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Patologia Polska 1990

[Effects of D-penicillamine and encorton on the fibrotic processes in experimental liver cirrhosis in rats].

Samo registrirani uporabniki lahko prevajajo članke
Prijava / prijava
Povezava se shrani v odložišče
M Rubaj
J Czarnecki
B Rubaj
T Piecińska

Ključne besede

Povzetek

The aim of the study was to evaluate the effects of D-penicillamine (cuprenil), encorton and both drugs in combination on fibrotic processes in the rat liver damaged by chronic use of CCl4. The studies comprised 80 white Wistar rats divided into 8 experimental groups. Group I receiving every day oral methylocellulose for 12 weeks was a control group. In group II the rats were given only CCl4 for 12 weeks. In the remaining experimental groups beside CCl4 the animals received drugs in various doses and for various periods. At 12 weeks all animals were killed and post-mortem studies were performed. The liver sections for histopathological studies were fixed in 10% buffered formaline. Paraffin specimens were stained with hematoxylin and eosine. Colour reactions to collagen fibers were performed by using Heidenhein's method and to reticuline fibers by Gomori's method. In the assessment of the severity of fatty degeneration, inflammatory infiltrates and fibrosis the 3-point scale was used, ranging from + for minor changes, ++ for moderate changes, for severe changes, and 0 for no changes. Morphological analysis of the liver showed that chronic administration of CCl4 produced an experimental model of cirrhosis of the liver in rats. Concomitant use of CCl4 and cuprenil revealed its inhibiting action on the fibrotic process in the rats' liver. Inhibition of fibrosis varied and was related to the dose and time of its action. The most optimal was a low dose, 10 mg kg of body weight, whereas a double dose used during the experiment appeared less favourable. Similarly less effective action was exhibited after encorton. After combined use of both drugs the inhibitory effect was negligible. In addition hepatotoxic effects were found manifested by marked fatty degeneration of hepatocytes.

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