Renoprotective activity of fermented Crescentia cujete in rats subjected to Unilateral Ureteral Obstruction

Unilateral ureteral obstruction (UUO) induces hydronephrosis in the affected kidney, with compensatory damages in the contralateral kidney. This study aimed to evaluate the renoprotective effects of fermented Crescentia cujete (FCC) on the contralateral kidney in UUO-induced rats. Based on a preliminary study, 14 days post-UUO-induction (dpi) was selected as the treatment baseline for initiating treatments. For the main study, 24 six-month-old male rats (weighing 315.05±3.22g) were subjected to right UUO and randomly assigned to three groups: G1 (sham-operated), G2 (untreated UUO), and G3 (UUO treated with 11.84mg/kg FCC). From 15 to 28 dpi, group G3 rats received oral FCC twice daily, while those of G1 and G2 remained untreated. On 29 dpi, rats were evaluated for lower limb oedema, blood pressure, SDMA, cystatin C, creatinine clearance and renal ultrasonography; and kidney macroscopy, histopathology for tubular injury, inflammation and fibrosis, and immunohistochemical expression of claudin-1, NGAL, SPP1, TNF-α following euthanasia. Results showed that right kidneys in groups G2 and G3 exhibited higher hydronephrosis, tubular injury, inflammation, and fibrosis scores compared to G1 (P<0.05), with no differences between G2 and G3. In the contralateral kidney, FCC improved length, width, thickness, volume, weight of kidney, hydronephrosis scores, and histopathological lesions compared to G2 (P<0.05), with non-significant differences in these parameters between rats of groups G1 and G3. Systemically, FCC reduced lower limb oedema, blood pressure, SDMA, and elevated creatinine clearance compared to UUO+FCC (P<0.05). Moreover, FCC downregulated the immunoexpression of NGAL, SPP1, and TNF-α in the contralateral kidney (P<0.05). FCC treatment also restored cystatin C level to sham-treated control group. In conclusion, FCC demonstrated renoprotective effects in the contralateral kidney of UUO rats by preserving renal morphology and suppressing pro-inflammatory and pro-fibrotic markers.

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