Galen medical journal · 2026
Effect of Tamsulosin on Osteopontin Gene Expression in Preventing Ethylene Glycol-Induced Kidney Stone in Male Wistar Rats : Short title: Effect of Tamsulosin on Osteopontin Gene Expression.
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Parvizrad Ramin, Ghorbani Marghamlki Elahe, Nikfar Somayeh, Khalili Dermani Sara
Аннотация
BACKGROUND: Tamsulosin, an α1-adrenergic receptor antagonist, has been proposed as a potential therapeutic agent against urolithiasis-induced renal damage. However, limited in vivo evidence exists regarding its renoprotective mechanisms.
MATERIALS AND METHODS: Forty male Wistar rats were randomly allocated into four groups (n=10/group): positive control, negative control (ethylene glycol-induced urolithiasis), prevention (tamsulosin administered simultaneously with ethylene glycol), and treatment (tamsulosin administered after model induction). Biochemical parameters including serum creatinine, urea, uric acid, calcium, and phosphorus were measured using rat-validated commercial kits (Pars Azmun, Iran). Normal ranges were defined based on published reference values. Gene expression was analyzed by qPCR using the 2^-ΔΔCt method. Study design and reporting followed the ARRIVE checklist.
RESULTS: At day 30, the prevention group exhibited significantly lower serum creatinine (0.60 ± 0.08 mg/dL) compared to the negative control (0.98 ± 0.12 mg/dL, P0.01). Although urea levels were slightly higher in the prevention group (4.0 ± 0.7 mg/dL) versus the negative control (3.22 ± 0.6 mg/dL), the calculated BUN/creatinine ratio was significantly improved (46.7 vs. 33.0, P0.05). No significant changes were observed in serum calcium or phosphorus. Gene expression analysis showed upregulation of protective markers in the prevention group.
CONCLUSION: In vivo findings on the beneficial effects of tamsulosin on the renal profile in ethylene glycol-induced urolithiasis illustrate its protective effects on the renal system through improvement of creatinine clearance and BUN/creatinine balance. This underscores its probable use as a protective therapeutic agent against renal injury of crystallization origin.
MATERIALS AND METHODS: Forty male Wistar rats were randomly allocated into four groups (n=10/group): positive control, negative control (ethylene glycol-induced urolithiasis), prevention (tamsulosin administered simultaneously with ethylene glycol), and treatment (tamsulosin administered after model induction). Biochemical parameters including serum creatinine, urea, uric acid, calcium, and phosphorus were measured using rat-validated commercial kits (Pars Azmun, Iran). Normal ranges were defined based on published reference values. Gene expression was analyzed by qPCR using the 2^-ΔΔCt method. Study design and reporting followed the ARRIVE checklist.
RESULTS: At day 30, the prevention group exhibited significantly lower serum creatinine (0.60 ± 0.08 mg/dL) compared to the negative control (0.98 ± 0.12 mg/dL, P0.01). Although urea levels were slightly higher in the prevention group (4.0 ± 0.7 mg/dL) versus the negative control (3.22 ± 0.6 mg/dL), the calculated BUN/creatinine ratio was significantly improved (46.7 vs. 33.0, P0.05). No significant changes were observed in serum calcium or phosphorus. Gene expression analysis showed upregulation of protective markers in the prevention group.
CONCLUSION: In vivo findings on the beneficial effects of tamsulosin on the renal profile in ethylene glycol-induced urolithiasis illustrate its protective effects on the renal system through improvement of creatinine clearance and BUN/creatinine balance. This underscores its probable use as a protective therapeutic agent against renal injury of crystallization origin.