregnant women. The aim of the study was to determine the level of mRNA expression of NLRP3-inflammasome and the distribution of NLRP3 +-cells in mesenteric lymph nodes in progeny of rats with experimental gestational diabetes and after administration of glibenclamide to pregnant Wistar rats. Materials and methods. A molecular-genetic study was carried out using polymerase chain reaction with real-time reverse transcription (RT-PCR) of mRNA expression level of the Nlrp3 gene. The distribution of NLRP3 +-cells in MLN of experimental animals was investigated by immunofluorescence and immunohistochemical methods. Results. The development of EGD is accompanied by transcriptional induction of the Nlrp3 gene in MLN in descendants, whose mRNA level increased five-fold (p < 0.05) in 1-month and 3-fold (p < 0.05) in 6-month-old animals. The administration of glibenclamide to pregnant rats inhibited the transcription of the Nlrp3 gene only at the age of 1 month (5.3 times, p < 0.05) and did not change it in the older age group. In the progeny of rats with EGD, the density of the NLRP3 +-lymphocyte population in the MLN increased, more clearly at early observation times. The intake of glibenclamide reduced the number of NLRP3 +-lymphocytes only at the age of 1 month (by 33 %, the cortex plateau), whereas their number in the medullary cords of 6-month-old progeny even increased. Conclusion. The increased mRNA expression of NLRP3-inflammasome and density of NLRP3 +-cells in MLN in descendants of rats with EGD indicates activation of pro-inflammatory signaling. Glibenclamide, as an inhibitor of the activation of the NLRP3-inflammasome, demonstrated its effectiveness only at early observation times.

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Increased expression of immune-related genes in leukocytes of patients with diagnosed gestational diabetes mellitus (GDM)

Cited by 26 publications

References 60 publications

Glycyrrhizic acid prevents enteritis through reduction of NF-κB p65 and p38MAPK expression in rat

Glycyrrhizic acid prevents enteritis through reduction of NF-κB p65 and p38MAPK expression in rat

Effect of various doses of vitamin D supplementation on pregnant women with gestational diabetes mellitus: A randomized controlled trial

Effect of experimental gestational diabetes and administration of glibenclamide on mRNA level of NLRP3-inflammasome and distribution of NLRP3+-cells in mesenteric lymph nodes in progeny

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