Glycodeoxycholic acid
Glycodeoxycholic acid levels could as prognostic biomarker in acetaminophen-induced acute liver failure patients. Glycodeoxycholic acid can induce the apoptosis of SMMC-7721 cells.
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Chinese Journal of Clinical Laboratory Science, 2009, 27(3):167-169.
The effect of glycodeoxycholic acid on P53 expression in the apoptosis of SMMC-7721 cells[Reference:
WebLink]
To investigate the effect of Glycodeoxycholic acid(GDCA) on apoptosis of and P53 expression in SMMC-7721 cells.
METHODS AND RESULTS:
Apoptotic rate was examined by Annexin V.P53 mRNA was analyzed by RT-PCR,and P53 protein was measured by immunohistochemistry technique.Compared with the control,SMMC-7721 cells treated with GDCA had significantly increased apoptotic rate in a dose-and time-dependent manner.After treated with 200 μmol/L GDCA,the apoptotic rates of the cells at 48 h and 72 h were(7.67±2.35)% and(12.93±1.48)% respectively.When the GDCA concentration was raised to 400 μmol/L,the apoptotic rates of the cells at 48 h and 72 h also increased to(13.14±2.56)% and(14.22±2.11)% respectively.The p53 mRNA in SMMC-7721 cells was up-regulated,whereas the mutant P53 protein was obviously inhibited after the cells were treated with GDCA.
CONCLUSIONS:
GDCA can induce the apoptosis of SMMC-7721 cells.
Toxicol Sci. 2014 Dec; 142(2): 436–444.
Glycodeoxycholic Acid Levels as Prognostic Biomarker in Acetaminophen-Induced Acute Liver Failure Patients[Pubmed:
25239633]
Acetaminophen (APAP)-induced acute liver failure (ALF) remains a major clinical problem. Although a majority of patients recovers after severe liver injury, a subpopulation of patients proceeds to ALF. Bile acids are generated in the liver and accumulate in blood during liver injury, and as such, have been proposed as biomarkers for liver injury and dysfunction. The goal of this study was to determine whether individual bile acid levels could determine outcome in patients with APAP-induced ALF (AALF).
METHODS AND RESULTS:
Serum bile acid levels were measured in AALF patients using mass spectrometry. Bile acid levels were elevated 5–80-fold above control values in injured patients on day 1 after the overdose and decreased over the course of hospital stay. Interestingly, Glycodeoxycholic acid (GDCA) was significantly increased in non-surviving AALF patients compared with survivors. GDCA values obtained at peak alanine aminotransferase (ALT) and from day 1 of admission indicated GDCA could predict survival in these patients by receiver-operating characteristic analysis (AUC = 0.70 for day 1, AUC = 0.68 for peak ALT). Of note, AALF patients also had significantly higher levels of serum bile acids than patients with active cholestatic liver injury.
CONCLUSIONS:
These data suggest measurements of GDCA in this patient cohort modestly predicted outcome and may serve as a prognostic biomarker. Furthermore, accumulation of bile acids in serum or plasma may be a result of liver cell dysfunction and not cholestasis, suggesting elevation of circulating bile acid levels may be a consequence and not a cause of liver injury.
