Abstract
BackgroundContrast-induced acute kidney injury (CI-AKI) occurs after the administration of intravenous iodinated contrast agents. Oxidative stress has been proposed as one of the most important mechanisms in the pathogenesis of CI-AKI. The objective of this study was to investigate the antioxidant effect of the extract from Phyllanthus emblica (PE) in preventing CI-AKI.MethodsMale Sprague Dawley rats were subjected into eight groups, were given water (control) or PE extract (125 or 250 or 500 mg/kg/day) for 5 days before the induction of CI-AKI. Renal function and oxidative stress markers; malondialdehyde (MDA), total antioxidant capacity (TAC), superoxide dismutase (SOD) and catalase (CAT) activity were determined in plasma and renal tissue. Kidney sections were performed for histopathological examination.ResultsIn the contrast media (CM) group, increases in blood urea nitrogen and serum creatinine were demonstrated which correlated with severity of tubular necrosis, peritubular capillary congestion and interstitial edema. Moreover, an increase in MDA and a decrease in TAC SOD and CAT activity in CM group were significantly changed when compared with the control (P < 0.05). In contrast, CI-AKI-induced rats administrated with PE extract 250 and 500 mg/kg/day significantly preserved renal function and attenuated the severity of pathological damage (P < 0.05) as well as significantly lower MDA and higher TAC, SOD and CAT than the CM group (P < 0.05).ConclusionsThis study demonstrated the protective role of PE extract against CI-AKI.
Highlights
Introduction of CIAKI in Rats Contrast-induced acute kidney injury (CI-AKI) rats were subjected to CI-AKI protocol as described [20,21,22] briefly; pentobarbital sodium (60 mg/kg) anesthesia by intraperitoneal injection was followed by CI-AKI induction, which was performed with drug administration into tail vein
Effect of Phyllanthus emblica (PE) extract on renal function parameters Both blood urea nitrogen (BUN) and serum Cr in the contrast media (CM) group were significantly increased when compared with the control (p < 0.05)
While BUN was significantly decreased in the PE extract 125 mg + CM group, PE extract 250 mg + CM group and PE extract 500 mg + CM group when compared with CM group (P < 0.05); Figure 2
Summary
Introduction of CIAKI in Rats CI-AKI rats were subjected to CI-AKI protocol as described [20,21,22] briefly; pentobarbital sodium (60 mg/kg) anesthesia by intraperitoneal injection was followed by CI-AKI induction, which was performed with drug administration into tail vein. Drug administered consisted of indomethacin at a dose of 10 mg/kg, followed at 15 min and 30 min later with Nw-nitro-L-Arginine methyl ester (L-NAME) at dose of 10 mg/kg and with lowosmolar, non-ionic contrast medium agent (Iopromide) at a dose of 1600 mg iodine/kg This quantity is the dose of contrast medium that is standard for clinical use and for other relevant experiments in rat models. The pathogenesis of CI-AKI is due to the ability of contrast agents could induce renal vasoconstriction followed by hypoxic condition in the kidney which promotes further ischemic renal injury by the increase of oxygen free-radicals through oxidative stress [4]. Active extracts of PE have been shown to posses anticancer [14,15], radioprotection [16], anti-inflammatory [17] and antioxidant [18,19] properties in several models of organ injury
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