Hepatic oval cell activation in response to injury following chemically induced periportal or pericentral damage in rats

Characterization of two distinct liver progenitor cell subpopulations of hematopoietic and hepatic origins

“…This model of hepatotoxicity has revealed massive oval cell proliferation by day 9 post-CCl 4 injection with activation continuing persistently through days 11 and 13 [33]. Hematoxylin-eosin staining clearly confirmed the efficacy of the treatment in destroying the classical hepatic tissue architecture in treated animals as compared to controls (Figs.…”

“…Inhibition of hepatocyte proliferation was attained through subcutaneous insertion of 2-AAF (70 mg pellet, 2.5 mg/day release; Innovative Research of America, Sarasota, FL). On day 7, hepatic injury was induced by a single intraperitoneal injection of CCl 4 (1.9 ml/kg; CCl 4 /corn oil 1:1) [33]. Treated and control animals were sacrificed and liver extracted at 9, 11 and 13 days post-CCl 4 treatment.…”

Liver precursor cells increase hepatic fibrosis induced by chronic carbon tetrachloride intoxication in rats

“…1 Metabolism of CCl 4 into highly reactive CCl 3 radicals by cytochrome P450 is responsible for centrilobular hepatocellular necrosis, which triggers matrix deposition starting around the central veins, with gradual formation of septa bridging neighboring central veins, without any ductular reaction. 25 In our model, administration of AAF before and during CCl 4 treatment blocks the proliferative hepatocyte response caused by CCl 4 -induced necrosis 27 and leads to the emergence of an alternate regenerative pathway with expansion of LPC in periportal regions as commonly reported in human fibrosis of various etiologies. [12][13][14]28 Using this new model, we investigated the involvement of LPC activation in fibrosis development by comparing the fibrogenic response in rats treated with a combination of CCl 4 and AAF to that obtained in animals treated with either CCl 4 or AAF alone.…”

Granulocyte–Colony Stimulating Factor Promotes Liver Repair and Induces Oval Cell Migration and Proliferation in Rats

“…The 2AAF/PH regimen for OC induction was performed as previously described. 19 Briefly, 4 weeks after BMTx, chimeric animals were implanted intraperitoneally with a time-released 2AAF pellet (70 mg/28-day release; Innovative Research of America, Sarasota, FL). Seven days later, rats underwent PH, as described elsewhere.…”

“…We used the well-established model of OC activation in rats, involving the administration of 2-acetylaminofluorene (2AAF) before partial hepatectomy (PH). 19 2AAF is metabolized selectively by hepatocytes to an N-hydroxyl derivative, which interferes with the cyclin-D 1 pathway. Therefore, the administration of 2AAF before PH inhibits hepatocyte proliferation and forces OC recruitment to mediate liver regeneration.…”