RESUMO
Objectives: To assess the protective effect of L-carnitine in reducing cisplatin toxicity via estimating biochemical tests, histomorphometric, and immunohistochemistry (IHC) of ß-catenin and cyclin D. Materials and Methods: Fifteen adult male rabbits were used in this study and allocated into 3 groups; Group 1 (Control negative), rabbits of this group were not given any treatment. In group 2, the animals were injected with cisplatin single-dose/per week. Group 3 rabbits were treated with Cisplatin+L-carnitine orally by gavage tube for 29 days. At the end of the experiments, blood samples from all rabbits were taken from the earlobe, and then the biochemical test was done, the kidney and tissue sections were prepared for both H& E and IHC for both ß-catenin and cyclin D genes. Results: Treatment with L-carnitine reduced the injury effect of cisplatin via a decline in serum creatinine, urea, bilirubin, GPT, GOP, and ALP significantly (P<0.05). Also, administration of LC attenuates the histopathologic abnormality in the kidney (15.71% vs 85.18%) and liver (score 3 vs 15 ) induced by cisplatin. L-carnitine elevates the expression of ß-catenin and cyclin D in renal and hepatic parenchyma by diffuse, moderate-strong positivity vs cisplatin that showed local-weak staining. Conclusion: These findings imply that L-carnitine, by its pleiotropic actions in activating Wnt signaling, alleviates cisplatin-induced renal and hepatic destruction. It might be a method of preventing cisplatin-related nephrotoxicity and hepatotoxicity.
RESUMO
BACKGROUND: Ultraviolet B (UVB) is the most damaging component of sunlight. It rapidly activates the epidermal growth factor receptor (EGFR) and generates reactive oxygen species (ROS) in excessive quantities that quickly overwhelm tissue antioxidants. SETTING AND DESIGN: To demonstrate the effects of UVB radiation on EGFR expression in mice skin and to evaluate the role of antioxidants in the exposed group. MATERIALS AND METHODS: After obtaining the approval of the ethical committee, forty mice from BALB/c strain were used in this experiment and were allocated into 3 groups; 10 (control group); 15 (exposure group); and 15 (exposed and treated with antioxidants). Antioxidants were administered through subcutaneous injection. Skin biopsies from all groups were stained with EGFR antibodies. Total antioxidant status (TAS) was evaluated in all groups. STATISTICAL ANALYSIS: The data obtained were analyzed using ANOVA, Duncan's test, and Pearson's Correlation. RESULTS: The highest EGFR expression in exposure group was of score 3(+) (53%). The highest EGFR expression in treatment group was score 0 (40%). Apoptotic bodies and dermal mast cells increased in exposure group while decreased in treatment group. The mean values for TAS were measured for each group; control group = 1.2 mmol/l; exposure group = 0.87 mmol/l; treatment group =1.3 mmol/l. CONCLUSIONS: UVB led to Seborrheic Keratosis (SK) in mice through enhancement of EGFR expression. Antioxidants effectively reduced UVB-induced SK, reduced epidermal changes, apoptotic bodies, and decreased dermal mast cells. TAS measurement declined in exposure group, while it was within normal range in most treated cases.
