Journal of

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Introduction: Curcumin is a major phenolic compound of Curcuma longa, which has long been used in traditional Indian medicine. Recently, curcumin has been reported to have antihyperglycemic activity in animal models. However, the molecular basis of this action has not been adequatedly described. In the present study the antihyperglycemic effect of curcumin was examined using C2C12 myoblast cells. Methods: The effects of curcumin were investigated in C2C12 myotubes by treating the cells with 40 µM of curcumin for 1.5 h. C2C12 myotubes were homogenized and the subcellular fractionation was prepared using ultracentrifugation Then protein assay was performed using Bradford method and Glut4 determination was done using SDS-PAGE. Moreover, western immunoblotting techniques were exerted for semi-quantitative measurement. Data analysis was performed via gene tools software of Gel documentation and SPSS. An ANOVA test was used to compare three groups together. Results: Comparison of Glut4 levels in C2C12 myotubes showed that myotubes which were exposed to1.5 hours of 40 µM curcunin had higher Glut4 percentages in both cytosolic and membrane fractions and Glut4 percentages were significant with a confidence interval (CI) of 95% ( P<0.05 ). Conclusion: The study results showed that curcumin can strongly induce the increase of Glut4 translocation in differentiated C2C12 cells, indicating its possible regulatory role in the glucose metabolism of skeletal muscle cells

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Introduction: Epilepsy is regarded as one of the prevalent neurological disorders in children. The role of anti-oxidants in protection of epilepsy has been discussed in several studies. Vitamin E can be mentioned as a natural antioxidant to neutralize free radicals. Therefore, the present study aimed to evaluate the effects of vitamin E on oxidative stress markers such as malone dialdehyde(MDA) and protein carbonyl(PC) in children suffering from idiopathic epilepsy and vitamin D deficiency.

Methods: In the current study, children suffering from idiopathic epilepsy and vitamin D deficiency were randomly divided into two groups. One group was treated with 50000 units of vitamin D oral capsules (per week) for 8 weeks and the other  group was treated with 100 units of vitamin E (per day) for one month as well as 50000 unit of vitamin D for 8 weeks. The amount of MDA and PC were measured by the spectrophotometer method. The obtained data were analyzed via the  SPSS software (ver, 19) using t-test.

Results: The results indicated that the amount of  MAD and PC revealed a significant decrease after the treatment. In fact, in the group treated with vitamin E, the amount of PC decreased significantly compared with the other group, though MDA reduction was not proved to be significant. 

Discussion: The findings of the present study revealed that treatment with vitamin E could reduce the PC amount in regard with epileptic patients.