A hydrophilic bile acid effects partial dissolution of cholesterol gallstones in the prairie dog

Lipids ◽  
1986 ◽  
Vol 21 (9) ◽  
pp. 575-579 ◽  
Author(s):  
Bertram I. Cohen ◽  
Erwin H. Mosbach ◽  
Charles K. McSherry ◽  
Beverly Rzigalinski ◽  
Syoji Kuroki
2020 ◽  
Vol 2020 ◽  
pp. 1-13
Author(s):  
Geng Chen ◽  
Shuodong Wu

This study was aimed at investigating the effect of baicalin on experimental cholesterol gallstones in mice. The mouse gallstone model was induced by feeding with a lithogenic diet, and cholesterol stones were found in the gallbladder. The lithogenic diet caused elevation of triglycerides, cholesterol, and low-density lipoprotein concentrations and descent of high-density lipoprotein concentration in serum. Hyperplasia and inflammatory infiltration were observed in the gallbladder wall of lithogenic diet-fed mice. We also found the increase of cholesterol content and the decrease of bile acid in bile. Real-time PCR and western blot results demonstrated that the expression levels of two enzymes (cholesterol 7α-hydroxylase (CYP7a1) and sterol 12α-hydroxylase (CYP8b1)) to catalyze the synthesis of bile acid from cholesterol were decreased and that two cholesterol transporters (ATP-binding cassette transporter G5/G8 (ABCG5/8)) were increased in the liver of lithogenic diet-fed mice. The lithogenic diet also led to enhanced activity of alanine aminotransferase and aspartate aminotransferase in serum; increased concentrations of tumor necrosis factor-α, interleukin- (IL-) 1β, IL-6, and malondialdehyde; and decreased superoxide dismutase activity in the liver, suggesting inflammatory and oxidative stress. In addition, liver X receptor alpha (LXRα) was increased in the liver. After gavage of baicalin, the lithogenic diet-induced gallstones, hyperlipidemia, gallbladder hyperplasia, inflammation, and oxidative stress in liver and cholesterol metabolism disorders were all alleviated to some degree. The expression of LXRα in the liver was inhibited by baicalin. In addition, the LXRα agonist T0901317 aggravated lithogenic diet-induced harmful symptoms in mice, including the increase of gallstone formation, hyperlipidemia, hepatic injury, inflammation, and oxidative stress. In conclusion, we demonstrated that baicalin played a protective role in a lithogenic diet-induced gallstone mouse model, which may be mediated by inhibition of LXRα activity. These findings may provide novel insights for prevention and therapy of gallstones in the clinic.


Lipids ◽  
1988 ◽  
Vol 23 (3) ◽  
pp. 220-224 ◽  
Author(s):  
Bertram I. Cohen ◽  
Erwin H. Mosbach ◽  
Syoji Kuroki ◽  
Charles K. McSherry

1972 ◽  
Vol 51 (6) ◽  
pp. 1495-1503 ◽  
Author(s):  
D. E. Brenneman ◽  
William E. Connor ◽  
E. L. Forker ◽  
Larry DenBesten

2021 ◽  
pp. 174341
Author(s):  
Xin Ye ◽  
Shuang Shen ◽  
Zhengjie Xu ◽  
Qian Zhuang ◽  
Jingxian Xu ◽  
...  

1994 ◽  
Vol 29 (1) ◽  
pp. 47-55 ◽  
Author(s):  
Shuichiro Okamoto ◽  
Kenji Nakano ◽  
Keigo Kosahara ◽  
Masanori Kishinaka ◽  
Hitoshi Oda ◽  
...  

1985 ◽  
Vol 69 (1) ◽  
pp. 71-79 ◽  
Author(s):  
A. Reuben ◽  
P. N. Maton ◽  
G. M. Murphy ◽  
R. H. Dowling

1. Biliary lipid secretion rates were measured in non-obese and obese individuals with and without cholesterol gallstones, using a steady-state, amino acid duodenal perfusion method. In addition, biliary lipid secretion rates were measured in five obese gallstone patients receiving high-dose chenodeoxycholic acid therapy (16-22 mg day−1 kg−1). 2. Bile acid secretion rates in the non-obese patients with cholesterol gallstones (563+sem 70 μmol/h, n = 6) were significantly lower than in the non-obese controls (1078 + 210 μmol/h, n = 10, P < 0.05), whereas cholesterol secretion rates were similar in the non-obese individuals with and without gallstones (51+7 and 42+4 μmol/h respectively). 3. In the obese, both with and without gallstones, the major abnormality was hypersecretion of cholesterol (107+7 μmol/h, n = 7, and 81 + 15 μmol/h, n = 7, respectively). Both these values were significantly greater than those in the non-obese controls (P < 0.01-0.02). 4. Biliary cholesterol secretion rates correlated significantly with bile acid secretion rates but, for every mole of bile acid secreted, the obese secreted more cholesterol than the non-obese. 5. Chenodeoxycholic acid treatment lowered biliary cholesterol saturation in obese gallstone patients by reducing biliary cholesterol secretion. 6. These results suggest that there are two major types of defect in biliary lipid secretion in gallstone patients: reduced biliary bile acid secretion in non-obese gallstone patients and excessive biliary cholesterol secretion in the obese.


Author(s):  
Flavio Lirussi ◽  
Rosa Maria Iemmolo ◽  
Rocco Orlando ◽  
Gino Nassuato ◽  
Maurizio Muraca ◽  
...  

1976 ◽  
Vol 21 (4) ◽  
pp. 233-237 ◽  
Author(s):  
Roderick M. McDougall ◽  
Keith Walker ◽  
Olin G. Thurston

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