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We constructed a similar model using bile miRNA alone.
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Yang et al. showed that the OPN-mediated inhibition of cholesterol stone nucleation is dose-dependent in an animal model and in vitro using bile from human gallbladders [ 27].
Similar proteomic strategies have been employed by other groups to identify potential biomarkers in GBC using bile, serum and cell line-based models [ 11– 11].
In another model of liver fibrosis, using bile-duct ligation, Bridle et al. [ 43] reported that rapamycin inhibited EMT, the activation of stellate cells, and the synthesis of procollagen I, cytokeratin 19 and α-smooth muscle actin (α-SMA) in treated rats.
Cholangiocyte physiology is studied in vivo using bile-duct cannulated animals and in vitro using freshly isolated cholangiocytes, cholangiocyte monolayers, cell lines, and isolated bile duct units.
Surgical bile duct ligation (BDL) is the most common model used to induce obstructive cholestatic injury in mice and rats.
Mouse model used in this study is in early stages, down-regulated expression of CYP27A might be a predictor for the destruction of bile duct.
Here, we unravel the interactions of bile acid derived dimeric phospholipid amphiphiles with model membranes using Laurdan-based hydration, DPH-based membrane fluidity, and differential scanning calorimetry studies.
Someone outside their system was using their bile as his platform, and beating the established candidates.
Therefore, we used the model of bile duct ligation (BDL) to induct liver fibrosis in C57/BL6 mice.
Cell culture models were used to investigate interactions between bile acids and ER stress.
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