Bile of animal(mainly chicken, pig, snake, cow, and bear) has long been used as medicine. As the major active components of bile, bile acids mainly include cholic acid, deoxycholic acid, chenodeoxycholic acid, ursodeoxycholic acid, and taurochenodeoxycholic acid. They interact with intestinal microorganisms in enterohepatic circulation, thereby playing an important part in nutrient absorption and allocation, metabolism regulation, and dynamic balance. Bile acids have pharmacological effects such as protecting liver, kidney, heart, brain, and nerves, promoting bile secretion, dissolving gallstones, anti-cancer, relieving cough and dyspnea, dispelling phlegm, treating eye diseases, and regulating intestinal function and blood glucose, which are widely used in clinical practice. This study summarized and analyzed the research on the chemical constituents and pharmacological effects of bile acids from medicinal animals, in a bid to provide scientific basis and reference for the further development and utilization of bile acids.
Animals ; Bile Acids and Salts ; Cattle ; Chenodeoxycholic Acid ; Cholic Acids ; Deoxycholic Acid ; Female ; Swine ; Ursodeoxycholic Acid

BACKGROUND: Bacterial and Helicobacter gene were commonly detected in diseased human bile, although the meaning of the presence of Helicobacter in biliary tract is still unclear. The aim of this study was to evaluate the changes of bile acid composition in bacterial and Helicobacter infected bile, and to determine whether Helicobacter pylori might grow in human bile or not. METHODS: Thirty bile samples were obtained by percutaneous transhepatic biliary drainage or gallbladder puncture during cholecystectomy. According to the polymerase chain reaction analysis using bacterial 16S rRNA and Helicobacter genus specific 16S rRNA primers, 3 groups were divided; Group I; no presence of any bacterial DNA, Group II; positive bacterial DNA only, Group III; positive bacterial and Helicobacter DNA. Bile acid analysis for deoxycholic acid (DCA), chenodeoxycholic acid (CDCA), lithocholic acid (LCA), and ursodeoxycholic acid (UDCA) was performed by high performance liquid chromatography. And then Helicobacter pylori was tried to culture in broth mixed with human bile at a final bile concentration of 50%. RESULTS: The concentrations of DCA in group II and III were very low and significantly reduced compared to group I (p<0.01, respectively). The concentrations of LCA or UDCA were not shown any relationships between groups. Helicobacter pylori has grown actively in the broth mixed with human bile containing both of less than 0.1 gm/L of DCA and CDCA, compared to no growth in media mixed with human bile containing more than 3.0 gm/L of DCA and/or CDCA. CONCLUSION: DCA seems to have the strongest antibacterial effect. Helicobacter pylori is likely to grow in human bile containg very low concentrations of CDCA and DCA.
Bile* ; Biliary Tract Diseases* ; Biliary Tract* ; Chenodeoxycholic Acid ; Cholecystectomy ; Chromatography, Liquid ; Deoxycholic Acid ; DNA ; DNA, Bacterial ; Drainage ; Gallbladder ; Helicobacter Infections* ; Helicobacter pylori ; Helicobacter* ; Humans ; Lithocholic Acid ; Polymerase Chain Reaction ; Punctures ; Ursodeoxycholic Acid

No abstract available.
Deoxycholic Acid* ; Phosphatidylcholines* ; Prurigo*

PURPOSE: Cytotoxicity of the bile acids on colon cancer cell lines was studied to know which bile acid was most cytotoxic to colonic mucosal epithelium. We performed agarose gel electrophoresis whether this toxicity was caused by detergent effect of the bile acids or by apoptotic pathway. MATERIALS AND METHODS: HT29, LoVo, SW620 colon cancer cell lines were exposed to lithocholate, cholate, deoxycholate and chenodeoxycholate with 50, 100, 150, 200, 250, 300 pM as final concentration in DMEM culture media for short time (for 2 hours) and for long time (for 5 days). Agarose gel electrophoresis was performed on each colon cancer cell lines (HT29, LoVo, SW620, SW480) after 1, 2, 3, 4, 5 days exposure to deoxycholate with 150 pM concentration to detect intemucleosomal fragmentation. RESULTS: There was no toxicity after short time exposure in all bile acids concentration and in all colon cancer cell lines. Of the bile acids, deoxycholate was most toxic for all colon cancer cell lines. And DNA fragmentation was noticed after 2 days exposure with deoxycholate. Only LoVo cell line showed apoptotic DNA pattern after 4 days of exposure with deoxycholate. CONCLUSION: Bile acids (especially deoxycholate) are suggested to be possible agents to cause apoptosis in colonic mucosal epithelium.
Apoptosis ; Bile Acids and Salts* ; Bile* ; Cell Line* ; Chenodeoxycholic Acid ; Cholates ; Colon* ; Colonic Neoplasms* ; Culture Media ; Deoxycholic Acid ; Detergents ; DNA ; DNA Fragmentation ; Electrophoresis, Agar Gel ; Epithelium ; Lithocholic Acid

OBJECTIVES: The purpose of this study is to shorten the decellularization time of trachea by using combination of physical, chemical, and enzymatic techniques. METHODS: Approximately 3.5-cm-long tracheal segments from 42 New Zealand rabbits (3.5±0.5 kg) were separated into seven groups according to decellularization protocols. After decellularization, cellular regions, matrix and strength and endurance of the scaffold were followed up. RESULTS: DNA content in all groups was measured under 50 ng/mg and there was no significant difference for the glycosaminoglycan content between group 3 (lyophilization+deoxycholic acid+de-oxyribonuclease method) and control group (P=0.46). None of the decellularized groups was different than the normal trachea in tensile stress values (P>0.05). Glucose consumption and lactic acid levels measured from supernatants of all decellularized groups were close to group with cells only (76 mg/dL and 53 mg/L). CONCLUSION: Using combination methods may reduce exposure to chemicals, prevent the excessive influence of the matrix, and shorten the decellularization time.
Deoxycholic Acid ; DNA ; Freeze Drying ; Glucose ; Lactic Acid ; Rabbits ; Tissue Engineering ; Trachea

BACKGROUND/AIMS: Deoxycholic acid (DCA) has been appeared to be an endogenous colon tumor promoter. In this study, we investigated whether DCA induces nuclear factor-kappa B (NF-kappa B) activation and IL-8 expression, and tauroursodeoxycholic acid (TUDC) inhibits this signaling in HT-29 cells. METHODS: After DCA treatments, time courses of NF-kappa B binding activity were determined by electrophoretic mobility shift assay (EMSA). Also, we performed Western blotting of I kappa B alpha to confirm NF-kappa B activation. Time and concentration courses of DCA-induced secretion of IL-8 were measured with ELISA in supernatants of cultured media from the cells. To evaluate the role of NF-kappa B, IL-8 levels were assessed after pretreatment with using phosphorothioate-modified anti-sense oligonucleotides (ODN). Moreover, DCA-induced secretions of IL-8 were measured after pretreatment with TUDC. RESULTS: DCA dose-dependently induced prominent NF-kappa B binding complexes from 30 min to 8 hr and degradation of I kappa B alpha. The secretions of IL-8 were increased with DCA (50~200 micro M) treatment in a time and dose-dependent manner. Pre-incubation of the cells with TUDC (0.1~10 micro M) for 2 hours caused significant decreases in DCA induced IL-8 secretion. However, transient transfection using p50 or p65 AS-ODN showed no effect on IL-8 secretion. CONCLUSIONS: DCA may play as a colonic tumor promoter through anti-apoptotic effect of NF-kappa B activation and IL-8 expression, and DCA-induced NF-kappa B independent IL-8 expression is inhibited by TUDC.
Blotting, Western ; Colonic Neoplasms ; Deoxycholic Acid/*pharmacology ; Dose-Response Relationship, Drug ; Electrophoretic Mobility Shift Assay ; English Abstract ; HT29 Cells ; Humans ; Interleukin-8/*metabolism ; NF-kappa B/*metabolism ; Oligonucleotides, Antisense/pharmacology ; Signal Transduction/*drug effects ; Taurochenodeoxycholic Acid/*pharmacology ; Trans-Activation (Genetics)/drug effects

Blood Platelets ; drug effects ; metabolism ; Calcium ; blood ; Deoxycholic Acid ; pharmacology ; Humans ; Quinazolines ; pharmacology ; Quinazolinones

OBJECTIVETo prepare puerarin deoxycholate/phospholipid mixed micelle to increase the solubility of puerarin.

METHODSodium deoxycholate and soybean phospholipids were used to prepare puerarin mixed micelle through orthogonal design experiments. With the solubility, shape and particle size as the response indexes, the preparing process of puerarin mixed micelle was optimized.

RESULTThe optimized process for the puerarin deoxycholate/phospholipid mixed micelle was that the puerarin, soya phosphatidylcholine and sodium deoxycholate with the mole ratio of 3:2:4 should be dissolved in methanol-chloroform (1:1), and the solvents should be evaporated rotatively at 30 degrees C. The particle diameter of the mixed micelle was (64.8 +/- 13) nm (volume-weighted particle size distribution), and the solubility was 0.811 1 g x L(-1) in water at the room temperature, which was 22.3 times as that of the raw puerarin (0.036 4 g x L-1).

CONCLUSIONThe puerarin deoxycholate/phospholipid mixed micelle can improve the solubility of puerarin significantly.

Deoxycholic Acid ; chemistry ; Isoflavones ; chemistry ; Micelles ; Particle Size ; Phospholipids ; chemistry ; Plant Extracts ; chemistry ; Solubility

BACKGROUND: The dimorphic yeast, Candida albicans, is considered as a dangerous opportunistic pathogen in immunocompromised hosts. Several phospholipases of C. albicans are known to be secreted into the culture medium. Phospholipases have been proposed as a virulence factor in the pathogenesis of Candida infections. OBJECTIVE: In order to investigate enzyme production, we examined culture condition of secreted phospholipase production from C. albicans. METHODS: C. albicans ATCC 10231 was cultivated in various media at 37 degrees C for 3 days. Phospholipase activity was measured by fatty acid soap precipitation in plate containing 0.04% lecithin, 0.1 M citrate buffer, pH 4.2 and 1.5% noble agar. RESULTS: Phospholipase was highly induced when C. albicans was cultivated in broth medium (containing glucose 2%, albumin 0.2% and Fe++ ion 0.01%) and Saboulaud's dextrose agar supplemented with 0.01% sodium deoxycholate. CONCLUSION: Highly induction of secreted phospholipase by albumin from C albicans may be play an important role in tissue invasion in the pathogenesis of C. albicans.
Agar ; Candida albicans* ; Candida* ; Citric Acid ; Deoxycholic Acid ; Glucose ; Hydrogen-Ion Concentration ; Immunocompromised Host ; Lecithins ; Phospholipases* ; Soaps ; Virulence ; Yeasts

PURPOSE: Bile acids (especially deoxycholate) was known to be toxic and mutagenic on colon epithelium. They proposed at least four mechanisms for the bile acid toxicity. It is the one of these mechanisms that bile acid inhibits the xenobiotic metabolizing enzyme activity (esp glutathione S-transferase, GST). So we measured the cytosolic GST level of colon carcinoma cell lines after deoxycholate exposure whether or not the deoxycholate lowered the cytosolic GST activity. METHODS: Three colon cancer cell lines (LoVo, SW480, HT29) were used for this study. We calculated the cellular toxicity by MTS method. And cytosolic GST activity was measured according to the method as Habig described. For total GST activity, 2.5 mM 1-chloro-2,4-dinitrobenzene was used for substrate, and measured as absorbance in 340 nm. RESULTS: Basal cytosolic GST level for LoVo, SW480, HT29 cell line was 514.59+/-27.01, 291.63+/-38.44 and 344.58+/-47.92 nmol/min/mg cytosol protein. GST level did not changed significantly after 5 days culture without DCA. But GST level was decreased significantly to 128.63+/-21.35, 134.33+/-41.76 and 163.10+/-22.73 nmol/min/mg cytosol protein each cell line after 5 days deoxycholate exposure (p<0.005). CONCLUSION: Cytosolic GST level was lowered significantly after deoxycholate exposure for 5 days. One of the mechanisms of bile acid toxicity for colon cancer cell is proposed to inhibit cytosolic GST activity.
Bile ; Bile Acids and Salts ; Cell Line* ; Colon* ; Colonic Neoplasms* ; Cytosol* ; Deoxycholic Acid* ; Dinitrochlorobenzene ; Epithelium ; Glutathione Transferase* ; Glutathione* ; HT29 Cells ; Humans