ABSTRACT
Background: Bone marrow mesenchymal stem cells [BM-MSCs] elicit neuroprotective effects, and their repair ability has been investigated in different experimental models. We aimed to investigate the effect of multiple i.p. BM-MSCs injections in the cuprizone model of multiple sclerosis in mice
Methods: Adult male C57BL/6 mice [n = 40] were fed a regular diet or a diet containing cuprizone [0.2% w/w] for six weeks. Bone marrow samples were taken from patients with spinal cord injury. BM-MSCs [2 * 10[6] in 1 milliliter medium] were administered intraperitoneally for two consecutive weeks at the end of the forth weeks of cuprizone administration. Animals [n = 12] were perfused with 10% paraformaldehyde at the end of sixth week. The brains were sectioned coronally in 6- 8-Mu m thickness [-2.3 to 1.8 mm from bregma]. The sections were stained by luxol fast blue-cresyl violet, and images were captured via a microscope. Demyelination ratio was estimated in corpus callosum in a blind manner. A quantitative real-time PCR was used to measure the myelin basic protein gene expression at sixth week
Results: Histologically, cuprizone induced demyelination in the corpus callosum. Demyelinated area was diminished in the corpus callosum of cell-administered group. Cuprizone could decrease myelin-binding protein mRNAs expression in corpus callosum, which was significantly recovered after BM-MSCs injections
Conclusion: Our data indicated a remyelination potency of multiple i.p. BM-MSCs in the cuprizone model of multiple sclerosis in mice
ABSTRACT
The autism spectrum disorders [ASD] are amongst the most heritable complex disorders. Although there have been many efforts to locate the genes associated with ASD risk, many has been remained to be disclosed about the genetics of ASD. Scrutiny's have only disclosed a small number of de novo and inherited variants significantly associated with susceptibility to ASD. These only comprise a small number of total genetic risk factors. Some studies confirm the contribution of mitochondrial genome mutations to the pathophysiology of the autism, but some other studies rejected such a contribution. In the current study we tried to scrutinize the association between mitochondrial tRNA genes mutations and the risk of Autism. DNA was extracted from the blood of 24 patients with ASD and 40 age-matched healthy controls from Special Medical Center in Tehran. 22 tRNA genes of mitochondrial genome were PCR amplified using 12 primer pairs and sequenced. Sequencing results were searched for mutations using clustalW Progran and then the association of mutations with the autism risk was assessed by statistical analysis using SPSS version 15. Many of the observed mutations were sporadic mutations without any significant relationship with the risk of autism, and the other mutations including those of high frequency showed no significant relationship with the risk of disease as well [P>0.05] except mutations 16126T>C [P=0.01], 14569G>A[P=0.02] and 1811A>G[P=0.04]. These three mutations were in the noncoding regions of the mitochondrial genome near tRNA genes. The mutation 16126T>C was in the mtDNA control region. Our study showed a significant relationship between the point mutations 16126T>C, 14569G>A and 1811A>G of the mitochondrial genome and the risk of autism
ABSTRACT
3,4-methylenedioxymethamphetamine [MDMA] is an illicit, recreational drug that causes cellular death and neurotoxicity. This study evaluates the effects of different doses of MDMA on the expression of apoptosis-related proteins and genes in the hippocampus of adult rats. In this experimental study, a total of 20 male Sprague Dawley rats [200-250 g] were treated with MDMA [0, 5, 10, 20 mg/kg i.p. twice daily] for 7 days. Seven days after the last administration of MDMA, the rats were killed. Bax and Bcl-2 genes in addition to protein expressions were detected by western blot and reverse transcription polymerase chain reaction [RT-PCR].Results were analyzed using one-way ANOVA and p