Abstract
to evaluate the influence of acetylsalicylic acid (ASA) on cell proliferation after partial hepatectomy in rats. 40 male Wistar rats were separated into four groups of ten rats each. Groups 1 and 2 (controls): undergoing 30% partial hepatectomy and, after one day (group 1) and seven days (group 2), to euthanasia; daily administration of 0.9% saline solution (1mL per 200g of body weight). Groups 3 and 4 (experimental): undergoing 30% partial hepatectomy and, after one day (group 3) and seven days (group 4), to euthanasia; daily administration of ASA (40mg/mL, 1mL per 200g of body weight). The absolute number of cells stained with PCNA was counted in photomicrographs, in five fields, and it was calculated the mean of positive cells per animal and per group. the final mean of PCNA+ cells per group was: in group 1, 17.57 ± 6.77; in group 2, 19.31 ± 5.30; in group 3, 27.46 ± 11.55; and, in group 4, 12.40 ± 5.23. There was no significant difference at the two evaluation times in the control group (p=0.491), but there was in the experimental group (p=0.020), with a lower number of PCNA+ cells on the seventh day. The comparison between the two groups, on the first day, showed more PCNA+ cells in the livers of the animals that received ASA (p=0.047), and on the seventh day the number was lower in the experimental group (p=0.007). ASA induced greater hepatocyte proliferation.
Highlights
One of the main characteristics of the liver is its ability to regenerate
The primary response of the organ to different lesions is not always this, and it may concur with fibrosis and hepatocyte necrosis[1]
Hepatic fibrosis results from a sustained response to chronic liver injuries and thrombosis of intrahepatic vessels, which stimulate the exacerbated secretion of the extracellular matrix by stellate cells[2]
Summary
The primary response of the organ to different lesions is not always this, and it may concur with fibrosis and hepatocyte necrosis[1]. Hepatic fibrosis results from a sustained response to chronic liver injuries and thrombosis of intrahepatic vessels, which stimulate the exacerbated secretion of the extracellular matrix by stellate cells[2]. Even after removing 70% of its total mass, the remaining tissue is able to regenerate, recovering its original volume and function[4]. This process depends on a series of cytokines and growth factors, which stimulate angiogenesis and coordinate hepatocyte hypertrophy and hyperplasia
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
