Abstract
ABSTRACTIntroduction:We investigated whether Oltipraz (OPZ) attenuated renal fibrosis in a unilateral ureteral obstruction (UUO) rat model.Materials and Methods:We randomly divided 32 rats into four groups, each consisting of eight animals as follows: Rats in group 1 underwent a sham operation and received no treatment. Rats in group 2 underwent a sham operation and received OPZ. Rats in group 3 underwent unilateral ureteral ligation and received no treatment. Group 4 rats were subjected to unilateral ureteral ligation plus OPZ administration. Transforming growth factor beta-1 (TGF-β1), E-cadherin, nitric oxide (NO) and hydroxyproline levels were measured. Histopathological and immunohistochemical examinations were carried out.Results:TGF-β1, NO and E-cadherin levels in the UUO group were significantly higher than the sham group and these values were significantly different in treated groups compared to the UUO group. In rats treated with UUO + OPZ, despite the presence of mild tubular degeneration and less severe tubular necrosis, glomeruli maintained a better morphology when compared to the UUO group. Expressions of α-SMA in immunohistochemistry showed that the staining positivity decreased in the tubules of the OPZ-treated group.Conclusions:While the precise mechanism of action remains unknown, our results demonstrated that OPZ exerted a protective role in the UUO-mediated renal fibrosis rat model highlighting a promising therapeutic potency of Nrf2-activators for alleviating the detrimental effects of unilateral obstruction in kidneys.
Highlights
We investigated whether Oltipraz (OPZ) attenuated renal fibrosis in a unilateral ureteral obstruction (UUO) rat model
TGF - β1, nitric oxide (NO), and E - cadherin levels were significantly higher in the UUO group than the sham group
UUO + OPZ group had lower levels of these markers compared to the UUO group
Summary
We investigated whether Oltipraz (OPZ) attenuated renal fibrosis in a unilateral ureteral obstruction (UUO) rat model. The histopathologic changes are characterized by tubular dilatation or atrophy, inflammatory cell infiltration, fibroblast activation and proliferation, increases in matrix proteins, and progressive tubulointerstitial fibrosis. These histopathologic processes might eventually result in the loss of renal parenchyma leading to permanent renal function deterioration. The expression of intercellular epithelial adhesion molecules such as E - cadherin decrease and mesenchymal cell markers such as α - smooth muscle actin (α - SMA), N - cadherin and vimentin increase For this reason, EMT is recognized as a molecular component of renal fibrosis [4,5,6]
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