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Abstract
Purpose: To investigate the anti-fibrotic effect and mechanism of action of quinolone oxizime in vitro and in vivo.Methods: Proliferation of renal fibroblasts was determined using 3-(4, 5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay, while laser confocal fluorescence microscope was used for immuno-cytochemical studies. Total TGF β1 was determined by enzyme linked immunosorbent assay (ELISA).Results: Quinolone oxizime decreased the proliferation of renal fibroblasts in a dose-dependent manner (p < 0.05) in vitro. Proliferation of renal fibroblasts was 39, 63, 82, 95, 97 and 99 % on treatment with quinolone oxizime at doses of 10, 8, 6, 4, 2 and 1 μM, respectively, after 48 h. The expression of TGF β1 in the peripheral blood lymphocytes was reduced significantly by quinolone oxizime treatment. In the animal model of renal fibrosis, quinolone oxizime treatment decreased development of lesions, prevented tubular dilation and expansion of interstitium. After 30 days of quinolone oxizime treatment, tubulo-interstitial lesions were completely absent in rats in the 5 mg/kg treatment group. Moreover, quinolone oxizime treatment for 30 days inhibited accumulation of extracellular matrix and prevented renal injury in rats.Conclusion: These results show that quinolone oxizime exhibits anti-fibrotic effects through targeting the expression of TGF β1. Therefore, quinolone can potentially be used for the treatment of fibrotic kidney diseases but further studies are required to ascertain this.Keywords: Quinolone oxizime, Anti-fibrosis, Tubulo-interstitium, Interstitium, Fibroblasts
Highlights
Kidney fibrosis is caused by a complex pathological condition involving processes like accumulation of inflammatory cells, aggregation of collagen and dilation of renal tubules [1]
Results from MTT assay showed that quinolone oxizime treatment exhibited inhibitory effect on the proliferation of kidney fibroblasts after 48 h
Significant (p < 0.05) decreases were observed in the percentage proliferation of kidney fibroblasts on treatment with 6, 8 and 10 μM doses of quinolone oxizime, when compared to the control fibroblasts (Figure 2)
Summary
Kidney fibrosis is caused by a complex pathological condition involving processes like accumulation of inflammatory cells, aggregation of collagen and dilation of renal tubules [1]. The progression of kidney fibrosis leads to the development of end-stage renal disease [1]. Mechanistic studies have shown that the expression of TGF-β activates interstitial fibroblasts which generates various components of matrix and results in renal fibrosis. These processes collectively cause tubule-interstitial fibrosis, and subsequently lead to end-stage renal disease [7]. The effect of quinolone oxizime on renal fibrosis was studied in vitro in fibroblasts and in vivo in a rat model. The effect of quinolone oxizime on renal fibrosis was investigated after unilateral ureteral obstruction mm3) sections and the sections put into 25 cm containers in Dulbecco's modified Eagle's medium (DMEM; Gibco Corp., Carlsbad, CA, USA). Available ELISA kit was used for determination of total TGF-β1 in the supernatant in accordance with the instructions of the kit manufacturer
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