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Severe skin damage not only causes a mass of tissue defect, but also leads to the loss of various sensory functions. Tissue engineering skin provides a new way for high-quality wound repair, while there are still many problems in the recovery of sensory function, such as abnormality or loss of sensation of pain, touch, and temperature. Therefore, when tissue engineering skin is used to promote wound healing, regeneration and functional recovery of sensory nerve have attracted more and more attention. This article introduces the kind, distribution, regeneration, and factors influencing regeneration of sensory nerve in skin, and explores strategies in promoting regeneration of sensory nerve from dermal scaffold, seed cell, and neurturin of tissue engineering skin.
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Objective: To investigate the effect and mechanism of brain-derived neurotrophic factor (BDNF) pretreatment for reducing myocardial ischemia/reperfusion (I/R) injury in experiment rats. Methods: Rat’s myocardial I/R model was established by left anterior descending artery ligation for 30min followed-by reperfusion for 180 min. The rats were divided into 5 groups:Sham operation group, I/R group and IR with BDNF pretreatment (1, 10, 100) nmol/(kg·ml) groups respectively. The LVSP, LVEDP, ±dp/dtmax were recorded after I/R;serum levels of LDH, CK and the cardiac tissue levels of MDA, SOD were examined;the ratios of left ventricular myocardial infarction area in different groups were observed by by Evans blue staining;cell apoptosis rates were evaluated by Tunel staining;the total-TrkB and p-TrkB in myocardium were detected by Western-blot analysis. Result: Compared with I/R group, in 3 IR with BDNF pretreatment groups, LVSP, ±dp/dtmax were gradually increasing and LVEDP were gradually decreasing, all P Conclusion: BDNF pretreatment could maintain the cardiac function in experiment rats after I/R injury, it may reduce MI area, decrease oxidative damage and apoptosis, therefore, protect myocardial cells for reducing IR injury.
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BACKGROUND:Studies have shown that neural stem cel transplantation has a certain effect on neuropathic pain, but the efficacy of transplanted cel number on neuropathic pain is not exactly understood. OBJECTIVE:To observe the effect of different amount of neural stem cels administered intrathecaly on the neuropathic pain and expression of glial-derived neurotrophic factor in the spinal cord dorsal horn and dorsal root ganglion in rats after partial sciatic nerve transaction. METHODS:A Sprague-Dawley rat at 14-16 days of pregnancy was used to prepare neural stem cel suspensions that were injected intrathecaly into rat models of partial sciatic nerve transaction at doses of 1×103, 1×104, 1×105, 1×106, 1×107cels per 30 μL, respectively. Additionaly, model group and sham-operated group were set up. Threshold values of mechanical and thermal pain were recorded 1 day before operation, 1, 3, 7, 14, 21 days after operation. Expressions of glial-derived neurotrophic factor protein and mRNA in the ipsilateral spinal cord dorsal horn and dorsal root ganglion were detected by immunohistochemistry and RT-PCR, respectively, at 7 and 21 days after partial sciatic nerve transaction. RESULTS AND CONCLUSION: Pain threshold values were decreased in al the groups except the sham-operated group at 1 day after operation, and reached the peak at 7 and 14 days after operation (P < 0.05). Compared with the model group, the pain threshold values and the expression of glial-derived neurotrophic factor protein and mRNA in the ipsilateral spinal cord dorsal horn and dorsal root ganglion were increased gradualy in a dose-dependent manner in the 1×104, 1×105, 1×106, 1×107 groups at 7 days after operation (P < 0.05). At 21 days post-operation, the pain threshold values showed no differences from the preoperative findings in the 1×105, 1×106, 1×107 groups, but the expression of glial-derived neurotrophic factor was significantly higher in the 1×105 group than the other groups (P < 0.05). Taken together, intrathecal transplantation of neural stem cels at a dose of 1×105 is the most effective in aleviating partial sciatic nerve transaction-induced neuropathic pain in rats.
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BACKGROUND:Transformation growth factor-β(TGF-β) and brain-derived neurotrophic factor (BDNF) are the main regulatory factors in the process of spinal cord injury. There are many researches for TGF-βand BDNF pathogenesis in the spinal cord injury, but the regulation of Ginsenoside Rg1 intervention on TGF-βand BDNF in the spinal cord injury is rarely reported. OBJECTIVE:To observe the effect of Ginsenoside Rg1 intervention on TGF-βand BDNF expression at themolecular protein levels, and to study the protection effect of Ginsenoside Rg1 on the spinal cord and nerve function after spinal cord injury. METHODS:Experimental rats were randomly divided into blank control group, model group and Ginsenoside Rg1 group. In the model and Ginsenoside Rg1 groups, spinal cord injury model was established with the impact method in rats. In the Ginsenoside Rg1 group, rats were intraperitoneal y injected with 10 mg/kg Ginsenoside Rg1 24 hours after modeling, once per day, for 14 days. Rats in the blank control and model groups were injected with equal saline. RESULTS AND CONCLUSION:Compared with the control group, serum malondialdehyde levels increased, the content of superoxide dismutase decreased, TGF-βexpression levels in spinal cord tissue increased, and BDNF expression levels decreased in the model and Ginsenoside Rg1 groups. Compared with the model group, serum malondialdehyde levels decreased, the content of superoxide dismutase increased, TGF-βexpression levels in spinal cord tissue decreased, and BDNF expression levels increased in the Ginsenoside Rg1 group. Ginsenoside Rg1 can protect the injury spinal cord in rats after spinal cord injury.
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Nerve growth factor (NGF) has been the focus in area of angiogenesis.In differential,survival,development of nerves,NGF plays a crucial role.In addition,NGF activates migration,differential of endothelial cells and vascular smooth muscle cells,and stimulate the activation of the endothelial progenitor cells in angiogenesis.Crosstalk between vascular endothelial growth factor and NGF is also critical in the development of vessels.The function of NGF in angiogenesis blazes a trail in therapy of ischemia diseases.
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BACKGROUND:Bone marrow mesenchymal stem cells (BMSCs) can be induced to differentiate into neuron-like cells directional y. Accordingly, BMSCs can be used as seed cells theoretical y in constructing tissue-engineered peripheral nerves. OBJECTIVE:Using combination of two cytokines to induce BMSCs differentiating into neuron-like cells directional y, and further to discusse its application in peripheral nerve injury. METHODS:BMSCs were isolated and purificated from the bone marrow of Wistar rats by using the differential adherence method. Basic fibroblast growth factor and epidermal growth factor were used to induce the BMSCs differentiating into neuron-like cells. The morphological change was observed and the neuronal specific markers were detected by immunohistochemistry technique. The morphological and immunohistological changes were also studied after the induce agent were removed. RESULTS AND CONCLUSION:With presence of morphological and immunohistochemical features of nerve cells induced by neurotrophic factors, BMSCs exhibited two or more processes that were interconnected as a meshwork;cellnucleus and nucleus could be observed with strong light refraction of cytoplasm. After immunohistochemical staining, neuroln specific enolase, neurofilament protein and synaptophysin protein positive cells were detected. A great amount of cells reversed to their original fibroblast-like morphology, and the expression of the three above-mentioned proteins decreased as the induce agent withdrawn. Our study showed that BMSCs can be induced to differentiate into neuron-like cells, but the transdifferentiation is a short-time reversible phenomenon.