Related Posts With Tag " Rat "


Effect of quercetin on the brain-derived neurotrophic factor gene expression in the rat brain

ABSTRACT: Quercetin is a ubiquitous fl avonoid found in many plants. Neuroprotective effects of quercetin have been shown in several in vitro and in vivo studies, but its mechanism of action has not been fully defi ned yet. Brain-derived neurotrophic factor (BDNF) is a fundamental neurotrophin with vital functions in the survival of neuronal cells. In the present study, we aimed to investigate the effects of quercetin on expression of BDNF mRNA in the hippocampus of rat brain. METHODS: Male rats were daily gavaged with quercetin (10, 20 or 50 mg/kg·bwt) for 30 days. Hippocampal levels of the BDNF transcripts were assessed using quantitative (q) RT-PCR. RESULTS: Quercetin at doses of 20 and 50 mg/kg caused a signifi cant increase in the mRNA expression of BDNF as compared with the control group. Quercetin treatment at a dose of 10 mg/kg failed to cause any signifi cant changes in the levels of BDNF mRNA CONCLUSION: Our fi ndings suggest that the neuroprotective effects of quercetin may be at least partly due to its .Author: Farideh Jalali Mashayekhi inducing effects on the expression levels of the BDNF mRNA

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Effects of Cobalamin (Vitamin B12) on Gentamicin Induced Nephrotoxicity in Rat

Abstra ct Background The main side effect of gentamicin is nephrotoxicity. The effect of cobalamin (Cob) was investigated on gentamicin nephrotoxicity in rats. Methods Renal injury induced by i.p. injection of gentamicin (100 mg/kg) for 8 consecutive days. Cobalamin (6 mg/kg/day, i.p) treatment was done for 8 consecutive days as co-treatment and post-treatment protocol. Results Cobalamin significantly increased creatinine clearance levels and renal blood flow which were reduced by gentamicin. Also, cobalamin significantly improved serum electrolytes (sodium and potassium) levels which were disturbed by gentamicin. Cobalamin significantly compensated deficits in the antioxidant defense mechanisms, suppressed lipid per oxidation and ameliorated renal tissue damage mediated by gentamicin. Conclusion The results of the current study indicated that cobalamin effectively protected the kidney tissue against gentamicin induced acute nephrotoxicity in rats. The antioxidant and anti-inflammatory activities can be supposed the main factors responsible for the nephroprotective effect of cobalamin

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Alteration in CatSper1 and 2 genes expression, sperm parameters and testis histology in varicocelized rats

Abstract Background: CatSper gene, a member of cation channel sperm family, has an essential role in sperm motility and male fertility. Following varicocele, sperm parameters especially sperm movement decreases. For this reason, we hypothesized that CatSper gene expression might be reduced after varicocele induction in an animal model. Objective: The aim of this study was to evaluate the expression of CatSper 1 and 2 genes, sperm parameters and testis histology following varicocele induction. Materials and Methods: A total of 30 Wistar male rats were randomly divided into three following groups (n=10/ each): control, sham, and varicocele group. Experimental varicocele was induced by partial ligation of the left renal vein. The epididymal sperm parameters, CatSper1 and 2 genes expression, and testes histology were studied two months after varicocele induction. Results: Our results revealed that motility (32.73±16.14%), morphology (48.80±17%) and viability (31.23±9.82%) of sperms significantly reduced following varicocele induction. In addition, we showed a significant decrease in the number of spermatogonia (43.63±5.31) and seminiferous tubules diameters (190.51±19.23 mm) in experimental varicocele rats. The level of CatSper1 and 2 genes expression evaluated using real-time polymerase chain reaction was significantly downregulated 2 months after varicocele induction. Conclusion: Our data indicated that experimental varicocele has deleterious effects on sperm parameters, testis structure as well as the expression of CatSper 1 and 2 genes

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