Double staining of b-galactosidase with fibrosis and XXXX markers reveals the chronological appearance of senescence in @entity409 induced by @entity107 .

@entity10740 @entity7504 @entity96 @entity5 @entity107 @entity409 @entity11754 @entity12003 @entity102 @entity19087 @entity7905 @entity35 @entity13963 @entity23305
UNASSIGNED: Cellular senescence is characterized by irreversible cell arrest and is associated with the development of @entity102 , including @entity5 . Here, we investigated the induction of cellular senescence during @entity409 . @entity96 was induced in Fischer 344 @entity35 with a weekly intraperitoneal injection of @entity107 (50mg/kg body weight) for 16 weeks. Double-detection of b-galactosidase with Ki67 for cell proliferation; a-SMA and @entity13963 for cell specificity; @entity10740 , @entity7504 , @entity11754 , and @entity12003 , @entity23305 , and @entity19087 for senescence-associated molecular pathways and y-glutamyltranspeptidase (GGT) for hepatocarcinogenesis was assessed to determine the association of these markers with cellular senescence. DNA damage was measured through @entity7905 ( @entity7905 ) detection. Progressive cellular senescence was observed in both fibrotic septa and hepatocytes from week 10 to 18. The maximum peak of positive senescent and fibrotic cells was observed at week 16 and decreased at week 18, but cell proliferation remained high. Whereas the increased @entity11754 expression and @entity7905 were concomitant with that of b-galactosidase, those of @entity10740 and @entity7504 were barely detected. Furthermore, b-galactosidase positive myofibroblast-like cells were mainly surrounding @entity5 . Our findings showed that in hepatocarcinogenesis by @entity107 , cellular senescence is associated with @entity11754 pathway activation and is mainly localized in myofibroblast-like cells.
