Cirrhosis in rats does not resolve in the long-term after induction by thioacetamide model

Abstract

Introductions: Hepatic cirrhosis is a final common pathway of all chronic liver diseases, characterized by deposit of fibrillar collagen and liver failure. Materials and Methods: In this experiment, hepatic cirrhosis was induced in 15 female Wistar rats by a 14-week period, with thioacetamide solution in a 200 mg/kg dosage, via intraperitoneal. Animals were submitted to liver biopsy, and euthanized after a 80-day post-induction period. Serum biochemical analysis was performed, in addition to histopathology by H.E., Picrosirius, Alcian Blue and P.A.S. stainings, following analysis of histological activity index and staging of fibrosis. Morphometric analysis of collagen on Picrosirius slides was also performed. Results: Mortality during experimental period was low (13.33%), and after 80-day period, liver function improved, cellular changes did not altered, and deposition of acidic mucopolysaccharides and glycogen were increased. Liver histological activity did not change significantly (7.25 ± 1.30 to 6.41 ± 1.32), but staging of fibrosis was altered (3.91 ± 0.76 to 4.70 ± 1.11). Interlobular collagen showed a significant decrease (5.14 ± 2.00 to 4.00 ± 1.20), while intralobular collagen was increased (0.23 ± 0.06 to 0.36 ± 0.08). Conclusions: These findings characterize thioacetamide as a safe experimental model for induction cirrhosis, which may be used for future therapy studies.

Evaluation Effect of Transplanted Mesenchymal Stem Cell on Rat with Liver Cirrhosis

“…Moreover, focal areas of necrosis and apoptotic changes with mononuclear leucocytes infiltration were also observed in the hepatic parenchyma. These results were in complete agreement with other results (Madani et al, 2008, Buko et al, 2014and Rui et al, 2014. These results recorded that these findings may be attributed to the metabolism of CCL4 due to the oxidation process which induced oxidative stress in the hepatic cells responsible for the changes in cell permeability, increase the intracellular concentration of Ca++, increase in nuclear volume, enlargement of nucleoli and also inhibits mitochondrial activity leads to cell death and severely affecting hepatic cells which are located in the previous acinus region as previously mentioned (Bigoniya et al, 2009).…”

Experimental pathological studies on the ability of Stem cells for regeneration of hepatocytes in rats

“…Moreover, focal areas of necrosis and apoptic changes with mononuclear leucocytic infiltration were also observed in the hepatic parenchyma. These results were in compelete agreement with the results of Geng et al, (2010), Madani et al, (2008), Buko et al, (2014 and Rui et al, (2014).These findings may be attributed to metabolism of TAA which metabolized by cytochrome P450 enzymes of liver microsomes and converted to a toxic intermediate called thioacetamide S-oxide due to oxidation process which induced oxidative stress in the hepatic cells responsible for the changes in cell permeability, increase intracellular concentration of Ca++, increase in nuclear volume, enlargement of nucleoli and also inhibits mitochondrial activity leads to cell death and severely affecting hepatic cells which are located in the perivenous acinus region as previesly mentioned by Zaragoza et al, (2000) and Bigoniya et al, (2009). Moderate degree of degenerative changes in hepatocytes were observed in treated rats with MSCs the form of vacuolar and hydropic degeneration.…”