morin and Kidney-Diseases

Oxidative stress is one of the important mechanisms of cisplatin-induced nephrotoxicity. Therefore, this study was designed to explore the potential protective effects of morin and/or hesperidin on oxidative stress in cisplatin-induced nephrotoxicity. This study was performed on 42 Wistar rats. Rats were divided into seven groups: control, morin, hesperidin, cisplatin, cisplatin + morin, cisplatin + hesperidin, and cisplatin + morin + hesperidin. Morin and/or hesperidin were given for 10 consecutive days by oral gavage and on the 4th day a single dose of cisplatin (7 mg/kg) was injected intraperitoneally. After administrations, on the 11th day of the experiment the animals were killed, and malondialdehyde (MDA), nitric oxide (NOx), glutathione (GSH) levels and myeloperoxidase (MPO), catalase (CAT), superoxide dismutase (SOD) activity were measured. Cisplatin-treated rats showed increased levels of MDA, and decreased levels of NOx also activity of CAT. Morin and/or hesperidin pretreatment prevent oxidative stress in kidney tissue, while they increase the NOx level, CAT activity, and decrease MPO activity. In conclusion, morin + hesperidin pretreatment may have a significant potential for protection of cisplatin-induced nephrotoxicity.

Topics: Animals; Antioxidants; Apoptosis; Catalase; Cisplatin; Flavonoids; Glutathione; Glutathione Peroxidase; Hesperidin; Kidney; Kidney Diseases; Male; Malondialdehyde; Nitric Oxide; Oxidative Stress; Peroxidase; Rats; Rats, Wistar; Superoxide Dismutase

Morin is a flavonoid that exists in nature and is the major component of traditional medicinal herbs. Here we evaluated morin for its hepatoprotective effect against chronic ethanol-induced biochemical changes in male Wistar rats. Ethanol administration (7.9 g/kg bwt) for 60 days induced hepatic and renal damage by increasing oxidative stress and decreasing antioxidant levels. The status of lipid peroxidation (thiobarbituric reactive substances (TBARS) and hydroperoxides (HP)), antioxidant (vitamin C, vitamin E, GSH), serum hepatic markers (AST, ALT, ALP, GGT, bilirubin), and renal markers (urea, creatinine) were assessed as biochemical endpoints to determine the hepatic protective effect of morin. Oral administration of morin (100 mg/kg b.w) to alcohol-intoxicated rats for 30 days showed significant decreases in lipid peroxidation and restoration of antioxidant, hepatic, and renal markers to normal. Histopathologic observations of liver were also in correlation with biochemical parameters. The results indicate that morin might be beneficial in ameliorating alcohol-induced oxidative damage in rat liver.

Topics: Animals; Antioxidants; Biomarkers; Ethanol; Flavonoids; Kidney Diseases; Lipid Peroxidation; Liver Diseases, Alcoholic; Liver Function Tests; Male; Oxidative Stress; Rats; Rats, Wistar

The present study investigated the protective effect of morin, a natural flavonoid, on the imipenem-induced nephrotoxicity in rabbits. Nephrotoxicity of imipenem was examined after the intravenous administrations of imipenem (200 mg/kg) to rabbits in the presence and the absence of morin (12, 25, 50 mg/kg, p.o.). Cytotoxicity of imipenem was also examined in the presence and the absence of morin (100 microM) by using MDCK cells overexpressing human organic anion transporter 1 and 3 (MDCK/hOAT1 or MDCK/hOAT3). Intravenous dosing of imipenem alone induced severe proximal tubular necrosis in rabbits, however, the concurrent use of morin (25 or 50 mg/kg, p.o.) significantly suppressed the histopathological damage in the kidney induced by imipenem. While imipenem was not cytotoxic in MDCK/hOAT1 cells over the tested concentrations up to 10 mM, it showed significant cellular toxicity with CC(50) of 0.77 mM in MDCK/hOAT3 cells, implying that OAT3 may involve more actively in the imipenem-induced nephrotoxicity. In addition, the cellular toxicity of imipenem decreased by approximately 20 folds in the presence of morin in MDCK/hOAT3 cells. In conclusion, the present study suggests that morin might be beneficial to reduce the nephrotoxicity of imipenem, at least in part, via the inhibition of OAT3-mediated renal excretion of imipenem.

Topics: Animals; Anti-Bacterial Agents; Antioxidants; Cell Line; Dogs; Flavonoids; Imipenem; Kidney; Kidney Diseases; Organic Anion Transport Protein 1; Organic Anion Transporters, Sodium-Independent; Rabbits; Transfection

The aim of this study was to analyze the protective effects of morin administered during the therapy of reperfusion injury of the laboratory rat kidney. Animals were randomly divided into five groups (n= 10). One group was left intact. Three medicated groups and one placebo group were subjected to ischemia (60 min) and reperfusion of the left kidney. Morin was suspended in a 2 ml of 0.5% Avicel solution and administered orally by a gastric probe at doses of 5, 10, and 20 mg.kg(-1) once a day for 15 days. The placebo group was given only 2 ml of 0.5% Avicel in the same way. On the 15th day, all the animals were exsanguinated and the reperfused kidneys were recovered. Selected biochemical markers in blood were assessed: superoxide dismutase, glutathion peroxidase, total antioxidative capacity, malondialdehyde, creatinine, urea, and uric acid. Creatinine, urea, and total protein were analyzed in urine, and a 24-hour diuresis was recorded. The kidney tissue samples were used for histopathological examination. Morin supported the organism's own defensive reactions against free radicals and decreased lipid peroxidation in the cell membranes and contributed to the recovery of kidney functions. The histopathological results confirm 20 mg x kg(-1) as the most effective dose.

Topics: Animals; Antioxidants; Flavonoids; Kidney; Kidney Diseases; Rats; Rats, Wistar; Reperfusion Injury