Both NOS inhibitors developed a clear pro-fibrotic effect in the liver. Aminoguanidine was more fibrotic than L-NAME. Our data suggest a significant anti-fibrotic role for iNOS rather than for eNOS. L-Arginine did not show any anti-fibrotic properties in the TAA-model used.

The purpose of this work was to study the effect of ursodeoxycholic acid (UDCA) on the morphological and functional alterations in pancreatic islet beta-cells in rats with diabetes induced by alloxan (150 mg kg(-1), i.p.). UDCA (40 mg kg(-1), i.g.) was administered daily from the fifth to the 35th day after the alloxan treatment. The treatment of diabetic rats with UDCA improved the pancreatic morphology disturbed by the alloxan treatment: UDCA increased the number of pancreatic islets and beta-cells, the beta-/alpha-cell ratio and decreased the number of alpha-cells. As the morphometric data suggest, the treatment of diabetic animals with UDCA significantly increased the area of beta-cell cytoplasmatic granules stained by paraldehyde-fuchsin. The concentration of blood glucose in diabetic rats was gradually decreased after the UDCA treatment, and at the end of the experiment reached the control value. The treatment with UDCA raised the serum insulin level in diabetic rats about 2.5-fold, but this concentration was significantly lower as compared to the control group. The content of lipid peroxidation end-products, hydroxyalkenals and malondialdehyde, was significantly elevated in the alloxan-treated rats, whereas the treatment with UDCA normalized these parameters. The present data indicate that UDCA acts as an effective antidiabetic agent in alloxan-induced diabetes and its beneficial effects in diabetic rats can be related to the antioxidant properties of UDCA.

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