Inhibitory effect of bile acids on renin angiotensinogen reaction system

1972 ◽  
Vol 28 (2) ◽  
pp. 165-166 ◽  
Author(s):  
T. Kokubu ◽  
K. Hiwada ◽  
E. Ueda ◽  
Y. Yamamura
Keyword(s):  
Bile Acids ◽  
Reaction System ◽  
Inhibitory Effect

scholarly journals Inhibitory Effect of Rabbit Bile on Renin Angiotensinogen Reaction System

1970 ◽  
Vol 33 (11) ◽  
pp. 1231-1233 ◽  
Author(s):  
KUNIO HIWADA ◽  
TATSUO KOKUBU ◽  
YUICHI YAMAMURA
Keyword(s):  
Reaction System ◽  
Inhibitory Effect

Role of amidation in bile acid effect on DNA synthesis by regenerating mouse liver

1995 ◽  
Vol 268 (6) ◽  
pp. G1051-G1059
Author(s):  
E. R. Barbero ◽  
M. C. Herrera ◽  
M. J. Monte ◽  
M. A. Serrano ◽  
J. J. Marin
Keyword(s):  
Bile Acid ◽  
Dna Synthesis ◽  
Bile Acids ◽  
High Performance ◽  
Cell Injury ◽  
Intraperitoneal Administration ◽  
Inhibitory Effect ◽  
Toxicity Tests ◽  
Maximal Effect

Effect of bile acids on DNA synthesis by the regenerating liver was investigated in mice in vivo after partial hepatectomy (PH). Radioactivity incorporation into DNA after [14C]thymidine intraperitoneal administration peaked at 48 h after PH. At this time a significant taurocholate-induced dose-dependent reduction in DNA synthesis without changes in total liver radioactivity content was found (half-maximal effect at approximately 0.1 mumol/g body wt). Effect of taurocholate (0.5 mumol/g body wt) was mimicked by chocolate, ursodeoxycholate, deoxycholate, dehydrocholate, tauroursodeoxycholate, taurochenodeoxycholate, and taurodeoxycholate. In contrast, chenodeoxycholate, glycocholate, glycochenodeoxycholate, glycoursodeoxycholate, glycodeoxycholate, 5 beta-cholestane, bromosulfophthalein, and free taurine lacked this effect. No relationship between hydrophobic-hydrophilic balance and inhibitory effect was observed. Analysis by high-performance liquid chromatography indicated that inhibition of thymidine incorporation into DNA was not accompanied by an accumulation of phosphorylated DNA precursors in the liver but rather by a parallel increase in nucleotide catabolism. Bile acid-induced modifications in DNA synthesis were observed in vivo even in the absence of changes in toxicity tests, which suggests that the inhibitory effect shared by most unconjugated and tauroconjugated bile acids but not by glycoconjugated bile acids should be accounted for by mechanisms other than nonselective liver cell injury.

scholarly journals Taurolithocholate-induced Ca2+ release is inhibited by phorbol esters in isolated hepatocytes

1992 ◽  
Vol 287 (3) ◽  
pp. 891-896 ◽  
Author(s):  
L Combettes ◽  
B Berthon ◽  
M Claret
Keyword(s):  
Bile Acid ◽  
Bile Acids ◽  
Phorbol Ester ◽  
Phorbol Esters ◽  
Rat Hepatocytes ◽  
Isolated Hepatocytes ◽  
Inhibitory Effect ◽  
Cell Uptake ◽  
Intracellular Binding ◽  
Pkc Activation

The monohydroxy bile acid taurolithocholate (TLC) causes a rapid and transient increase in free cytosolic Ca2+ concentration ([Ca2+]i) in suspensions of rat hepatocytes similar to that elicited by the InsP3-dependent hormone vasopressin. The effect of the bile acid is due to a mobilization of Ca2+, independent of InsP3, from the endoplasmic reticulum (ER). Short-term preincubation of cells with the phorbol ester 4 beta-phorbol 12 beta-myristate 13 alpha-acetate (PMA), which activates protein kinase C (PKC), blocked the increase in [Ca2+]i induced by TLC, but did not alter that mediated by vasopressin. We obtained the following results, indicating that the effect of PMA is mediated by the activation of PKC. (1) Phorbol esters were effective over a concentration range where they activate PKC (IC50 = 0.5 nM); (2) phorbol esters that do not activate PKC did not inhibit the effects of TLC; (3) the permeant analogue oleoylacetylglycerol mimicked the inhibitory effect of PMA; (4) lastly, the inhibition of the TLC-induced Ca2+ mobilization by phorbol esters was partially prevented by preincubating the cells with the PKC inhibitors H7 and AMG-C16. Preincubating hepatocytes with PMA had no effect on the cell uptake of labelled TLC, indicating that the phorbol ester does not interfere with the transport system responsible for the accumulation of bile acids. In saponin-treated liver cells, PMA added before or after permeabilization failed to abolish TLC-induced Ca2+ release from the ER. The possibility is discussed that PMA, via PKC activation, may alter the intracellular binding or the transfer of bile acids in the liver.

Effect of protein on the determination of total bile acids in serum.

1983 ◽  
Vol 29 (1) ◽  
pp. 171-175 ◽  
Author(s):  
N Q Hanson ◽  
E F Freier
Keyword(s):  
Bile Acid ◽  
Bile Acids ◽  
Hydroxysteroid Dehydrogenase ◽  
Inhibitory Effect ◽  
Normal Serum ◽  
Total Serum ◽  
Enzyme Preparations ◽  
Analytical Recovery ◽  
Fluorescence Light

Abstract We measured total serum bile acids on a fluorescence-light-scattering micro centrifugal analyzer by the direct enzymatic method with 3 alpha-hydroxysteroid dehydrogenase (EC 1.1.1.50) and with resazurin as a fluorogenic electron acceptor. We found that serum protein has an inhibitory effect on the measurement of bile acids, but this effect was eliminated by adding bovine serum albumin to the reaction mixture in a final protein concentration (12.2 g/L) that was high compared with that contributed by a normal serum specimen. The assay is a sensitive method that reaches equilibrium in 5 min. The method is microscale (5 microL of sample, 150 microL of working reagent), is easy to perform, and is accurate (analytical recovery = 104.1%) and precise (CV = 11.1 and 5.7% on specimens with bile acid concentrations of 7.6 and 35.4 mumol/L, respectively). Normal values are 1-12 and less than 9 mumol/L on nonfasting and fasting individuals, respectively. Pure 3 alpha-hydroxysteroid dehydrogenase must be used: we found several enzyme preparations that gave falsely high values for bile acid.

scholarly journals Degradation of 17β-estradiol by UV/persulfate in different water samples

2021 ◽  
Author(s):  
Yunjie Zhu ◽  
Yanan Shao ◽  
Min Wei ◽  
Kefu Yu ◽  
Yuanyuan Zhang ◽  
...  
Keyword(s):  
Degradation Rate ◽  
Reaction System ◽  
Degradation Process ◽  
Inhibitory Effect ◽  
Bond Breakage ◽  
Benzene Rings ◽  
Optimum Ph ◽  
17Β Estradiol ◽  
By Products ◽  
Potential Use

Abstract Sulfate radical (•SO4−)-based advanced oxidation processes are widely used for wastewater treatment. This study explored the potential use of UV/persulfate (UV/PS) system for the degradation of 17β-estradiol (E2). The pH of the reaction system can affect the degradation rate of E2 by UV/PS and the optimum pH was 7.0; Br− and Cl− in water can promote the degradation rate, HCO3− has an inhibitory effect on the reaction, SO42− and cations (Na+, Mg2+, K+) have no effect on the degradation rate. The degradation of E2 by UV/PS was a mineralization process, with the mineralization rate reaching 90.97% at 8 h. E2 in the UV/PS system was mainly degraded by hydroxylation, deoxygenation, and hydrogenation. E2 reaction sites were mainly located on benzene rings, mainly carbonylation on quinary rings, and bond breakage between C10 and C5 resulted in the removal of benzene rings and carboxyl at C2 and C3 sites. In the presence of halogen ions, halogenated disinfection by-products were not formed in the degradation process of E2 by UV/PS. E2 in the UV/PS system could inhibit the formation of bromate. The results of this study suggest that UV/PS is a safe and reliable method to degrade E2.

Ursodeoxycholic acid inhibits glucagon-induced cAMP formation in hamster hepatocytes: a role for PKC

1995 ◽  
Vol 268 (2) ◽  
pp. G300-G310 ◽  
Author(s):  
B. Bouscarel ◽  
T. W. Gettys ◽  
H. Fromm ◽  
H. Dubner
Keyword(s):  
Ursodeoxycholic Acid ◽  
Bile Acids ◽  
Inhibitory Effect ◽  
Camp Production ◽  
Glucagon Receptor ◽  
Pkc Inhibitor ◽  
Camp Synthesis ◽  
Kinase C ◽  
Camp Formation ◽  
Pkc Activation

The effect of bile acids on adenosine 3',5'-cyclic monophosphate (cAMP) synthesis was investigated in isolated hamster hepatocytes. Bile acids had no direct effect on cAMP production. However, ursodeoxycholic acid (UDCA) and tauroursodeoxycholic acid inhibited, by approximately 45%, cAMP formation induced by concentrations of glucagon greater than 1 nM, with a respective half-maximum inhibitory effect observed at 4 +/- 2 microM. Similar inhibition was observed with phorbol 12-myristate 13-acetate (PMA). Chenodeoxycholic, murocholic, and taurodeoxycholic acids were the next most potent bile acids. Taurolithocholic acid was 100-fold less potent than UDCA, whereas both ursocholic and taurocholic acids had no effect at concentrations up to 0.5 mM. Neither bile acids nor PMA affected either the binding of glucagon to its receptor, the cAMP-dependent phosphodiesterase, adenylate cyclase, or the inhibitory and stimulatory (Gs) GTP-binding proteins. The inhibitory effect of PMA and UDCA on glucagon-induced cAMP synthesis was abolished in the presence of the protein kinase C (PKC) inhibitor, staurosporine. Furthermore, UDCA induced PKC translocation from cytosol to membrane and stimulated phosphorylation of an 80-kDa protein substrate for PKC. In conclusion, mediated by PKC activation, bile acids inhibit glucagon-induced cAMP synthesis by uncoupling the glucagon receptor and Gs.

Inhibition of interferon-α-induced signaling by hyperosmolarity and hydrophobic bile acids

2010 ◽  
Vol 391 (10) ◽  
Author(s):  
Dirk Graf ◽  
Katrin Haselow ◽  
Ivo Münks ◽  
Johannes G. Bode ◽  
Dieter Häussinger
Keyword(s):  
Protein Expression ◽  
Bile Acids ◽  
Hepatoma Cell ◽  
Protein A ◽  
Sodium Taurocholate ◽  
Inhibitory Effect ◽  
Interferon Α ◽  
Hepatoma Cell Line ◽  
Human Hepatoma Cell ◽  
Mrna And Protein Expression

Abstract Apart from viral conditions, host factors such as elevated bile acid concentrations are determinants of successful interferon-α (IFN-α) treatment in patients with chronic hepatitis C or B. The present study demonstrates that hydrophobic bile acids inhibit Jak1- and Tyk2-phosphorylation, which lead to blockade of STAT1-mediated IFN-α-signaling in the sodium-taurocholate cotransporting peptide (NTCP)-transfected human hepatoma cell line HepG2, resulting in a decreased mRNA and protein expression of IFN-stimulated genes such as myxovirus resistance protein A (MxA) or dsRNA-activated protein kinase (PKR). In addition, hyperosmotic stress leads to an inhibition of IFN-α-induced Jak1- and Tyk2-phosphorylation, and STAT1/STAT2-phosphorylation and gene expression. This inhibitory effect of hydrophobic bile acids or hyperosmolarity is not due to caspase-mediated cleavage or lysosomal degradation of the cognate receptors or to the generation of oxidative stress, activation of p38- or Erk-mediated MAPK pathways or phosphatase activity. Preincubation with the organic osmolyte betaine blocked the inhibitory effect of bile acids or hyperosmolarity on MxA protein expression, but had no effect on transcript levels or activation of STAT1, suggesting that betaine mediates its effects on MxA expression at a translational or post-translational level. Our findings could provide a rationale for betaine use in cholestatic HBV/HCV patients undergoing interferon therapy.

scholarly journals Ursodeoxycholic acid suppresses the malignant progression of colorectal cancer through TGR5-YAP axis

2021 ◽  
Vol 7 (1) ◽  
Author(s):  
Huan Zhang ◽  
Huanji Xu ◽  
Chenliang Zhang ◽  
Qiulin Tang ◽  
Feng Bi
Keyword(s):  
Colorectal Cancer ◽  
Bile Acid ◽  
Ursodeoxycholic Acid ◽  
Bile Acids ◽  
Inhibitory Effect ◽  
Bile Acid Metabolism ◽  
Dependent Manner ◽  
Concentration Dependent Manner ◽  
Rhoa Activity ◽  
Relationship Of

AbstractThe Hippo/YAP pathway plays an important role in the development of cancers. Previous studies have reported that bile acids can activate YAP (Yes Associated Protein) to promote tumorigenesis and tumor progression. Ursodeoxycholic acid (UDCA) is a long-established old drug used for cholestasis treatment. So far, the effect of UDCA on YAP signaling in colorectal cancer (CRC) is not well defined. This study means to explore relationship of UDCA and YAP in CRC. UDCA suppressed YAP signaling by activating the membrane G-protein-coupled bile acid receptor (TGR5). TGR5 mainly regulated cAMP/PKA signaling pathway to inhibit RhoA activity, thereby suppressing YAP signaling. Moreover, the restoration of YAP expression alleviated the inhibitory effect of UDCA on CRC cell proliferation. In AOM/DSS-induced CRC model, UDCA inhibited tumor growth in a concentration-dependent manner and decreased expression of YAP and Ki67. UDCA plays a distinguished role in regulating YAP signaling and CRC growth from the primary bile acids and partial secondary bile acids, demonstrating the importance of maintaining normal intestinal bile acid metabolism in cancer patients. It also presents a potential therapeutic intervention for CRC.

Molecular Mechanisms Triggered by Bile Acids on Intestinal Ca2+ Absorption

2018 ◽  
Vol 25 (18) ◽  
pp. 2122-2132 ◽  
Author(s):  
Ana Marchionatti ◽  
Maria Rivoira ◽  
Valeria Rodriguez ◽  
Adriana Perez ◽  
Nori Tolosa de Talamoni
Keyword(s):  
Bile Acids ◽  
Redox State ◽  
Molecular Mechanisms ◽  
Nitrosative Stress ◽  
Metabolic Diseases ◽  
Sodium Deoxycholate ◽  
Inhibitory Effect ◽  
Single Administration ◽  
Pubmed Database ◽  
Main Components

Background: Bile acids (BAs) are among the main components of bile. Lately, they are also considered important signaling molecules, not only by regulating their own synthesis, but also having a role in several metabolic diseases. Objective: In this review we focus on the effect of sodium deoxycholate (NaDOC), ursodeoxycholic (UDCA) and litocholic (LCA) acids and their combination upon the intestinal Ca2+ absorption. To make clear the actions of those BAs on this physiological process, an overview of current information about the mechanisms by which the intestinal Ca2+ occurs is described. Methods: The PubMed database was searched until 2017, using the keywords bile acids, NaDOC, UDCA and LCA and redox state, apoptosis, autophagy and intestinal Ca2+ absorption. Results: The modulation of redox state, apoptosis and autophagy are mechanisms that are involved in the action of BAs on intestinal Ca2+ absorption. Although the mechanisms are still not completely understood, we provide the latest knowledge regarding the effect of BAs on intestinal Ca2+ absorption. Conclusion: The response of the intestine to absorb Ca2+ is affected by BAs, but it is different according to the type and dose of BA. When there is a single administration, NaDOC has an inhibitory effect, UDCA is an stimulator whereas LCA does not have any influence. However, the combination of BAs modifies the response. Either UDCA or LCA protects the intestine against the oxidative injury caused by NaDOC by blocking the oxidative/nitrosative stress, apoptosis and autophagy.

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