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Fig. 5 | BMC Biotechnology

Fig. 5

From: Engineered FGF19ΔKLB protects against intrahepatic cholestatic liver injury in ANIT-induced and Mdr2-/- mice model

Fig. 5

FGF19ΔKLB inhibited BA biosynthesis and regulated BA homeostasis. Four-week-old Mdr2−/− mice were treated by daily i.p. injections of PBS, FGF19WT or FGF19ΔKLB (n = 5 per group) for eight weeks. (A-B) Serum total BA (TBA) (E) and hepatic BA pool (F) levels after treated by FGF19WT or FGF19. (C-G) Western blotting analysis of hepatic Cyp7a1, Cyp27a1, Cyp8b1 and Cyp7b1 protein expression levels (C) and its semi-quantification (D-G). (H-K) Hepatic Cyp7a1 (H), Cyp27a1(I), Cyp8b1(J), and Cyp7b1(K) mRNA levels were evaluated by RT-PCR. (L-P) Expression profiles of BA canalicular efflux transporter (Bsep and Mrp2) (L-M) and basolateral uptake transporter (Ntcp, Oatp1 and Oatp2) (N-P) were determined by RT-PCR. Mean ± SEM was chosen to represent the data; *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001; ns, not significant; (A-D, F-M) conventional one-way ANOVA, then Tukey

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