Volume 26, Issue 4 (2023)
mjms 2023, 26(4): 17-25 |
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Ahmadi M, Rahbari A, Hajihashemi S, Ghanbari F. The effect of prostaglandin E2 on gentamicin- induced nephrotoxicity in rats. mjms 2023; 26 (4) :17-25
URL: http://mjms.modares.ac.ir/article-30-77417-en.html
URL: http://mjms.modares.ac.ir/article-30-77417-en.html
1- Department of Physiology, School of MedicineArak University of Medical Sciences , s.hajihashemi@gmail.com
Abstract: (500 Views)
Introduction: Gentamicin (GM) is a widely used aminoglycoside antibiotic. The nephrotoxicity of gentamicin causes reducing renal blood flow via vasoconstriction. Given PGE2's vasodilatory effects and the mechanisms of tissue damage in GM-induced nephrotoxicity, such as vasoconstriction, the aim of this study was to investigate the protective role of PGE2 in GM-induced nephrotoxicity. The diclofenac sodium was used to assess the direct effects of exogenous PGE2 by blocking endogenous production.
Materials and methods: The experiment was conducted on 56 male Wistar rats (200–250 g). Renal nephrotoxicity was induced by intraperitoneal (i.p.) injection of gentamicin (100 mg/kg). The therapeutic effects of PGE2 (0.2 µg/kg) and diclofenac (0.5 mg/kg) were assessed. The rats were placed in individual metabolic cages to collect urine. The systolic blood pressure and renal blood flow were measured. Levels of urea, creatinine, sodium, potassium, magnesium, and osmolarity were analyzed in plasma and urine samples. The left kidney was used for histological analysis.
Results: Administration of gentamicin for eight consecutive days resulted in a significant increase (p<0.001) in serum creatinine, blood urea nitrogen (BUN), absolute sodium excretion (UNaV), and fractional excretion of sodium and potassium (FENa and FEK), while creatinine clearance, urine osmolarity, and renal blood flow significantly decreased (p<0.001) compared to the control group.
Treatment with PGE2 significantly reducing serum creatinine, UNaV, FENa, FEK (p<0.001), and BUN (p<0.05), while significantly increasing creatinine clearance, urine osmolarity, and renal blood flow (p<0.001).
Conclusion: Prostaglandin E2 provided substantial protective effects against gentamicin induced acute nephrotoxicity in rats.
Materials and methods: The experiment was conducted on 56 male Wistar rats (200–250 g). Renal nephrotoxicity was induced by intraperitoneal (i.p.) injection of gentamicin (100 mg/kg). The therapeutic effects of PGE2 (0.2 µg/kg) and diclofenac (0.5 mg/kg) were assessed. The rats were placed in individual metabolic cages to collect urine. The systolic blood pressure and renal blood flow were measured. Levels of urea, creatinine, sodium, potassium, magnesium, and osmolarity were analyzed in plasma and urine samples. The left kidney was used for histological analysis.
Results: Administration of gentamicin for eight consecutive days resulted in a significant increase (p<0.001) in serum creatinine, blood urea nitrogen (BUN), absolute sodium excretion (UNaV), and fractional excretion of sodium and potassium (FENa and FEK), while creatinine clearance, urine osmolarity, and renal blood flow significantly decreased (p<0.001) compared to the control group.
Treatment with PGE2 significantly reducing serum creatinine, UNaV, FENa, FEK (p<0.001), and BUN (p<0.05), while significantly increasing creatinine clearance, urine osmolarity, and renal blood flow (p<0.001).
Conclusion: Prostaglandin E2 provided substantial protective effects against gentamicin induced acute nephrotoxicity in rats.
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