Temat: cytoprotection - Katalog OPAC zbiorów

Skocz do pozycji: 1.

Tytuł:: An endogenous defensive concept, renewed cytoprotection/adaptive cytoprotection: intra(per)-oral/intragastric administration of strong alcohol in rat. Involvement of pentadecapeptide BPC 157 and nitric oxide system
Autorzy:: Becejac, T.
Cesarec, V.
Drmic, D.
Hirsl, D.
Madzarac, G.
Djakovic, Z.
Bunjevac, I.
Zenko Sever, A.
Sepac, A.
Batelja Vuletic, L.
Stancic Rokotov, D.
Seiwerth, S.
Sikiric, P.
Powiązania:: https://bibliotekanauki.pl/articles/70217.pdf
Data publikacji:: 2018
Wydawca:: Polskie Towarzystwo Fizjologiczne
Tematy:: cytoprotection
adaptive cytoprotection
pentadecapeptide BPC 157
alcohol
oral application
oesophageal lesion
low sphincter pressure
L-arginine
rat
Źródło:: Journal of Physiology and Pharmacology; 2018, 69, 3
0867-5910
Pojawia się w:: Journal of Physiology and Pharmacology
Dostawca treści:: Biblioteka Nauki

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Skocz do pozycji: 2.

Tytuł:: Heme oxygenase-1 expression in disease states.
Autorzy:: Deshane, Jessy
Wright, Marcienne
Agarwal, Anupam
Powiązania:: https://bibliotekanauki.pl/articles/1041399.pdf
Data publikacji:: 2005
Wydawca:: Polskie Towarzystwo Biochemiczne
Tematy:: heme oxygenase-1
heme
cytoprotection
polymorphisms
disease
Opis:: Heme oxygenase-1 (HO-1) is an enzyme which catalyzes the rate-limiting step in heme degradation resulting in the formation of iron, carbon monoxide and biliverdin, which is subsequently converted to bilirubin by biliverdin reductase. The biological effects exerted by the products of this enzymatic reaction have gained much attention. The anti-oxidant, anti-inflammatory and cytoprotective functions associated with HO-1 are attributable to one or more of its degradation products. Induction of HO-1 occurs as an adaptive and beneficial response to several injurious stimuli including heme and this inducible nature of HO-1 signifies its importance in several pathophysiological disease states. The beneficial role of HO-1 has been implicated in several clinically relevant disease states involving multiple organ systems as well as significant biological processes such as ischemia-reperfusion injury, inflammation/immune dysfunction and transplantation. HO-1 has thus emerged as a key target molecule with therapeutic implications.
Źródło:: Acta Biochimica Polonica; 2005, 52, 2; 273-284
0001-527X
Pojawia się w:: Acta Biochimica Polonica
Dostawca treści:: Biblioteka Nauki

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Skocz do pozycji: 3.

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