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
Introduction: It has shown that listening to Mozart music can potentiate spatial tasks in human; and reduce seizure attacks in epileptic patients. A few studies have reported the effects of prenatal plus postpartum exposure of mice to the Mozart music on brain-drived neurotrophic factor [BDNF] in the hippocampus. Here we investigated the effect of postpartum exposure to The Mozart music on BDNF concentration in the hippocampus of rat. Methods: Thirty male one day old newborn Wistar rats divided randomly in two equal experimental and control groups. Experimental group exposed to slow rhythm Mozart music [Mozart Sonata for two pianos KV 448, 6 hour per day; sound pressure levels, between 80 and 100 dB] for 60 successive days. The control group was kept in separate room with housing conditions like experimental group except music exposure. After 60 days the rats were euthanized and hippocampuses extracted; then the content of BDNF protein was measured using ELISA sandwich method. Results: Data analysis revealed that rats exposed to Mozart Sonata music had significantly increased BDNF content in the hippocampus as compared to control rats [P +/- 0.01]. The concentrations of BDNF were 86.30 +/- 2.26 and 94.60 +/- 6.22 ng/g wet weight in control and music exposure groups respectively. Discussion: Exposure to the Mozart music early in life can increase the BDNF concentration in the hippocampus in rats
ABSTRACT
Congenital nephrotic syndrome may be caused by mutations in NPHS1 and NPHS2, which encode nephrin and podocin, respectively. Since the identification of the NPHS2 gene, various investigators have demonstrated that its mutation is an important cause of steroid-resistant nephrotic syndrome. We aimed to evaluate frequency and spectrum of podocin mutations in the Iranian children with steroid-resistant nephritic syndrome. We examined 20 children with steroid-resistant nephritic syndrome referred to Ali Asghar Children's Hospital, in Tehran, Iran. Mutations in the 5th and 7th exons of NPHS2 were assessed. The mutational analysis of NPHS2 was performed by DNA sequencing. The mean age at the onset of proteinuria was 6.4 +/- 3.6 years. None of the children had mutations in the exons 5 or 7. Our study suggests that NPHS2 mutations in exons 5 and 7 are not seen in our children. Therefore, we cannot recommend NPHS2 [exons 5 and 7] mutation for screening in Iranian children with steroid-resistant nephritic syndrome. Other exons of podocin or other podocyte proteins in Iranian children may play a role in pathogenesis of steroid-resistant nephritic syndrome
Subject(s)
Humans , Male , Female , Child , Membrane Proteins/genetics , Intracellular Signaling Peptides and Proteins/genetics , Mutation , Steroids , Drug Resistance , Nephrotic Syndrome/therapy , Base Sequence , Sequence Analysis, DNA , DNA Mutational AnalysisABSTRACT
Even today there is no effective drug therapy to prevent neuronal loss after brain stroke. The objective of this research was to study effects of the mitochondrial K-ATP [MAK] channel regulators on neuronal cell population and neurological function after ischemia reperfusion in the rat. Rats were temporarily subjected to four vessels occlusion for 15 minutes followed by 24 hours reperfusion with or without MAK channel regulators. The normal cell count of neuronal population significantly increased in the K-ATP channel opener [diazoxide] treated ischemia-reperfusion group compared with the control group. Cell count and neurological function scores were dose dependent to MAK channel regulators in vivo. Our results showed that diazoxide treatment leads to better preservation of cortical neurons in rat