The effect of the ginger on the apoptosis of hippochampal cells according to the expression of BAX and Cyclin D1 genes and histological characteristics of brain in streptozotocin male diabetic rats.

Diabetes is the most common endocrine disorder in humans with multiple complications including nervous system damages. The aim of the present study was to determine the effect of ginger extract on apoptosis of the neurons of hippocampus, via evaluation of BAX and Cyclin D1 and also histological analysis, in male diabetic rats. In this experimental study, 60 Wistar rats (220 ± 30gr) were conducted in 5 groups as follow: diabetic group treated with saline (group 1), normal group treated with saline (group 2), diabetic group treated with ginger (group 3), diabetic group treated with ginger-insulin (group 4), diabetic group treated with insulin (group 5). STZ (60 mg/kg) was intraperitoneally used to induce the diabetes. Expression levels of BAX and Cyclin D1 were examined using Real-Time PCR technique and the normality of neurons was evaluated using H&E staining method. The results showed that blood glucose level significantly decreased in group 4 when compared to group 1. In molecular analysis, there was no significant difference between groups regarding the expression of BAX gens, while, the expression of Cyclin D1 were significantly decreased in group 4 compared with group 1. Histological analysis revealed that pathological symptoms were lower in group 4 than the other diabetic groups. The results of present study showed that the ginger in addition to lowering blood sugar level, changes the expression of Cyclin D1 gene and histological characteristics in a positive manner. This means that the ginger may protects neurons of the hippocampus from apoptosis in diabetic patients.

Different ideas associated renal malformation and laminin α5 expression caused by maternal nicotine exposures.

The number of smokers is increasing specially in pregnant mothers and millions of children with health problems are born from the smoker mothers. Nicotine as a toxic substance crosses from placenta and accumulates in the developing organs of fetus. In this study, the effects of maternal nicotine exposure on expression levels of kidney laminin α5 in newborn mice were examined. Timed pregnant mice were injected subcutaneously with nicotine at a dose of 2 mg/kg/day from day 7 of gestation to the last day of the pregnancy (Group 1) and from day 7 until the two weeks of postnatal (Group 2). Sham control groups were injected with saline. After the last injection, all the newborn mice were anesthetized; their kidneys were removed and prepared for analysis of mRNA and protein expression of laminin α5 using Real-Time PCR and immunohistochemical techniques, respectively. Our results showed that mRNA levels of kidney laminin α5 in newborn mice were increased in group 1 when compared to sham control group and also group 2. Immunohistochemical analysis demonstrated that the protein levels of laminin α5 in the glomerulus have significantly increased in group 1 when compared to group 2. In the proximal convoluted tubules, the parameter had a high significant increase in group 1 in comparison to control and also group 2. According to the results, it seems that maternal nicotine exposure may induce abnormal laminin α5 expression which may cause defects in kidney function during life time.

DNA Methylation and microRNA patterns are in association with the expression of BRCA1 in ovarian cancer.

Ovarian cancer is the sixth most prevalent cancer in women and is considered the most lethal gynecological malignancy. It can be inherited as a familial disease but also has a strong spontaneous occurrence. Although the disease is associated with genome instability brought on by genetics and environmental factors there is evidence that mutations in the gene encoding for the breast cancer type 1 susceptibility protein (BRCA1) or its down-regulation are involved in its development. Down-regulation of BRCA1 expression by hypermethylation of its promoter may account for some cases of ovarian cancer but this does not explain the cause of the majority of the disease. This review explores the role of BRCA1 promoter hypermethylation and micro-RNAs (miRNA) involved in the regulation of BRCA1 and their role in ovarian cancer development as well as some of the exciting discoveries which could lead to targeting miRNA with a view to restoring BRCA1 expression in diseased tissues.