ABSTRACT
Objective: To explore the possible effects of naringin on acrylamide-induced nephrotoxicity in rats. Methods: Sprague-Dawley rats weighing 200-250 g were randomly divided into five groups. The control group was given intragastric (i.g.) saline (1 mL) for 10 d. The acrylamide group was given i.g. acrylamide in saline (38.27 mg/kg titrated to 1 mL) for 10 d. The treatment groups were administered with naringin in saline (50 and 100 mg/kg, respectively) for 10 d and given i.g. acrylamide (38.27 mg/kg) 1 h after naringin injection. The naringin group was given i.g. naringin (100 mg/kg) alone for 10 d. On day 11, intracardiac blood samples were obtained from the rats when they were under anesthesia, after which they were euthanized. Urea and creatinine concentrations of blood serum samples were analyzed with an autoanalyzer. Enzyme-linked immunosorbent assay was used to quantify malondialdehyde, superoxide dismutase, glutathione, glutathione peroxidase, catalase, tumor necrosis factor-β, nuclear factor-κB, interleukin (IL)-33, IL-6, IL-1β, cyclooxygenase-2, kidney injury molecule-1, mitogen-activated protein kinase-1, and caspase-3 in kidney tissues. Renal tissues were also evaluated by histopathological and immunohistochemical examinations for 8-OHdG and Bcl-2. Results: Naringin attenuated acrylamide-induced nephrotoxicity by significantly decreasing serum urea and creatinine levels. Naringin increased superoxide dismutase, glutathione, glutathione peroxidase, and catalase activities and decreased malondialdehyde levels in kidney tissues. In addition, naringin reduced the levels of inflammatory and apoptotic parameters in kidney tissues. The histopathological assay showed that acrylamide caused histopathological changes and DNA damage, which were ameliorated by naringin. Conclusions: Naringin attenuated inflammation, apoptosis, oxidative stress, and oxidative DNA damage in acrylamide-induced nephrotoxicity in rats.
ABSTRACT
Objective: To explore the possible effects of naringin on acrylamide-induced nephrotoxicity in rats. Methods: Sprague-Dawley rats weighing 200-250 g were randomly divided into five groups. The control group was given intragastric (i.g.) saline (1 mL) for 10 d. The acrylamide group was given i.g. acrylamide in saline (38.27 mg/kg titrated to 1 mL) for 10 d. The treatment groups were administered with naringin in saline (50 and 100 mg/kg, respectively) for 10 d and given i.g. acrylamide (38.27 mg/kg) 1 h after naringin injection. The naringin group was given i.g. naringin (100 mg/kg) alone for 10 d. On day 11, intracardiac blood samples were obtained from the rats when they were under anesthesia, after which they were euthanized. Urea and creatinine concentrations of blood serum samples were analyzed with an autoanalyzer. Enzyme-linked immunosorbent assay was used to quantify malondialdehyde, superoxide dismutase, glutathione, glutathione peroxidase, catalase, tumor necrosis factor-β, nuclear factor-κB, interleukin (IL)-33, IL-6, IL-1β, cyclooxygenase-2, kidney injury molecule-1, mitogen-activated protein kinase-1, and caspase-3 in kidney tissues. Renal tissues were also evaluated by histopathological and immunohistochemical examinations for 8-OHdG and Bcl-2. Results: Naringin attenuated acrylamide-induced nephrotoxicity by significantly decreasing serum urea and creatinine levels. Naringin increased superoxide dismutase, glutathione, glutathione peroxidase, and catalase activities and decreased malondialdehyde levels in kidney tissues. In addition, naringin reduced the levels of inflammatory and apoptotic parameters in kidney tissues. The histopathological assay showed that acrylamide caused histopathological changes and DNA damage, which were ameliorated by naringin. Conclusions: Naringin attenuated inflammation, apoptosis, oxidative stress, and oxidative DNA damage in acrylamide-induced nephrotoxicity in rats.
ABSTRACT
Objective To investigate the effects of quercetin (Q) and rutin on 5-fluorouracil (5-FU)-induced hepatotoxicity. Methods The control group was corn oil. The 5-FU group rats were corn oil and injected intraperitoneal 5-FU 50 mg/kg. Groups rutin 50 + 5-FU and rutin 100 + 5-FU were respectively 50 mg/kg and 100 mg/kg rutin. These groups were given 5-FU (50 mg/kg) in the 18th day. The group rutin 100 was rutin (100 mg/kg i.g.). Groups Q50 + 5-FU and Q100 + 5-FU were respectively 50 mg/kg and 100 mg/kg quercetin. These groups were given 5-FU (50 mg/kg) in the 18th day of quercetin application. The group Q100 was quercetin (100 mg/kg i.g.). In the end of experimental applications, blood was collected from anesthetized rats. Results The MDA level was significantly higher in the 5-FU group compared with control group, and determined to be decreased in other groups. GPx and GSH levels were significantly decreased in the 5-FU group compared to the control, rutin 100 + 5-FU and Q100 + 5-FU groups. AST, ALT, LDH and ALP levels in the serum were significantly increased in the 5-FU group compared with the other groups. The results from this analysis show that while the caspase-3 level increases in the 5-FU group, it decreases in the Q50 + 5-FU, Q100 + 5-FU, rutin 50 + 5-FU and rutin 100 + 5-FU groups. Bcl-2 level decreased in the 5-FU group compared to the control group, but increased in the rutin 100 + 5-FU, Q50 + 5-FU and Q100 + 5-FU groups. Conclusions In this study it was determined that the rutin and Q have protective effects on 5-FU-induced hepatotoxicity.