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Wyszukujesz frazę "β-cells" wg kryterium: Temat


Wyświetlanie 1-5 z 5
Tytuł:
Effects of olive leaf polyphenols against H2O2 toxicity in insulin secreting β-cells
Autorzy:
Cumaoğlu, Ahmet
Rackova, Lucia
Stefek, Milan
Kartal, Murat
Maechler, Pierre
Karasu, Çimen
Powiązania:
https://bibliotekanauki.pl/articles/1039946.pdf
Data publikacji:
2011
Wydawca:
Polskie Towarzystwo Biochemiczne
Tematy:
olive
glucose
insulin
hydrogen peroxide
polyphenol
apoptosis
β-cells
oxidative stress
oleuropein
Opis:
In pancreatic β-cells, although H2O2 is a metabolic signal for glucose stimulated insulin secretion, it may induce injury in the presence of increased oxidative stress (OS) as in the case of diabetic chronic hyperglycemia. Olea europea L. (olive) leaves contain polyphenolic compounds that may protect insulin-secreting cells against OS. The major polyphenolic compound in ethanolic olive leaf extract (OLE) is oleuropein (about 20 %), thus we compared the effects of OLE with the effects of standard oleuropein on INS-1 cells. The cells were incubated with increasing concentrations of OLE or oleuropein for 24 h followed by exposure to H2O2 (0.035 mM) for 45 min. H2O2 alone resulted in a significantly decreased viability (MTT assay), depressed glucose-stimulated insulin secretion, increased apoptotic and necrotic cell death (AO/EB staining), inhibited glutathione peroxidase activity (GPx) and stimulated catalase activity that were associated with increased intracellular generation of reactive oxygen species (ROS) (fluorescence DCF). OLE and oleuropein partly improved the viability, attenuated necrotic and apoptotic death, inhibited the ROS generation and improved insulin secretion in H2O2-exposed cells. The effects of oleuropein on insulin secretion were more pronounced than those of OLE, while OLE exerted a stronger anti-cytotoxic effect than oleuropein. Unlike OLE, oleuropein had no significant preserving effect on GPx; however, both compounds stimulated the activity of catalase in H2O2-exposed cells. These findings indicate different modulatory roles of polyphenolic constituents of olive leaves on redox homeostasis that may have a role in the maintenance of β-cell physiology against OS.
Źródło:
Acta Biochimica Polonica; 2011, 58, 1; 45-50
0001-527X
Pojawia się w:
Acta Biochimica Polonica
Dostawca treści:
Biblioteka Nauki
Artykuł
Tytuł:
Inhibition of CYP17 expression by adrenal androgens and transforming growth factor β in adrenocortical cells.
Autorzy:
Biernacka-Łukanty, Justyna
Lehmann, Tomasz
Trzeciak, Wiesław
Powiązania:
https://bibliotekanauki.pl/articles/1041500.pdf
Data publikacji:
2004
Wydawca:
Polskie Towarzystwo Biochemiczne
Tematy:
CYP17
adrenocortical cells
TGF-β
androgens
expression
Opis:
Cytochrome P450c17, encoded by the CYP17 gene, is a component of the 17a-hydroxylase/17,20-lyase enzyme complex essential for production of adrenal glucocorticoids and androgens as well as gonadal androgens. The expression of CYP17 in adrenocortical cells is stimulated by corticotropin (ACTH) via the signal transduction pathway involving cAMP and protein kinase A (PKA). Thus, in addition to glucocorticoids, ACTH stimulates formation of adrenal androgens, which are known to induce transforming growth factor β (TGF-β) secretion. TGF-β in turn inhibits steroid hormone output by attenuating both basal and ACTH-dependent expression of CYP17. The present study revealed that treatment of bovine and human H295R adrenocortical cells with androgens resulted in a decrease in the basal level of CYP17 transcript and cortisol secretion, without affecting forskolin-stimulated levels. We also demonstrated that in H295R cells TGF-β inhibited both basal and forskolin-stimulated accumulation of CYP17 mRNA. Determination of promoter activity, directing luciferase reporter gene expression in H295R cells transfected with deletion fragments of bovine CYP17 promoter, indicated that the -483 to -433 bp fragment of the promoter was necessary for the inhibitory action of TGF-β on CYP17 expression. It is concluded that in bovine and human adrenocortical cells, androgens inhibit basal CYP17 expression probably at the transcriptional level and independently of the effect of TGF-β.
Źródło:
Acta Biochimica Polonica; 2004, 51, 4; 907-917
0001-527X
Pojawia się w:
Acta Biochimica Polonica
Dostawca treści:
Biblioteka Nauki
Artykuł
Tytuł:
Simvastatin modulates β-catenin/MDR1 expression on spheres derived from CF41.Mg canine mammary carcinoma cells
Autorzy:
Cruz, P.
Reyes, F.
Torres, C.G.
Powiązania:
https://bibliotekanauki.pl/articles/2087784.pdf
Data publikacji:
2018
Wydawca:
Polska Akademia Nauk. Czytelnia Czasopism PAN
Tematy:
β-catenin
MDR1
simvastatin
canine mammary carcinoma cells
cancer stem cells
Źródło:
Polish Journal of Veterinary Sciences; 2018, 21, 1; 95-99
1505-1773
Pojawia się w:
Polish Journal of Veterinary Sciences
Dostawca treści:
Biblioteka Nauki
Artykuł
Tytuł:
Limited GADD45α expression and function in IL-1β toxicity towards insulin-producing cells
Autorzy:
Skalniak, Lukasz
Gurgul-Convey, Ewa
Okreglicka, Katarzyna
Skalniak, Anna
Jura, Jolanta
Powiązania:
https://bibliotekanauki.pl/articles/1039450.pdf
Data publikacji:
2013
Wydawca:
Polskie Towarzystwo Biochemiczne
Tematy:
GADD45
IL-1β
insulin-producing cells
type 1 diabetes
Opis:
Growth arrest and DNA damage-inducible (GADD) 45 proteins are regulators of cell death and survival. The proinflammatory cytokine IL-1β strongly increases the level of the transcript encoding GADD45α in rat insulin-producing INS-1E cells. The activation of Gadd45α gene is clearly dependent on JNK and NF-κB activation and the synthesis of the secondary mediator nitric oxide (NO). Interestingly, the observed twelve-fold increase in the GADD45α-coding transcript level is not followed by increased expression of GADD45α at the protein level. An analysis of IL-1β toxicity in INS-1E cells overexpressing GADD45α revealed no correlation between the GADD45α protein level and the sensitivity to IL-1β toxicity. These findings suggest that the potential engagement of GADD45α in IL-1β toxicity towards beta cells is limited to the effects induced by the basal expression level of this protein.
Źródło:
Acta Biochimica Polonica; 2013, 60, 4; 595-602
0001-527X
Pojawia się w:
Acta Biochimica Polonica
Dostawca treści:
Biblioteka Nauki
Artykuł
Tytuł:
Elevated level of ambient glucose stimulates the synthesis of high-molecular-weight hyaluronic acid by human mesangial cells. The involvement of transforming growth factor β1 and its activation by thrombospondin-1
Autorzy:
Yevdokimova, Natalia
Powiązania:
https://bibliotekanauki.pl/articles/1041253.pdf
Data publikacji:
2006
Wydawca:
Polskie Towarzystwo Biochemiczne
Tematy:
mesangial cells
high glucose
transforming growth factor β1
hyaluronic acid
thrombospondin-1
Opis:
The dysregulation of the metabolism of glycosaminoglycan and protein components of extracellular matrix (ECM) is a typical feature of diabetic complications. High glucose-induced enrichment of ECM with hyaluronan (HA) not only affects tissue structural integrity, but influences cell metabolic response due to the variety of effects depending on the HA polymer molecular weight. TSP-1-dependent activation of TGFβ1 axis is known to mediate numerous matrix disorders in diabetes, but its role concerning HA has not been studied so far. In this work we demonstrated that 30 mM D-glucose increased the incorporation of [3H]glucosamine in high-molecular-weight (> 2000 kDa) HA of medium and matrix compartments of human mesangial cultures. Simultaneously, the synthesis of HA with lower molecular weight and HA degradation were not altered. The cause of the increased high-molecular-weight HA synthesis consisted in the up-regulation of hyaluronan synthase (HAS) 2 mRNA without alterations of the expression of HAS3, which generates HA of lower molecular weight. D-Glucose at 30 mM also stimulated the production of transforming growth factor β1 (TGFβ1), the excessive activation of which was determined by the up-regulation of thrombospondin-1 (TSP-1). The blockage of TGFβ1 action either by neutralizing anti-TGFβ1 antibodies or by quenching the TGFβ1 activation (with TSP-1-derived synthetic GGWSHW peptide) abolished the effect of high glucose on HAS2 mRNA expression and normalized the synthesis of HA. Exogenous human TGFβ1 had the same effect on HAS2 expression and HA synthesis as high glucose treatment. Therefore, we supposed that TSP-1-dependent TGFβ1 activation is involved in the observed high glucose effect on HA metabolism. Since high-molecular-weight HA polymers, unlike middle- and low-molecular weight HA oligosaccharides, are known to possess anti-inflammatory and anti-fibrotic functions, we suppose that the enrichment of mesangial matrix with high-molecular-weight HA may represent an endogenous mechanism to limit renal injury in diabetes.
Źródło:
Acta Biochimica Polonica; 2006, 53, 2; 383-393
0001-527X
Pojawia się w:
Acta Biochimica Polonica
Dostawca treści:
Biblioteka Nauki
Artykuł
    Wyświetlanie 1-5 z 5

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