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BACKGROUND: Differentiation of bone marrow stromal cells (BMSCs) into neurons requires two processes: orientation and differentiation. Orientation and differentiation are results from different gene expression in cells with the same gene bank. Gene expression requires a certain condition. Changes in extracellular matrix can induce changes in cell morphology and gene expression manner. OBJECTIVE: To explore the possibility of BMSC differentiation into neuron-like cells under tissue extract from rat damaged brain. METHODS: The fifth passage of green fluorescent protein (GFP)-transfected BMSCs was induced to differentiate in brain tissue extract from ischemia/reperfusion rats or normal rats. A blank control was set. Cell morphology change was observed under the phase contrast microscope, and then evaluated using immunohistochemical staining. RESULTS AND CONCLUSION: Primarily cultured BMSCs were purified and amplified, and then showed even spindle shape. The third passage of BMSCs was positive for CD44 and CD106, but negative for CD34. Under the fluorescence microscope, BMSCs showed fluorescence expression, but the strength was weak 24 hours following GFP transfection. Numerous cells presented significant green fluorescence 48 hours later. Following adding brain tissue extract from ischemia/reperfusion rats. Induced cells presented neuron-like feature, but neuron specific enolase specific antibody presented positive expression. Compared with the blank control group, the differentiation rate of BMSCs was significantly increased in the ischemia/reperfusion group and normal group (P < 0.05). The increased range was significantly greater in the ischemia/reperfusion group than the normal group (P < 0.05). These results indicated that brain tissue extract from ischemia/reperfusion rats can successfully induce the differentiation of BMSCs into neuron-like cells.
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Objective To investigate the effect of 17?-estradiol (E2) on the expression of hepatocyte growth factor (HGF) mRNA in the myocardial tissues in rats during myocardial ischemia-reperfusion (I/R) process, and explore the relationship between HGF mRNA expression and myocardial apoptosis. Methods Using the random number table, 40 male SD rats were divided into 2 groups (20 rats in each group) randomly, ischemia-reperfusion (control) group and E2 treatment group. Myocardial I/R models of rats were duplicated by ligating the left anterior descending coronary artery for 20 min then reperfusion for 30 min. The expression of HGF and the apoptosis of myocardiocytes were observed with RT-PCR, TUNEL and flow cytometry. Results At the points of cardiac ischemia for 20 min and reperfusion for 30 min, in the E2 treatment group, the expressions of HGF mRNA were significantly higher than corresponding points of the control group (P
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AIM To observe the expression of inducible nitric ox ide synthase (iNOS) in the rats' hippocampus of kainic acid (KA) induced-seizur es and the effect of L-arginine(L-Arg) or L-nitroarginine(L- NNA) chronic intervention before KA. METHODS The expression of iN OS mRNA by RT-PCR and behaviour were observed after administration of convulsan t dose of KA (10 mg?kg -1 ) and pretreatment with NO predecessor (L-Ar g, 40 mg?kg -1 ) or a inhibitor of NOS(L-NNA, 50 mg?kg -1 ) befo re KA. RESULTS The time-dependent seizures were induced on rats after giving KA, and were improved and serious in the animals with L-NNA pr etreatment, but they were alleviated by L-Arg pretreatment before KA. Compa red with control, iNOS mRNA expression was feebly at KA 3 h, continuative improv ement accompanying KA time prolonged, and it was markedly enhanced at KA 24 h. I t couldn't be examined at KA 2 d or 3 d, and was obviously improved at KA 7 d a gain. iNOS mRNA appeared weak in the rats hippocampus with L-Arg pretreatme nt after KA 1 h, whereas it wasn't found in L-NNA pretreatment animals. CONCLUSION iNOS mRNA expression appeared in the hippocampus of seizu re rats at a few time after KA, and L-Arg chronic intervention before KA ha s a little effect on it.
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AIM To explore the role of nitric oxide (NO) mediators in seizure behavior and the related expression of interlukin 6(IL 6). METHODS The IL 6 immunoreactivity (IL 6 ir) and behaviour were observed in kainic acid (KA) induced seizure following pretreatment with L nitroarginine( L NNA), a inhibitor of nitric oxide synthase(NOS), or the same number of moles of L arginine( L Arg). RESULTS The results showed that time dependent seizures were induced on animals after administration of KA (10 mg?kg -1 ), accompanied by the immediate enhancement of IL 6 ir in hippocampal structure, piriform area and cortex. The behaviors of rats were not markedly altered by chronic pretreatment with L NNA (50 mg?kg -1 ) or L Arg (40 mg?kg -1 ). However, after the administration of KA, the seizure behaviors were obviously different in the group of L NNA and L Arg respectively. Seizure was agrevated in the animals with L NNA pretreatment and many rats died at KA 3 hours, whereas seizure was alleviated after KA in the group of L Arg. IL 6 expression was apparently up regulated in some brain areas such as hippocampus in the group of KA pretreated with L NNA, but opposite effects appeared in the group pretreated with L Arg before KA injection. CONCLUSION These results indicate that endogenous NO mediators may alleviate the seizure behaviors and may down regulated the early expression of IL 6 in KA challenged seizure, but it the mechanism of the early expression of IL 6 with the homeostasis of endogenous NO mediator merits further study.nismoftheearlyexpressionofIL 6withthehome