From the cow's bile, which is by product of food manufacture installations in Ho Chi Minh city, was surveyed and built up a progress for isolating cholic acide. From cholic acide by five steps obtained chenodeoxycholic acide. The product come up to the standard of BP 2000
Cholic Acid ; Animal Experimentation ; Chenodeoxycholic Acid

Bcl-2 protects tumor cells from the apoptotic effects of various anti-neoplastic agents. Increased expression of Bcl-2 has been associated with a poor response to chemotherapy in various malignancies, including leukemia. Hence, bypassing the resistance conferred by anti-apoptotic factors such as Bcl-2 represents an attractive therapeutic strategy against cancer cells, including leukemic cells. This study was undertaken to examine whether the anticancer drug, cisplatin and the synthetic chenodeoxycholic acid (CDCA) derivative, HS-1200 show anti-tumor activity in U937 and U937/Bcl-2 cells. Viability assays revealed that HS-1200 overcomes the resistance conferred by Bcl-2 in human leukemic U937 cells. Various apoptosis assessment assays further demonstrated that HS-1200 overcomes the resistance conferred by Bcl-2 in human leukemic U937 cells by inducing apoptosis. In addition HS-1200, but not cisplatin, overcomes the anti-apoptotic effects of Bcl-2 in Bcl-2 over-expressing human leukemic cells (U937/Bcl-2 cells). Notably, we observed that the HS-1200-induced formation of mature promyelocytic leukemia (PML) nuclear bodies (NBs) correlates with a suppression of the anti-apoptotic effects of Bcl-2 in human leukemic cells over-expressing this protein (U937/Bcl-2 cells). Furthermore, HS-1200 was found to induce the association between PML and SUMO-1, Daxx, Sp100, p53 or CBP in the aggregated PML-NBs of U937/Bcl-2 cells. Thus, PML protein and the formation of mature PML-NBs could be considered as therapeutic targets that may help to bypass the resistance to apoptosis conferred by Bcl-2. Elucidating the exact mechanism by which PML regulates Bcl-2 will require further work.
Apoptosis ; Chenodeoxycholic Acid ; Cisplatin ; Humans ; Leukemia ; U937 Cells

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

Bile acids and synthetic its derivatives induced apoptosis in various kinds of cancer cells and had anticancer effects. However, it wasn`t discovered those materials have apoptosis induced effects on osteosarcoma cells. The present study was done to examine the synthetic bile acid derivatives induced apoptosis on osteosarcoma cells and such these apoptosis events. The synthetic bile acid derivatives, chenodeoxycholic acid (CDCA) induced the cell death on human osteosarcoma (HOS) cells contrary to ursodeoxycholic acid (UDCA). HS-1200, a synthetic derivative of CDCAs, was chosen to experiment apoptosis events in HOS cells. HOS cells treated with HS-1200 showed nucleus condensation, cytochrom c release, Bax/Bcl-xL alteration, activation of caspase-3 and caspase-activated deoxyribonuclease (CAD), and degradation of poly (ADP-ribose) polymerase (PARP). Though this study needs more investigations, these in vitro data suggest that treatment of the synthetic bile acid derivatives can give medical therapy on HOS cells.
Apoptosis* ; Bile Acids and Salts ; Bile* ; Caspase 3 ; Cell Death ; Chenodeoxycholic Acid ; Humans* ; Osteosarcoma* ; Ursodeoxycholic Acid

Bile acids and synthetic bile acid derivatives induce apoptosis in various kinds of cancer cells and thus have anticancer properties. Recently, it has been suggested that autophagy may play an important role in cancer therapy. However, few data are available regarding the role of autophagy in oral cancers and there have been no reports of autophagic cell death in OSCCs (oral squamous cell carcinoma cells) induced by HS-1200, a synthetic bile acid derivative. We thus examine whether HS-1200 modulates autophagy in OSCCs. Our findings indicate that HS-1200 has anticancer effects in OSCCs, and we observed in these cells that autophagic vacuoles were visible by monodansylcadaverine (MDC)and acridine orange staining. When we analyzed HS-1200-treated OSCC cells for the presence of biochemical markers, we observed that this treatment directly affects the conversion of LC-3II, degradation of p62/SQSTM1 and full-length beclin-1, cleavage of ATG5-12 and the activation of caspase. An autophagy inhibitor suppressed HS-1200-induced cell death in OSCCs, confirming that autophagy acts as a pro-death signal in these cells. Furthermore, HS-1200 shows anticancer activity against OSCCs via both autophagy and apoptosis. Our current findings suggest that HS-1200 may potentially contribute to oral cancer treatment and thus provide useful information for the future development of a new therapeutic agent.
Acridine Orange ; Apoptosis ; Autophagy ; Bile ; Bile Acids and Salts ; Biomarkers ; Cadaverine ; Carcinoma, Squamous Cell ; Cell Death ; Chenodeoxycholic Acid ; Mouth Neoplasms ; Vacuoles

OBJECTIVETo analyze epidemiological characteristics of norovirus variant of GII.4 Sydney from January 2012 to June 2014 in sentinel hospitals of Guangdong province, as well as the outbreaks caused by norovirus variant of GII.4 Sydney.

METHODSDuring January 2012 to June 2014, a total of 10 750 fecal samples were obtained from 22 hospitals of surveillance sites in Guangdong province. Those samples were sent to the local municipal CDCs for extracting and detecting norovirus nucleic acid. Then, all the positive samples were delivered to Guangdong provincial CDC that used Random Number Method to draw 855 positive samples for norovirus genotyping, and 690 samples were successfully sequenced. Chi-square tests were used to compare norovirus infection status of diarrhea cases in different age groups as well as during different periods. Epidemiological data of 13 outbreaks which were caused by norovirus variant of GII.4 Sydney from January 2012 to June 2014 were collected from the Public Health Emergency Management Information System of Guangdong Province, and the epidemiological characteristics were analyzed.

RESULTSThe norovirus variant of GII.4 Sydney was first detected in August 2012 and the detection rate was 13/15 in November 2012. During November 2012 to January 2013 (period T1), the norovirus positive rate of each month was 23.8% (100/421), 15.9% (61/383) and 19.2% (95/495), respectively. During November 2013 to January 2014 (period T2), the norovirus positive rate of each month was 17.0% (90/529), 8.7% (37/426) and 11.2% (46/409), respectively which were significantly lower than that of period T1 (χ² alue was 6.65, 9.93 and 10.74. P value was 0.010, 0.002, and 0.001, respectively). In period T1, the norovirus positive rate of people ages 15 and older was 26.3% (143/543) and the rate of people under 15 was 14.9% (113/756) (χ² = 2.90, P < 0.001). In period T2, the norovirus positive rate of people ages 15 and older was 10.1% (52/516) and the rate of people under 15 (14.3% (121/848)) (χ²= 5.09, P = 0.024). The foodborne transmission was the infection source for ten of thirteen outbreaks.

CONCLUSIONThe norovirus variant of GII.4 Sydney was first detected in August 2012. The epidemic began to occur in the community since November 2012, and the strength of the epidemic declined 1 year later. The foodborne transmission was the main infection sources for the outbreaks caused by norovirus variant of GII.4 Sydney.

Adolescent ; Adult ; Chenodeoxycholic Acid ; analogs & derivatives ; Child ; China ; Diarrhea ; Disease Outbreaks ; Epidemics ; Foodborne Diseases ; Genotype ; Humans ; Norovirus ; Sentinel Surveillance

OBJECTIVE: To explore the effects of taurolithocholic acid (tLCA) and chenodeoxycholic acid (CDCA) on the expression of aorexigenic neuropeptide in mouse hypothalamus GT1-7 cells. METHODS: Mouse hypothalamic GT1-7 cells were treated with culture medium containing 10% FBS (control group, =3) or with 10 nmol/L, 100 nmol/L, 1 μmol/L and 10 μmol/L tLCA (tLCA group, =3) or CDCA (CDCA group, =3) for 12, 24 or 48 h. Real-time PCR was performed to determine the expression levels of proopiomelanocortin (POMC) mRNA in the cells, and the production levels of α-melanocyte-stimulating hormone (α-MSH) were assessed using an ELISA kit. Signal transduction and activator of transcription 3 phosphorylation (p-STAT3), threonine kinase phosphorylation (p-AKT), suppressor of cytokine signaling 3 (SOCS3), G protein-coupled bile acid receptor-1 (TGR5) and farnesoid X receptor (FXR) protein were detected by Western blotting. RESULTS: Western blotting results showed that mouse hypothalamic GT1-7 cells expressed two bile acid receptors, TGR5 and FXR, whose expressions were regulated by bile acids. Real-time PCR showed that the expression of POMC mRNA was significantly increased in the cells after treatment with 10 μmol/L tLCA or CDCA for 24 h. POMC-derived anorexigenic peptide α-MSH increased significantly in GT1-7 cells after treatment with 10 μmol/L tLCA or CDCA for 24 h. Treatment of the cells with tLCA or CDCA significantly increased the expressions of intracellular signaling proteins including p-STAT3, p-AKT and SOCS3. CONCLUSIONS Mouse hypothalamic GT1-7 cells express bile acid receptors TGR5 and FXR. Bile acids tLCA or CDCA can promote the expression of POMC mRNA and increase the production of the anorexigenic peptide α-MSH. The intracellular signaling proteins p-AKT, p-STAT3 and SOCS3 are likely involved in bile acid-induced anorexigenic peptide production.
Animals ; Bile Acids and Salts ; Chenodeoxycholic Acid ; Hypothalamus ; Mice ; Neuropeptides ; Phosphorylation ; STAT3 Transcription Factor ; Signal Transduction ; Suppressor of Cytokine Signaling 3 Protein

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

Cerebrotendinous Xanthomatosis is a rare inherited autosomal recessive disorder characterized by an increased plasma cholestanol level and the accumulation of sterol in tendon and nervous system. The primary biochemical abnormality is a defect in the synthesis of bile acid due to a lack of hepatic mitochondrial sterol-26-hydroxylase activity. The clinical symptoms usually begin in the 2nd decade and include cataract, xanthoma, and progressive neurological dysfunction. There are variable abnormal findings in the eletrophysiologic and radiologic evaluation. The usual treatment consists of long-term administration of the chenodeoxycholic acid (CDCA or UDCA) or cholic acid, which may correct the biochemical abnormality. We report a case of Cerebrotendinous Xanthomatosis in a 32 year old male patient suffered from gait disturbance and tendon xanthoma in both achilles tendons and left knee area.
Achilles Tendon ; Adult ; Bile ; Cataract ; Chenodeoxycholic Acid ; Cholestanol ; Cholic Acid ; Gait ; Humans ; Knee ; Male ; Nervous System ; Plasma ; Tendons ; Xanthomatosis ; Xanthomatosis, Cerebrotendinous*

PURPOSE: To examine whether a synthetic bile acid derivatives (HS-1200) sensitizes the radiation-induced apoptosis in human breast cancer cells (MCF-7) and to investigate the underlying mechanism. MATERIALS AND MEHTODS: Human breast cancer cells (MCF-7) in exponential growth phase were treated with HS-1200 for 24 hours at 37degrees C with 5% CO2 in air atmosphere. After removal of HS-1200, cells were irradiated with 2~8 Gy X-ray, and then cultured in drug-free media for 24-96 hours. The effect of radiation on the clonogenicity of MCF-7 cells was determined with clonogenic cell survival assay with 16muM of HS-1200. The induction of apoptosis was determined using agarose gel electrophoresis and Hoechst staining. The expression level of apoptosis-related molecules, such as PARP, Bax, Bcl-2, Bak and AIF, were assayed by Western blotting analysis with 40muM of HS-1200 combined with 8 Gy irradiation. To examine the cellular location of cytochrome c, bax and AIF immunofluorescent stainings were undertaken RESULTS: Treatment of MCF-7 cells with 40muM of HS-1200 combined with 8 Gy irradiation showed several changes associated with enhanced apoptosis by agarose gel electrophoresis and Hoechst staining. HS-1200 combined with 8 Gy irradiation treatment also enhanced production of PARP cleavage products and increased Bax/Bcl-2 ratio by Western blotting. Loss of mitochondrial membrane potential (delta psi m) and increased cytochrome c staining indicated that cytochrome c had been released from the mitochondria in HS-1200 treated cells. CONCLUSION: We demonstrated that combination treatment with a synthetic chenodeoxycholic acid derivative HS-1200 and irradiation enhanced radiation-induced apoptosis of human breast cancer cells (MCF-7). We suggest that the increased Bax/Bcl-2 ratio in HS-1200 co-treatment group underlies the increased radiosensitivity of MCF-7 cells. Further futures studies are remained elusive.
Apoptosis* ; Atmosphere ; Bile ; Blotting, Western ; Breast Neoplasms* ; Breast* ; Cell Survival ; Chenodeoxycholic Acid ; Cytochromes c ; Electrophoresis, Agar Gel ; Humans* ; MCF-7 Cells ; Membrane Potential, Mitochondrial ; Mitochondria ; Radiation Tolerance