ABSTRACT
It is difficult for regeneration of central nervous system (CNS) in adult mammals, and myelin-associated inhibitors (MAIs) are believed to be major contributors. Paired immunoglobulin-like receptor B (PirB), as a co-receptor of MAIs, and expresses highly in CNS after injury, plays a vital role in the signal transduction of inhibition in the injured CNS. Knockout or block of PirB in vitro and in vivo may promote the neuro-regeneration after spinal cord injury or hypoxic-ischemic brain damage, release the damage induced byβ-amyloid in Al-zheimer's disease, recover the neural function in brain inflammation models, improve the reconstruction of vision after optic nerve injury, and so on. PirB may be a potential therapeutic target for neuro-regeneration and synaptic plasticity.
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Aim To investigate the effect of Salidroside on the focal celebral ischemia/reperfusion injury in rats and its underlying mechanism. Methods Adult male Sprague-Dawley rats, weighing 260-300 g, were ran-domly divided into three groups: sham, MCAO, MCAO+salidroside ( Sal ) groups. The rats were sub-jected to local celebral ischemia reperfusion with su- ture-occluded method. The rats of MCAO +Sal group were treated intraperitoneally with salidroside ( 50 mg ·kg-1 ) for 6 days. Neurological deficit testing was performed with Longa’ s Scale. The mRNA expressions of Neun,Nogo-A,and NgR were detected by RT-qPCR in ischemic brain. The protein expressions of Neun, NGF , BDNF , Nogo-A and NgR were determined by Western blot. Results Compared with MCAO group, salidroside significantly improved the neurological defi-cit,promoted the expressions of Bcl-2,Neun,NGF,BD-NF, and inhibited the expressions of Nogo-A, NgR. Conclusion Salidroside can reduce neurological defi-cit, increase the number of Nissl’ s Body and the ex-pression of Neun, and protect rats against focal cele- bral ischemia/reperfusion injury,which may be accom-plished by increasing the expressions of Bcl-2, NGF, BDNF, and inhibiting the expressions of Nogo-A, NgR.
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Objective To investigate the effects of bone mesenchymal stem cells (BMSCs)transplantation on the neurological function recovery of injured spinal cord and the underlying mechanism.Methods Rats were subjected to contusive spinal cord injury by using NYU spinal cord contusive impactor system ( NYC lmpactor).Seven days after spinal cord injury,the transplantation of BMSCs ( BMSCs group) or injection of PBS ( PBS group) was performed around the epicenter of injured spinal cord in rats.Basso-Beattie-Bresnahan (BBB) score was used to evaluate the function of spinal cord.The cavity volume of the injured spinal cord was measured and the axons in the injury center of spinal cord were examined under transmission electron microscopy.The BMSCs of the green fluorescent protein (GFP)transgenic rats were used to trace the transplanted cells and the survivor of BMSCs in the injured spinal cord and their differentiation into neural cells were observed.A mini-channel implantation model was employed to further investigate the role of BMSCs transplantation on the axonal regeneration.Results The BMSCs group showed a higher BBB score and a smaller lesion volume as compared with the PBS group.Transmission electron microscopy examination displayed that the number of axons in the BMSCs group was far more than that in the PBS group.A great number of BMSCs-GFP were founded around the center of the injured spinal cord at 4 weeks after BMSCs transplantation.lmmunohistochemistry showed that the implanted BMSCs-GFP did not express the surface marker of neurons,astrocytes and oligodendrocytes.In the mini-channel implantation model,NF-positive nerve fibers grew into the BMSCs-seeded channel,while there were no nerve fibers in the channel without seeding of BMSCs.Conclusions The BMSCs transplantation for the injured spinal cord promotes its functional recovery,and the related mechanism is in correlation with BMSCs transplantation inducing axonal regeneration.
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@#The injury of peripheral nerve is generally accompanied with active regeneration responses. This paper is to summarize the molecular mechanism to promote the nerve regeneration, including various reactions of the neuronal body, nerve fiber, and regulatory molecules in the microenvironment, such as transcription factors, inflammatory mediators, nerve growth factors, etc., aiming to investigate the possible mechanism in the nerve regeneration after injury.
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Objective To identify the cellular distribution of a my elin-associated protein (Nogo-A) in the central nervous system (CNS) of mice a nd explore its possible inhibition on the CNS axon regeneration after spinal cor d injury. Methods Brain, spinal cord, peripheral tissues and w eight-dropping injuried spinal cord from the adult C57BL/6 mice were studied. N ogo-A protein expression was localized immunohistochemically. Chick E12DRG neur ons were cultured and growth cone collapse assessed. Results N ogo-A protein expression detected was mainly in the oligodendrocyte cell body a nd the myelinated axons surrounded by cell processes rather than in the peripher al tissues. After spinal cord injury, Nogo-A was up-regulated at a moderate de gree in the area around the lesion. Chick E12 DRG growth cone collapse rate was as high as 70%, significantly higher than that in the blank control and vector control groups with a significant difference ( P