RESUMEN
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
RESUMEN
Introduction: X chromosome inactivation [XCI] is a process during which one of the two X chromosomes in female human is silenced leading to equal gene expression with males who have only one X chromosome. Here we have investigated XCI ratio in females with opioid addiction to see whether XCI skewness in women could be a risk factor for opioid addiction
Methods: 30 adult females meeting DSM IV criteria for opioid addiction and 30 control females with no known history of addiction were included in the study. Digested and undigested DNA samples which were extracted from blood were analyzed after amplification of the polymorphic androgen receptor [AR] gene located on the X chromosome. XCI skewness was studied in 3 ranges: 50: 50-64: 36 [random inactivation], 65: 35-80: 20 [moderately skewed] and >80: 20 [highly skewed]
Results: XCI from informative females in control group was 63% [N=19] random, 27% [N=8] moderately skewed and 10% [N=3] highly skewed. Addicted women showed 57%, 23% and 20%, respectively. The distribution and frequency of XCI status in women with opioid addiction was not significantly different from control group [P=0.55]
Discussion: Our data did not approve our hypothesis of increased XCI skewness among women with opioid addiction or unbalanced [non-random] expression of genes associated with X chromosome in female opioid addicted subjects
RESUMEN
The role of nitric oxide [NO] in many well-known effects of morphine is well defined. NO is involved in the signaling pathway of the N-methyl-D-aspartate [NMDA] receptor, which is proposed to mediate some of morphine's effects. This research studies the effect of morphine and NMDA on lipopolysaccharide [LPS]-stimulated NO production by clonal rat pheochromocytoma [PC12] cells. We used the Griess reaction to measure NO concentrations in cell culture medium. PC12 cells that were incubated for 24 h with varying concentrations of morphine [0.1, 1, 10, 100, and 1000microM] plus LPS [1 microg/ml] did not significantly alter the concentration of NO in the medium. However, NO production increased when cells were treated for both 48 h with 100 and 1000 microM morphine and for 72 h with 10,100, and 1000 microM of morphine. After 72 h, 1 microM naloxone significantly decreased NO concentration. Naloxone, at doses of 0.1, 1, and 10microM prevented NO production by 1000 microM of morphine. NMDA [0.1, 1, and 10 microM] did not alter NO concentrations after 24, 48 or 72 h. Morphine [1 microM]-induced NO production was inhibited by 10 microM NMDA after 48 h. Inhibition of NO was also noted with1 and 10 microM concentrations of morphine after 72 h. Chronic treatment of PC12 cells with morphine significantly increases LPS-stimulated NO production via naloxone-sensitive receptors. The cells seem to release endogenous morphine in medium. NMDA does not affect NO production, which may be due to the lack of functional NMDA receptor expression in PC12 cells