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The outer membrane protein K, OmpK first identified in Vibrio parahaemolyticus has been shown to be a receptor for a broad host range vibriophage KVP40 infecting members of the Vibrionaceae. In the study, the effect of culture conditions on the expression of ompK in V. anguillarum was studied using real-time PCR. The expression increased significantly in the presence of bile salts and iron chelating agent 2, 2’ bipyridine, suggesting a role for this protein in bile resistance and also in iron acquisition by V. anguillarum. OmpK induction by iron limitation and the presence of bile salts was reconfirmed by western blot technique after growing the cells in trypticase soy broth supplemented with bile salts, blood and 2, 2’ bipyridine. We surmise that the expression of OmpK protein of V. anguillarum is bile salt and iron chelating agent-dependent.
Four calves were implanted a micro-radio-pressure capsule into their gallbladders in order to measure continuously pressure changes over 3 months. A special programme was designed to compute an electric signal on pressure value expressed in mm Hg. During fasting state, permanent rhythmic pressure changes were superimposed on a cyclic tonic increase in the gallbladder pressure. While rhythmic pressure changes at a frequency of 4,0 ± 0,7 cycles/10 min lasted usually 90,00 ± 7,00 s, the duration of tonic pressure changes was around 24,00 ± 2,90 min being repeated every 95,00 ± 7,00 min. After feeding, the rhythmic pressure changes exhibited a greater amplitude, and occasional long duration of a tonic increase in pressure was prolonged up to 110 min. Caerulein (1 Hg/kg) significantly increased tonic pressure changes. The most abundant response of the gallbladder was seen during the first 20 min of postinjection period, indicating direct actions on its musculature. When injecting pilocarpine (1 mg/kg) of cholinergic potency, the tonic response was more dilated and of a smaller amplitude, but rhythmic pressure changes were distinct. Infusion of 30 μM/min/20 min TCHNa (sodium taurocholate) induced a two phasic increase in gallbladder pressure lasting 35,90 ± 4,70 min. These data suggest that long duration of tonic pressure changes of the gallbladder are controlled by the hormonal, CCK dependent mechanism, but permanent rhythmic pressure changes are influenced by vagal stimulation. It also appears that bile salts can modulate pressure changes of gallbladder, especially trihyd- roksy-derivatives in the form of TCHNa, but the mechanism by which bile salts exert a contractile effect remains to be elucidated.
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Bile acids are multifunctional modulators of the Barrett’s carcinogenesis

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Bile salts play an important pathogenic role in the development of Barrett adenocarcinoma (BA). However, the precise role of different bile salts in this process is still unknown. The aim of the present study was to compare the effects of two different bile salts, deoxycholic acid (DCA) and ursodeoxycholic acid (UDCA) on the expression of COX-2, CDX-2 and DNA repair enzymes (MUTYH, OGG-1) in the Barrett epithelial cancer cells (OE-19). OE-19 cells were incubated with DCA or UDCA (100 µM or 300 µM at pH=7.0) over 24 h. To investigate the involvement of NFB, in separate experiments the cells were incubated with DCA in the presence of proteosome inhibitor (MG-132). Cells cycle and apoptosis were analyzed by FACS analysis. After incubation of OE-19 cells with bile salts, the expression of mRNA of COX-2, DNA repair enzymes (MUTYH, OGG-1) and caudal-related homebox transcription factor CDX-2 were measured by quantitative RT-PCR. OE-19 cell were also transfected with siRNA-RelA (p65) to asses effect of NFB inactivation on COX-2 and CDX2 expression. DCA caused a stronger reduction in cell survival of OE-19 cells than UDCA. In addition, DCA stimulated directly the translocation of NFB p65 (active form) in the nuclei of OE-19 cells. DCA caused stronger than UDCA stimulation of the COX-2 mRNA expression in these cells and this effect was significantly attenuated by the addition of inhibitor of NFB activity (proteosome inhibitor MG-132). siRNA-RelA reduced expression not only of NFB but also expression of COX-2 as well as CDX-2 mRNA. DCA caused stronger downregulation of mRNA for DNA repair enzymes MUTYH and OGG-1 than UDCA. In contrast, UDCA induced stronger CDX-2 mRNA expression than DCA in OE-19 cells. We conclude that bile salts are involved in the carcinogenesis of Barrett adenocarcinoma via inhibition of DNA repair enzymes and induction of COX-2 and this last effect is, at least partly, mediated by NFB. DCA shows carcinogenic potential due to high upregulation of COX-2, CDX-2 and downregulation of DNA repair enzymes.
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