Research Paper Volume 15, Issue 11 pp 4576—4599

Senescence and senotherapies in biliary atresia and biliary cirrhosis

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Figure 5. HALPC administration in BDL rats. (A) Operated rats received HALPC (n=12) through peripheral vein injection 48 hours after BDL and were compared to vehicle-treated controls (n=6). (B) HALPC decreased the early marker of senescence p21 gene expression, but no significant effect was observed on later markers (SA-β-gal activity and p16 gene expression). (C) HALPC decreased cholangiocytes injury (serum γGT) and biliary proliferation (Sox9), but had no significant effect on biochemical cholestasis (serum total bilirubin). (D, E) HALPC slightly reduced the hepatocytes mass loss (Hnf4a) while having no significant effect on serum AST nor on liver histological fibrosis. (F) HALPC reduced Gpx1 expression. BDL: bile duct ligation; HALPC: human allogenic liver-derived progenitor cells; SA-β-gal: senescence-associated β-galactosidase; ULN: upper limit of normal. Data is presented as mean ± SEM; *p≤0.05; **p<0.01.