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Tytuł:
NOD1 and NOD2 receptors: integral members of the innate and adaptive immunity system
Autorzy:
Antosz, Halina
Osiak, Magdalena
Powiązania:
https://bibliotekanauki.pl/articles/1039530.pdf
Data publikacji:
2013
Wydawca:
Polskie Towarzystwo Biochemiczne
Tematy:
NOD1
NOD2
CARD
NF-κB
Opis:
NOD-like proteins (NLR) are a specialized group of intracellular receptors, which constitute an essential component of the host innate immune system. They were discovered more than a decade ago, but research on this particular class of microbial detectors is still ongoing to allow for a better understanding of the mechanisms, recognition of microorganisms, transmission of signals, and carrying out the activation of inflammatory signaling pathways. In this review, we discuss the construction of NOD1 and NOD2 receptors, their functions, and significance in the pathogenesis of inflammatory diseases in humans.
Źródło:
Acta Biochimica Polonica; 2013, 60, 3; 351-360
0001-527X
Pojawia się w:
Acta Biochimica Polonica
Dostawca treści:
Biblioteka Nauki
Artykuł
Tytuł:
The response of L5178Y lymphoma sublines to oxidative stress: Antioxidant defence, iron content and nuclear translocation of the p65 subunit of NF-κB.
Autorzy:
Boużyk, Elżbieta
Grądzka, Iwona
Iwaneńko, Teresa
Kruszewski, Marcin
Sochanowicz, Barbara
Szumiel, Irena
Powiązania:
https://bibliotekanauki.pl/articles/1044205.pdf
Data publikacji:
2000
Wydawca:
Polskie Towarzystwo Biochemiczne
Tematy:
iron
L5178Y murine lymphoma sublines
NF-κB
lovastatin
sensitivity to hydrogen peroxide
antioxidant defence
oxidative stress
Opis:
We examined the response to hydrogen peroxide of two L5178Y (LY) sublines which are inversely cross-sensitive to hydrogen peroxide and X-rays: LY-R cells are radioresistant and hydrogen peroxide-sensitive, whereas LY-S cells are radiosensitive and hydrogen peroxide-resistant. Higher initial DNA breaks and higher iron content (potentially active in the Fenton reaction) were found in the hydrogen peroxide sensitive LY-R cells than in the hydrogen peroxide resistant LY-S cells, whereas the antioxidant defence of LY-R cells was weaker. In particular, catalase activity is twofold higher in LY-S than in LY-R cells. The content of monobromobimane-reactive thiols is 54% higher in LY-S than in LY-R cells. In contrast, the activity of glutathione peroxidase (GPx) is about two times higher in LY-R than in LY-S cells; however, upon induction with selenium the activity increases 15.6-fold in LY-R cells and 50.3-fold in LY-S cells. Altogether, the sensitivity difference is related to the iron content, the amount of the initial DNA damage, as well as to the efficiency of the antioxidant defence system. Differential nuclear translocation of p65-NF-κB in LY sublines is due to the more efficient antioxidant defence in LY-S than in LY-R cells.
Źródło:
Acta Biochimica Polonica; 2000, 47, 4; 881-888
0001-527X
Pojawia się w:
Acta Biochimica Polonica
Dostawca treści:
Biblioteka Nauki
Artykuł
Tytuł:
MGF360-12L of ASFV-SY18 is an immune-evasion protein that inhibits host type I IFN, NF-κB, and JAK/STAT pathways
Autorzy:
Chen, Q.
Wang, X.X.
Jiang, S.W.
Gao, X.T.
Huang, S.Y.
Liang, Y.
Jia, H.
Zhu, H.F.
Powiązania:
https://bibliotekanauki.pl/articles/16647496.pdf
Data publikacji:
2023
Wydawca:
Polska Akademia Nauk. Czasopisma i Monografie PAN
Tematy:
African swine fever virus
MGF360-12L
type I IFN
NF-κB
JAK/STAT
Opis:
African swine fever virus (ASFV) causes feverous and hemorrhagic disease of domestic pigs and European wild boars with high mortality, yet no commercial vaccine is currently available. Several ASFV strains with natural deletion or gene-targeted knockout of multiple MGF360 and MGF505 genes are attenuated in vitro and in vivo, and can offer full protection against homologous challenge. However, the mechanisms underlying the protection are not fully understood. This study aims to investigate the effects of MGF360-12L of ASFV-SY18 on the cGAS-STING signaling pathway and explore the potential mechanisms. We identified that ASFV-SY18 MGF360-12L could inhibit cGAS-STING, TBK1, or IRF3-5D-stimulated IFN-β expression and ISRE activation. Specifically, MGF360-12L inhibits both the activation of PRD(III-I) in a dose-dependent manner, and suppresses the exogenous expression of TBK1 and IRF3-5D. MGF360-12L could block NF-κB activation induced by overexpression of cGAS-STING, TBK1, IKKβ. Downstream of the IFN-β signaling, MGF360-12L blocks the ISRE promoter activation by reducing total protein level of IRF9. Moreover, MGF360-12L protein can inhibit IFN-β-mediated antiviral effects. In conclusion, our findings suggest that MGF360-12L is a multifunctional immune-evasion protein that inhibits both the expression and effect of IFN-β, which could partially explain the attenuation of relevant gene-deleted ASFV strains, and shed light on the development of efficient ASFV live attenuated vaccines in the future.
Źródło:
Polish Journal of Veterinary Sciences; 2023, 26, 1; 119-130
1505-1773
Pojawia się w:
Polish Journal of Veterinary Sciences
Dostawca treści:
Biblioteka Nauki
Artykuł
Tytuł:
Metal responsive transcription factor 1 (MTF-1) regulates zinc dependent cellular processes at the molecular level
Autorzy:
Grzywacz, Agata
Gdula-Argasińska, Joanna
Muszyńska, Bożena
Tyszka-Czochara, Małgorzata
Librowski, Tadeusz
Opoka, Włodzimierz
Powiązania:
https://bibliotekanauki.pl/articles/1038990.pdf
Data publikacji:
2015
Wydawca:
Polskie Towarzystwo Biochemiczne
Tematy:
metal responsive-transcription factor 1
cell signaling
inflammation
NF-κB
Opis:
Metal responsive transcription factor 1 (MTF-1) is a zinc dependent transcription factor which is involved in the regulation of intracellular signaling pathways. MTF-1 regulates the expression of two streams of genes functioning in metal homeostasis and anti-oxidative response. MTF-1 acts in the process of binding of toxic metal ions in the cell, due to the activation of the expression of metallothioneins (MTs). Additionally, MTF-1 regulates transcription of genes involved in the sequestration of zinc and its intracellular transport. Disruption of zinc and MT homeostasis has an indispensable influence on the development of several pathological states. Moreover, by increasing MT activity, MTF-1 can effectively protect cells from oxidative and hypoxic stresses. The mechanism of MTF-1 action in cells includes the regulation of the proper immune response through activation/repression of anti- and pro-inflammatory cytokines. MTF-1 function in immune response is related to nuclear factor-κB (NF-κB) activity. Synthesis of insulin is also related to the activity of this transcription factor and zinc balance. Insulin transport also depends on zinc. In pancreatic β-cells, several types of the zinc transporters are found. Zinc transporters coordinated action is crucial for the synthesis and secretion of insulin. Disturbances in the regulation of signaling pathways connected with MTF-1 function can entail further alterations in zinc intracellular status and this growing imbalance can promote the pathophysiology of degenerative disorders.
Źródło:
Acta Biochimica Polonica; 2015, 62, 3; 491-498
0001-527X
Pojawia się w:
Acta Biochimica Polonica
Dostawca treści:
Biblioteka Nauki
Artykuł
Tytuł:
Nuclear Factor kappa B activation by Ag, Au nanoparticles, CdTe quantum dots or their binary mixtures in HepG2 cells
Autorzy:
Kapka-Skrzypczak, L.
Męczyńska-Wielgosz, S.
Matysiak-Kucharek, M.
Czajka, M.
Sawicki, K.
Kruszewski, M.
Brzóska, K.
Powiązania:
https://bibliotekanauki.pl/articles/2085648.pdf
Data publikacji:
2020
Wydawca:
Instytut Medycyny Wsi
Tematy:
nanomaterials
NF-κB
dual-luciferase reporter system
nanoparticles binary mixtures
Opis:
Introduction and Objective. Nuclear factor kappa B (NF-κB) signalling pathway plays a central role in the regulation of cellular response to stress. The aim of the study was to investigate the ability of silver nanoparticles (AgNPs), gold nanoparticles (AuNPs), CdTe quantum dots (CdTeQDs) or their binary mixtures to stimulate NF-κB binding in HepG2 cells. A dual luciferase reporter system was used to investigate NF-κB binding. Materials and method. Cells were transiently transfected with a firefly luciferase reporter system and Renilla luciferase expression plasmid as a transfection efficiency control. Twenty- four hours after transfection, the cells were treated with nanoparticles (10 µg/cm3 AgNPs, 10 µg/cm3 AuNPs, 3 µg/cm3 CdTeQDs) or with 10 ng/cm3 TNFα as a positive control. Six hours later, the cells were lysed and the activities of the luminescence of firefly and Renilla luciferases were measured using the Dual-Luciferase Reporter Assay System. Results. AuNPs and CdTeQDs alone significantly inhibited NF-κB binding activity. Co-treatment with AgNPs and CdTeQDs resulted in an additive effect, whereas the presence of AgNPs diminished the inhibitory effect of AuNPs. Interestingly, significant antagonism was observed between AuNPs and CdTeQDs, suggesting a similar mode of action. Conclusions. Comparison of the NF-κB binding activity induced by the mixtures of NPs suggests that in some cases NF-κB binding activity might differ from that observed for the NPs alone.
Źródło:
Annals of Agricultural and Environmental Medicine; 2020, 27, 2; 231-234
1232-1966
Pojawia się w:
Annals of Agricultural and Environmental Medicine
Dostawca treści:
Biblioteka Nauki
Artykuł
Tytuł:
p53-dependent suppression of the human calcyclin gene (S100A6): the role of Sp1 and of NFκB
Autorzy:
Króliczak, Weronika
Pietrzak, Maciej
Puzianowska-Kuznicka, Monika
Powiązania:
https://bibliotekanauki.pl/articles/1040715.pdf
Data publikacji:
2008
Wydawca:
Polskie Towarzystwo Biochemiczne
Tematy:
gene suppression
wild type and mutant p53
Sp1
calcyclin gene (S100A6)
NFκB
Opis:
Calcyclin (S100A6) is believed to participate in cell cycle control. It was, however, unclear if its expression depends on p53, a key regulator of apoptosis and cell cycle. We therefore performed transcription regulation assays in HeLa cells and found that wild type p53 suppressed the S100A6 promoter up to 12-fold in a dose-dependent manner. In contrast, the well-characterized V143A, R175H, R249S, and L344A p53 mutants cloned from human cancers suppressed this promoter with a 6 to 9-fold lower efficiency. All the sites mediating the p53-dependent suppression were contained in the -167 to +134 fragment of the S100A6 promoter. Separate overexpression of either Sp1 or of NFκB only partially counteracted the p53 inhibitory effect on the S100A6 promoter, while simultaneous overexpression of both these transactivators resulted in a complete abolishment of the p53 inhibitory effect on this promoter. Sp1 and NFκB binding to the probes resembling their putative binding sites present in the S100A6 promoter was decreased in the presence of wild type p53. We propose that the suppression of S100A6 is yet another mechanism by which p53 inhibits proliferation. Insufficient suppression of this gene by p53 mutants could well be responsible for calcyclin overexpression and cell cycle deregulation observed in cancer tissues.
Źródło:
Acta Biochimica Polonica; 2008, 55, 3; 559-570
0001-527X
Pojawia się w:
Acta Biochimica Polonica
Dostawca treści:
Biblioteka Nauki
Artykuł
Tytuł:
The role of nuclear factor-κB in the development of autoimmune diseases: a link between genes and environment
Autorzy:
Kuryłowicz, Alina
Nauman, Janusz
Powiązania:
https://bibliotekanauki.pl/articles/1040661.pdf
Data publikacji:
2008
Wydawca:
Polskie Towarzystwo Biochemiczne
Tematy:
autoimmune diseases
nuclear factor-κB (NF-κB)
genetic polymorphism
NF-κB targeted strategies
Opis:
Although autoimmune diseases are relatively common, mechanisms that lead to their development remain largely unknown. Nuclear factor-κB (NF-κB), as a key transcription factor involved in the regulation of immune responses and apoptosis, appears to be a good candidate for studies on the pathogenesis of autoimmunity. This review presents how perturbations of the NF-κB signaling pathway may contribute to self-tolerance failure, initiation of autoimmune inflammatory response as well as its persistent maintenance and therefore to the development of common autoimmune diseases including rheumatoid arthritis, multiple sclerosis, type 1 diabetes mellitus, thyroid autoimmune diseases, systemic lupus erythematosus as well as inflammatory bowel diseases and psoriasis. A special emphasis is put on the genetic variations in the NF-κB related genes and their possible association with susceptibility to autoimmune diseases, as well as on the therapeutic potential of the NF-κB targeted strategies in the treatment of autoimmunity.
Źródło:
Acta Biochimica Polonica; 2008, 55, 4; 629-647
0001-527X
Pojawia się w:
Acta Biochimica Polonica
Dostawca treści:
Biblioteka Nauki
Artykuł
Tytuł:
Flavanols from Japanese quince (Chaenomeles japonica) fruit suppress expression of cyclooxygenase-2, metalloproteinase-9, and nuclear factor-kappaB in human colon cancer cells
Autorzy:
Owczarek, Katarzyna
Hrabec, Elżbieta
Fichna, Jakub
Sosnowska, Dorota
Koziołkiewicz, Maria
Szymański, Jacek
Lewandowska, Urszula
Powiązania:
https://bibliotekanauki.pl/articles/1038623.pdf
Data publikacji:
2017
Wydawca:
Polskie Towarzystwo Biochemiczne
Tematy:
flavanols
Japanese quince (Chaenomeles japonica)
colon cells
COX-2
MMP-9
NF-κB
Opis:
Natural polyphenols and polyphenol-rich extracts have been found to possess preventive and therapeutic potential against several types of cancers, including colorectal cancer (CRC), which is an example of an inflammation-associated cancer. This study examines the chemopreventive effect of a Japanese quince (Chaenomeles japonica) fruit flavanol preparation (JQFFP) on colon cancer SW-480 cells. JQFFP, rich in procyanidin monomers and oligomers, was found to inhibit the SW-480 cell viability by 40% at 150 µM catechin equivalents (CE) after 72 h incubation when compared to control, but it was non-toxic to normal colon fibroblast CCD-18Co cells. Furthermore, 100 µM CE JQFFP suppressed COX-2 mRNA expression to 36.7% of control values and protein expression to 77%. In addition, JQFFP reduced the MMP-9 protein expression (to 24% vs. control at 100 µM CE) and caused inhibition of its enzymatic activity (to 35% vs. control at 100 µM CE). Not only did JQFFP inhibit the COX-2 and MMP-9 levels, but it also reduced the NF-κB protein expression (to 65% of control) and phosphorylation of its p65 subunit (to 51%) at 100 µM CE. These results provide the first evidence that JQFFP inhibits COX-2, MMP-9, and NF-κB expression, suggesting that it has cytotoxic, anti-inflammatory, and anti-metastatic activities towards the colon cancer SW-480 cells.
Źródło:
Acta Biochimica Polonica; 2017, 64, 3; 567-576
0001-527X
Pojawia się w:
Acta Biochimica Polonica
Dostawca treści:
Biblioteka Nauki
Artykuł
Tytuł:
Computational evaluation of bioactive compounds in Curcuma zanthorrhiza targeting SIRT1 and NFκB
Autorzy:
Prasetyawan, Sasangka
Safitri, Anna
Atho'illah, Mochammad Fitri
Rahayu, Sri
Powiązania:
https://bibliotekanauki.pl/articles/16693393.pdf
Data publikacji:
2023
Wydawca:
Polska Akademia Nauk. Czasopisma i Monografie PAN
Tematy:
curcuma
diabetes mellitus
NFκB
Sesquiterpenoid
SIRT1
Opis:
Type 2 diabetes mellitus (T2DM) is a metabolic disease with a high risk of complications and mortality. Novel T2DM therapeutic interventions are needed to combat this disease. This study aimed to identify pathways involved in T2DM and investigate sesquiterpenoid compounds from Curcuma zanthorrhiza that could act as SIRT1 activators and NFκB inhibitors. Protein–protein interaction and bioactive compound analysis were conducted using the STRING and STITCH databases, respectively. Molecular docking was used to determine the compounds’ interactions with SIRT1 and NFκB, while toxicity prediction was performed using Protox II. The results showed that curcumin could act as a SIRT1 activator (4I5I, 4ZZJ, and 5BTR) and NFκB inhibitor on the p52 relB complex and p50–p65 heterodimer, while xanthorrhizol could function as an IκK inhibitor. The toxicity prediction indicated that the active compounds of C. zanthorrhiza were relatively nontoxic because beta-curcumene, curcumin, and xanthorrizol belong to toxicity classes 4 or 5. These findings suggest that the bioactive compounds of C. zanthorrhiza could be promising candidates for developing SIRT1 activators and NFκB inhibitors to combat T2DM.
Źródło:
BioTechnologia. Journal of Biotechnology Computational Biology and Bionanotechnology; 2023, 104, 2; 171-182
0860-7796
Pojawia się w:
BioTechnologia. Journal of Biotechnology Computational Biology and Bionanotechnology
Dostawca treści:
Biblioteka Nauki
Artykuł
Tytuł:
Cu,Zn-superoxide dismutase deficiency in mice leads to organ-specific increase in oxidatively damaged DNA and NF-κB1 protein activity
Autorzy:
Siomek, Agnieszka
Brzoska, Kamil
Sochanowicz, Barbara
Gackowski, Daniel
Rozalski, Rafal
Foksinski, Marek
Zarakowska, Ewelina
Szpila, Anna
Guz, Jolanta
Bartlomiejczyk, Teresa
Kalinowski, Bartlomiej
Kruszewski, Marcin
Olinski, Ryszard
Powiązania:
https://bibliotekanauki.pl/articles/1042730.pdf
Data publikacji:
2010
Wydawca:
Polskie Towarzystwo Biochemiczne
Tematy:
Cu,Zn-SOD deficiency
NF-κB pathway
oxidative stress
Opis:
Earlier experimental studies have demonstrated that: i) Cu,Zn-superoxide dismutase deficiency leads to oxidative stress and carcinogenesis; ii) dysregulation of NF-κB pathway can mediate a wide variety of diseases, including cancer. Therefore, we decided, for the first time, to examine the level of oxidative DNA damage and the DNA binding activity of NF-κB proteins in SOD1 knockout, heterozygous and wild-type mice. Two kinds of biomarkers of oxidatively damaged DNA: urinary excretion of 8-oxodG and 8-oxoGua, and the level of oxidatively damaged DNA were analysed using HPLC-GC-MS and HPLC-EC. The DNA binding activity of p50 and p65 proteins in a nuclear extracts was assessed using NF-κB p50/p65 EZ-TFA transcription factor assay. These parameters were determined in the brain, liver, kidney and urine of SOD1 knockout, heterozygous and wild-type mice. The level of 8-oxodG in DNA was higher in the liver and kidney of knockout mice than in wild type. No differences were found in urinary excretion of 8-oxoGua and 8-oxodG between wild type and the SOD1-deficient animals. The activity of the p50 protein was higher in the kidneys, but surprisingly not in the livers of SOD1-deficient mice, whereas p65 activity did not show any variability. Our results indicate that in Cu,Zn-SOD-deficient animals the level of oxidative DNA damage and NF-κB1 activity are elevated in certain organs only, which may provide some explanation for organ-specific ROS-induced carcinogenesis.
Źródło:
Acta Biochimica Polonica; 2010, 57, 4; 577-583
0001-527X
Pojawia się w:
Acta Biochimica Polonica
Dostawca treści:
Biblioteka Nauki
Artykuł
Tytuł:
NF-κB signaling pathway and free radical impact
Autorzy:
Siomek, Agnieszka
Powiązania:
https://bibliotekanauki.pl/articles/1039704.pdf
Data publikacji:
2012
Wydawca:
Polskie Towarzystwo Biochemiczne
Tematy:
nitrogen oxygen species
NF-κB transcription factors
reactive oxygen species
Opis:
The activation of NF-κB transcription factor is critical for a wide range of processes such as immunity, inflammation, cell development, growth and survival. It is activated by a variety of stimuli including cytokines, ionizing radiation and oxidative stress. Redox modulations of NF-κB pathway have been widely demonstrated. Studies carried out during last years have advanced our knowledge about possible connections between NF-κB pathway and the impact of free radicals. This review is an endeavor to gather recent results focused on this issue, although an important question, whether oxidative stress plays a physiological role in NF-κB activation, seems to be still unanswered.
Źródło:
Acta Biochimica Polonica; 2012, 59, 3; 323-331
0001-527X
Pojawia się w:
Acta Biochimica Polonica
Dostawca treści:
Biblioteka Nauki
Artykuł
Tytuł:
TNFα-induced activation of NFκB protects against UV-induced apoptosis specifically in p53-proficient cells
Autorzy:
Szołtysek, Katarzyna
Pietranek, Katarzyna
Kalinowska-Herok, Magdalena
Pietrowska, Monika
Kimmel, Marek
Widłak, Piotr
Powiązania:
https://bibliotekanauki.pl/articles/1040680.pdf
Data publikacji:
2008
Wydawca:
Polskie Towarzystwo Biochemiczne
Tematy:
signaling
NF-κB
apoptosis
cytoprotection
TP53
Opis:
The signaling pathways that depend on p53 or NFκB transcription factors are essential components of cellular responses to stress. In general, p53 is involved in either activation of cell cycle arrest or induction of apoptosis, while NFκB exerts mostly anti-apoptotic functions; both regulatory pathways apparently interfere with each other. Here we aimed to analyze the effects of NFκB activation on DNA damage-induced apoptosis, either p53-dependent or p53-independent, in a set of human cell lines. Four cell lines, HCT116 and RKO colon carcinoma, NCI-H1299 lung carcinoma and HL60 myeloblastoma, each of them in two congenic variants either containing or lacking transcriptionally competent p53, were used. Cells were incubated with TNFα cytokine to activate NFκB and then treated with ultraviolet or ionizing radiation to induce apoptosis, which was assessed by measurement of the sub-G1 cell fraction. We observed that treatment with TNFα resulted in a significant reduction in the frequency of apoptotic cells in UV-irradiated p53-proficient lines (with exception of the UV-resistant NCI-H1299 cells). This anti-apoptotic effect was lost when cells were pretreated with parthenolide, an inhibitor of NFκB activation. In marked contrast, TNFα-pretreatment of p53-deficient lines resulted in an increased frequency of apoptotic cells after UV irradiation (with exception of HL60 cells). Such anti- and pro-apoptotic influence of TNFα was less obvious in cells treated with ionizing radiation. The data clearly indicates functional interference of both signaling pathways upon the damage-induced apoptotic response, yet the observed effects are both cell type- and stimulus-specific.
Źródło:
Acta Biochimica Polonica; 2008, 55, 4; 741-748
0001-527X
Pojawia się w:
Acta Biochimica Polonica
Dostawca treści:
Biblioteka Nauki
Artykuł
Tytuł:
Regulatory effects of 1,25-dihydroxyvitamin D3 on vascular smooth muscle cells
Autorzy:
Tukaj, Stefan
Trzonkowski, Piotr
Tukaj, Cecylia
Powiązania:
https://bibliotekanauki.pl/articles/1039718.pdf
Data publikacji:
2012
Wydawca:
Polskie Towarzystwo Biochemiczne
Tematy:
IκB-α
TNF-α
calcitriol
HSP70
NF-κB
IL-6
vitamin D
VSMC
Opis:
Inflammatory response has been recognized as a central feature in the development and progression of atherosclerosis, and VSMCs (Vascular Smooth Muscle Cells) - the main cellular component of media, play an important role in this process. Many reports indicate that the biologically active vitamin D metabolite - 1,25-dihydroxyvitamin D3 (1,25(OH)2D3 = calcitriol), besides its well established role in calcium homeostasis, plays an essential role in the regulation of the inflammation process. The aim of this study was to determine the regulatory effects of calcitriol, applied at two supra-physiological doses (10 nM and 100 nM), in VSMC culture. Secretion of the pro-inflammatory cytokines, IL-6 and TNF-α, was significantly attenuated in calcitriol-treated VSMC culture, but the level of anti-inflammatory TGF-β was generally unchanged. Since in advanced atherosclerosis lesions several cell types, including VSMCs, overproduce the HSP70 chaperone protein, we also checked the effects of calcitriol on its synthesis. The presence of 1,25(OH)2D3 did not affect HSP70 synthesis under physiological conditions but the synthesis of HSP70 in VSMCs exposed to heat shock was significantly inhibited by calcitriol (=100 nM). We observed that 1,25(OH)2D3 induced SOD 1 activity, stimulated the expression of IκB-α, and did not influence the level of NF-κB-p65 in VSMCs. The results of our study suggest that 1,25(OH)2D3 may serve as a natural anti-inflammatory agent and may therefore play a beneficial role in the physiology of VSMC in some contexts of atherosclerosis.
Źródło:
Acta Biochimica Polonica; 2012, 59, 3; 395-400
0001-527X
Pojawia się w:
Acta Biochimica Polonica
Dostawca treści:
Biblioteka Nauki
Artykuł
Tytuł:
The nuclear factor-kappaB (NF-κB): from a versatile transcription factor to a ubiquitous therapeutic target
Autorzy:
Yates, Laura
Górecki, Dariusz
Powiązania:
https://bibliotekanauki.pl/articles/1041153.pdf
Data publikacji:
2006
Wydawca:
Polskie Towarzystwo Biochemiczne
Tematy:
nuclear factor-kappaB (NF-κB)
IκB kinase complex (IKK)
transcription factors
inhibitory-kappaB (IκB)
Opis:
The nuclear factor-kappaB (NF-κB) transcription factors regulate a plethora of cellular pathways and processes including the immune response, inflammation, proliferation, apoptosis and calcium homeostasis. In addition to the complexity of its physiological roles, the composition and function of this family of proteins is very complicated. While the basic understanding of NF-κB signalling is extensive, relatively little is know of the in vivo dynamics of this pathway or what controls the balance between various outcomes. Although we know a large number of NF-κB-responsive genes, the contribution of these genes to a specific response is not always clear. Finally, the involvement of NF-κB in pathological processes is only now beginning to be unravelled. In addition to cancer and immunodeficiency disorders, altered regulation of NF-κB has been associated with several inherited diseases. These findings indicate that modulation of the NF-κB pathways may be beneficial. However, our limited knowledge of NF-κB signalling hinders therapeutic approaches: in many situations it is not clear whether the enhancement or inhibition of NF-κB activity would be beneficial or which pathways to interfere with and what the required level of activation is. Further studies of the role of NF-κB are needed as these may result in novel therapeutic strategies for a wide variety of diseases.
Źródło:
Acta Biochimica Polonica; 2006, 53, 4; 651-662
0001-527X
Pojawia się w:
Acta Biochimica Polonica
Dostawca treści:
Biblioteka Nauki
Artykuł
Tytuł:
Subcutaneous administration of infliximab-attenuated silica-induced lung fibrosis
Autorzy:
Zhang, Hua
Sui, Jun-Na
Gao, Lei
Guo, Jian
Powiązania:
https://bibliotekanauki.pl/articles/2162006.pdf
Data publikacji:
2018-07-04
Wydawca:
Instytut Medycyny Pracy im. prof. dra Jerzego Nofera w Łodzi
Tematy:
infliximab
silicosis
TNF-α
rat model
NF-κB
iNOS
Opis:
Objectives To investigate the influence of the anti-tumor necrosis factor-α infliximab (IFX) in the case of rats with silicosis. Material and Methods Forty-eight Wistar rats were randomly divided into 3 groups. The study group (N = 16) – silicosis was induced by intratracheal instillation of 50 mg silica on day 1, and IFX was subcutaneously administered at a dose of 15 mg/kg of body weight from day 2 to day 6, the vehicle group (N = 16) – silica used as the study group but without IFX, the sham group (N = 16) – 1 ml of saline was intratracheal-used. Eight rats in each group were euthanized on day 7 and on day 14, respectively. Lung tissue sections were stained with hematoxylin and eosin or Masson’s trichromedye. The nuclear factor-κB p65 (NF-κB p65) positioning in the lung tissues were determined by immunohistochemical staining. Levels of tumor necrosis factor α (TNF-α) in rat serum and bronchoalveolar lavage fluid were measured with enzyme linked immunosorbent assay. The inducible nitric oxide synthase (iNOS) mRNA in the lung tissues was measured by quantitative real-time polymerase chain reaction, as well as inhibitor protein-κB (I-κB) and NF-κB p65 expression were measured quantitatively by western blotting. Results Silica installation increased the lung tissues inflammation reaction, oxidative stress and pulmonary fibrosis. Infliximab treatment significantly improved silica-induced lung pathological changes (inflammatory cells, collagen deposition), decreased the TNF-α inhibited NF-κB signaling (I-κB, NF-κB p65) as well as oxidant status (iNOS). Conclusions Infliximab may improve silica-induced pulmonary inflammation by decreasing the TNF-α, inhibiting NF-κB signaling (I-κB, NF-κB p65) as well as oxidant status (iNOS), which suggest that IFX has potential role in the treatment of silica-induced lung damage. Int J Occup Med Environ Health 2018;31(4):503–515
Źródło:
International Journal of Occupational Medicine and Environmental Health; 2018, 31, 4; 503-515
1232-1087
1896-494X
Pojawia się w:
International Journal of Occupational Medicine and Environmental Health
Dostawca treści:
Biblioteka Nauki
Artykuł
Wyświetlanie 1-15 z 16

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