Avicenna journal of phytomedicine · 2025
Evaluating the effect of rutin on contrast-induced nephropathy in rats.
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Esparham Faezeh, Rajabian Fatemeh, Ghasemzadeh Rahbardar Mahboobeh, Razavi Bibi Marjan, Khajavi Rad Abolfazl, Amoueian Sakineh, Hosseinzadeh Hossein
Аннотация
OBJECTIVE: Contrast-induced nephropathy is a common cause of acute kidney injury, and oxidative stress plays an important role in its development. The flavonoid rutin is of interest for its potential antioxidant properties. This study aimed to assess the protective effects of rutin against contrast-induced renal toxicity in rats.
MATERIALS AND METHODS: Eight groups of male Wistar rats (n=6 in each group) were designed: (1) Sham, (2) Premedication-control (N(ω)-nitro-L-arginine methyl ester (L-NAME, 10 mg/kg, i.p.)+indomethacin (10 mg/kg, i.p.)), (3) Contrast medium (L-NAME+indomethacin+diatrizoate (12.5 ml/kg, i.p)), (4-6) Rutin (25, 50, and 100 mg/kg, p.o., for 7 days)+L-NAME+indomethacin+ diatrizoate, (7) N-acetylcysteine (NAC, 125 mg/kg, i.p.), L-NAME+indomethacin+diatrizoate, and (8) Rutin-alone (100 mg/kg). All study groups except for the sham and rutin-alone were subjected to 48 hr of water deprivation. On day 8, blood and kidney samples were isolated to evaluate oxidative stress, biochemical and histopathological changes.
RESULTS: The levels of serum blood urea nitrogen (BUN), creatinine, and malondialdehyde (MDA) were raised by diatrizoate, while glutathione (GSH) levels in renal tissue were reduced. Rutin (25, 50, and 100 mg/kg) improved biochemical parameters and oxidative stress. Diatrizoate also resulted in interstitial edema, medullary congestion, proteinaceous casts, and severe tubular necrosis in kidney tissue. Rutin (100 mg/kg) reduced tubular necrosis and interstitial edema but had no significant effect on the formation of medullary congestion and proteinaceous casts in renal tissue.
CONCLUSION: Oxidative stress triggered by contrast-induced nephropathy is caused by a rise in MDA and a decline in GSH amounts. Rutin protects kidney tissue against contrast-induced damage through its antioxidant effect.
MATERIALS AND METHODS: Eight groups of male Wistar rats (n=6 in each group) were designed: (1) Sham, (2) Premedication-control (N(ω)-nitro-L-arginine methyl ester (L-NAME, 10 mg/kg, i.p.)+indomethacin (10 mg/kg, i.p.)), (3) Contrast medium (L-NAME+indomethacin+diatrizoate (12.5 ml/kg, i.p)), (4-6) Rutin (25, 50, and 100 mg/kg, p.o., for 7 days)+L-NAME+indomethacin+ diatrizoate, (7) N-acetylcysteine (NAC, 125 mg/kg, i.p.), L-NAME+indomethacin+diatrizoate, and (8) Rutin-alone (100 mg/kg). All study groups except for the sham and rutin-alone were subjected to 48 hr of water deprivation. On day 8, blood and kidney samples were isolated to evaluate oxidative stress, biochemical and histopathological changes.
RESULTS: The levels of serum blood urea nitrogen (BUN), creatinine, and malondialdehyde (MDA) were raised by diatrizoate, while glutathione (GSH) levels in renal tissue were reduced. Rutin (25, 50, and 100 mg/kg) improved biochemical parameters and oxidative stress. Diatrizoate also resulted in interstitial edema, medullary congestion, proteinaceous casts, and severe tubular necrosis in kidney tissue. Rutin (100 mg/kg) reduced tubular necrosis and interstitial edema but had no significant effect on the formation of medullary congestion and proteinaceous casts in renal tissue.
CONCLUSION: Oxidative stress triggered by contrast-induced nephropathy is caused by a rise in MDA and a decline in GSH amounts. Rutin protects kidney tissue against contrast-induced damage through its antioxidant effect.