• Proceedings of the PSK Conference
• /
• 2003.04a
• /
• pp.207.1-207.1
• /
• 2003

Ursodeoxycholic acid (UDCA) has been known commonly improving hyperbilirubinemia and excretion abnormality of bromsulphalein, which are appeared in the liver, and reducing the release of cholesterol from bile duct. In our study, UDCA was aimed to know if the agent can inhibit the pathogenesis of AD by suppressing the microglial activation when stimulated particularly by A${\beta}$ peptide, which is known a major cause of AD. (omitted)

• Archives of Pharmacal Research
• /
• v.13 no.1
• /
• pp.38-42
• /
• 1990

The present study was undertaken to determine the inhibitory effects of cholane compounds, unsodeoxycholic acid (UDCA) and chenodeoxycholic acid (CDCA) on the development of morphine-induced tolerance and physical dependence, and also to determine the hepatic glutathione contents. UDCA and CDCA inhibited the development of morphine-induced tolerance and physical dependence significantly. UDCA inhibited the hepatic glutathione decrease induced by morphine multiple injections, while this effect was not observed in CDCA treated mice. It was throught that the inhibitory effects of hepatic glutathione decrease in morphine-treated mice by UDCA and CDCA showed a tendency of inhibitory effects of development of morphine tolerance and dependence.

• Biomolecules & Therapeutics
• /
• v.6 no.3
• /
• pp.232-241
• /
• 1998

This study was done to investigate whether cholic acid derivatives have anti-stress activity in various stress models. Two cholic acid derivatives, ursodeoxycholic acid (UDCA) and tauroursodeoxycholic acid (WDCA), were used. physical, psychological, chemical and environmental stress models were performed. Adrenal weight, serum glucose levels and ALP activity were elevated in restraint stress model, but this elevation was prevented by UDCA treatment. Moreover, UDCA and TUDCA inhibited exploratory and spontaneous movements in oscillation stress model. In alcohol-induced stress model, TUDCA improved rotarod performance. UDCA and TUDCA significantly reduced the involution of lymphoid organs and the increment of WBC counts in cold stress model. These findings suggest that choric acid derivatives have antistress effects in various stress models.

• Biomolecules & Therapeutics
• /
• v.16 no.2
• /
• pp.126-131
• /
• 2008

Immunosuppressive therapy after organ transplantation is routinely used to prevent rejection of the organ, because this decreases the risk of adverse events, infection, and malignancies. Recently, ursodeoxycholic acid (UDCA), which is isolated from the dried bile of adult Chinese bears, has been shown to reduce the incidence and severity of acute rejection of liver allograft during early phase of liver transplantation. Therefore, in this study, we investigated the effect of UDCA on the proliferation of splenocytes exposed to PMA plus ionomycin. Our results demonstrated that UDCA decreased the splenocytes' proliferation in a dose-dependent manner. The decreased cell proliferation was accompanied with the decreased secretion of cytokines such as IL-2, IFN-${\gamma}$ and TNF-${\alpha}$. In addition, the pretreatment of UDCA on splenocytes stimulated with PMA plus ionomycin decreased the mRNA levels of cytokines (IL-2, IFN-${\gamma}$ and TNF-${\alpha}$) and costimulatory molecules (B7.2 and PD-L1). These results suggest the beneficial effect of UDCA on organ transplantation by decreasing lymphocyte proliferation.

• Archives of Pharmacal Research
• /
• v.20 no.1
• /
• pp.29-33
• /
• 1997

The effects of ursodeoxycholic acid (UDCA) and its novel derivative, named as HS-1030, on the proliferation of HepG2, human hepatocellular carcinoma cells were investigated. Whereas UDCA had no significant effect in a concentration range we have tested, HS-1030 inhibited the proliferation of HepG2 cells in a concentration dependent manner. Surprisingly, HS-1030 had no effect on the proliferation of Human Chang liver cell which is a normal liver cell line. We also found that proliferation-inhibitory effect of HS-1030 was due to the induction of apoptosis of HepG2 cells, which was confirmed by observing the internucleosomal DNA fragmentation and morphological changes (ie., cell shrinkage, nuclear condensation and the formation of apoptotic bodies). These results suggest that HS-1030 may be a good candidate as a drug for the treatment of liver cancer.

• Proceedings of the Korean Society of Applied Pharmacology
• /
• 1998.11a
• /
• pp.199-199
• /
• 1998

In this study, the effects of ursodeoxycholic acid (UDCA) on ischemia/reperfusion injury were investigated on retrograded aortic perfusion model. Hearts from Sprague-Dawley rats were perfused with oxygenated Krebs-Henseleit solution (pH 7.4, 37) on a Langendorff apparatus. After equilibration, hearts were treated with ursodeoxycholic acid 10, 20, 40 and 800 M or vehicle (0.04% DMSO) for 10 min before the onset of ischemia. Following 25 min of global ischemia, ischemic hearts were reperfused and allowed to recover for 30 min. The physiological (i.e. heart rate, left ventricular diastolic pressure, coronary flow and time to contracture formation) and biochemical (lactate dehydrogenase, LDH) endpoints were evaluated. In vehicle group, time to contracture formation (TTC) value was 19.5 min during ischemia, LVDP was 20.8 mmHg at the endpoint of reperfusion and LDH activity in reperfusate was 59.7 U/L. Cardioprotective effects of UDCA following ischemia/reperfusion consisted of a reduced TTC (EC$\_$25/ = 16.10 M), reduced LDH release and enhanced recovery of contractile function during reperfusion. Especially, the treatments of UDCA 80 M remarkably increased LVDP (68.1 mmHg) and reduced LDH release (33.2 U/L). Our findings suggest that UDCA ameliorates ischemia/reperfusion-induced myocardial damage, in agreement with physiological and biochemical parameters.

• Journal of Food Hygiene and Safety
• /
• v.9 no.2
• /
• pp.75-80
• /
• 1994

The effects of ursodeoxycholic acid (UDCA) were studied on the hepatotoxicity induced by several hepatotoxicants such as carbonte trachloride, thioacetamide and 1-naphthylisothiocyanate in ICR male mice. UDCA (50 mg/kg, 100 mg/kg) decreased the elevated serum bilirubin in carbon tetrachloride intoxicated mice, the elevated serum AST, alkaline phosphatase in thioacetamide intoxicated mice, the elevated serum AST and bilirubin in 1-naphthylisothiocyanate intoxicated mice.

• 대한치주과학회:학술대회논문집
• /
• 1998.11a
• /
• pp.92-93
• /
• 1998

• IMMUNE NETWORK
• /
• v.5 no.1
• /
• pp.45-49
• /
• 2005

Background: Inflammation in the brain has known to be associated with the development of a various neurological diseases. The hallmark of neuro-inflammation is the activation of microglia, brain macrophage. Pro-inflammatory compounds including nitric oxide (NO) are the main cause of neuro-degenerative disease such as Alzheimer's disease (AD) which is resulted in cell death. Among those pro-inflammatory compounds, NO contributes to the cell death by directly or indirectly. Methods: In the study, we examined whether ursodeoxycholic acid (UDCA), a non-toxic hydrophilic bile acid, inhibits the NO production by a direct method using Griess reagent and by RT-PCR in the gene expression of inducible nitric oxide synthase (iNOS). In signal transduction, we also examined the NF-${\kappa}B$ (p65/p50), IKK, and I ${\kappa}B$, which are associated with the expression of iNOS gene using western blots. Results: In the present study, we found that UDCA effectively inhibited NO production in BV-2 microglial cell, and NF-${\kappa}B$ activation was reduced by suppressing IKK gene expression and by increasing the I${\kappa}B$ in cytosol comparing those to the positive control LPS. Conclusion: Taken together, these data suggested that UDCA may playa crucial role in inhibiting the NO production and the results imply that UDCA suppresses a cue signal of the microglial activation via stimulators, such as ${\beta}$-amyloid peptides which are known to stimulate microglia in AD pathogenesis.

• YAKHAK HOEJI
• /
• v.38 no.6
• /
• pp.646-653
• /
• 1994

The pharmacokinetics of DWP305, a new combined preparation for hepatic disorders was examined in rats. DWP305 was composed of ursodeoxycholic acid(UDCA), Cardus marianus extract(silymarin 74.5%), fursulthiamine and riboflavin tetrabutyrate(RTB). Especially, this study was focused on the possibilities of drug interaction that the administration of DWP305 may affect the oral absorption of each component. After oral administration of DWP305 and each component drug to rats, the biliary excretion of silybin and tauroursodeoxycholic acid(TUDCA), and the urinary excretion of vitamins were measured by HPLC up to 48 hours. The cumulative amount of TUDCA or silybin in bile was not significantly different between DWP305 and UDCA/silymarin administered groups at doses of 25 and 100 mg/kg. In the case of vitamin study, the urinary thiamine excretion of equivalent molar fursulthiamine administered group was significantly higher than that of thiamine administered group. Urinary riboflavin level of equivalent molar RTB administered group was lower than that of riboflavin administered group, but not significant. These results suggest that the combined preparation may not affect the oral absorption of each component in respect of drug interaction. Also, fursulthiamine and RTB were more effective in oral absorption than thiamine and riboflavin, respectively.