Astrocytoma ; metabolism ; Glial Fibrillary Acidic Protein ; metabolism ; Humans ; In Vitro Techniques ; Nestin ; metabolism

AIM AND METHODSThe relation between AT sclerosis (loss of neurons and proliferation of astrocytes) and long-lasting epileptic susceptibility was investigated by thionine staining, GFAP immunohistochemistry and observing the behavior of rats, after scorpion venom (SV) or normal saline (NS) administrated for three week.

RESULTSCompared with NS+ NS group, both the loss of neurons and proliferation of astrocytes were very marked in KA+ NS group (epileptic susceptible rats) (P < 0.05), but those changes were not visible in KA+ NS group (epileptic nonsusceptible rats).

CONCLUSIONSIt suggested that AT sclerosis may be one of important reasons of the long-lasting epileptic susceptibility.

Animals ; Astrocytes ; pathology ; Epilepsy ; pathology ; Glial Fibrillary Acidic Protein ; metabolism ; Male ; Neurons ; metabolism ; pathology ; Rats ; Rats, Sprague-Dawley

In order to study whether marrow stromal cells (MSCs) can be induced into nerve-like cells in vitro, and the mechanism, the MSCs in Wistar rats were isolated and cultured, and then induced with DMSO and BHA in vitro. The expression of specific marking proteins in neurons, glia and neural stem cells were detected before preinduction, at 24 h of preinduction, at 6 h, 24 h, and 48 h of neuronal induction by using immunohistochemistry and Western blotting. The ultrastructural changes after the inducement were observed. The results showed that after the inducement, many MSCs turned into bipolar, multipolar and taper, and then intersected as network structure. At the same time, some MSCs had the typical neuron-like ultrastructure. Immunohistochemistry revealed that NeuN and Nestin expression was detectable after inducement, but there was no GFAP and CNP expression. Western blotting showed the expression of Nestin was strong at 6 h of neuronal induction, and decreased at 24 h, 48 h of the induction. NeuN was detectable at 6 h of neuronal induction, and increased at 24 h, 48 h of the induction. It was concluded MSCs were induced into neural stem cells, and then differentiated into neuron-like cells in vitro.
Bone Marrow Cells/*cytology ; *Cell Differentiation ; Cells, Cultured ; Glial Fibrillary Acidic Protein/metabolism ; Neurons/*cytology ; Rats, Wistar ; Stromal Cells/cytology

Adult ; Cerebral Ventricle Neoplasms ; diagnosis ; metabolism ; Diagnosis, Differential ; Glial Fibrillary Acidic Protein ; analysis ; Humans ; Immunohistochemistry ; Lateral Ventricles ; chemistry ; pathology ; Male

OBJECTIVETo study the potential interaction between PrP protein and glial fibrillary acidic protein (GFAP) and identify the binding region within PrP with GFAP.

METHODSThe supernatant of healthy and scrapie-infected hamsters' brain homogenate was prepared, while various recombinant PrP or GFAP proteins were expressed using prokaryotic-expressing or in-vitro translation system. The possible molecular interaction between PrP proteins and GFAP was tested by Pull-down and immunoprecipitation assays.

RESULTSBoth native PrP(C) and its protease-resistant isoform (PrP(Sc)) formed complexes with the native GFAP. The full-length recombinant PrP proteins interacted with GFAP. The domain responsible for interacting GFAP was located at C-terminal of PrP (residues 91 to 231).

CONCLUSIONThe studies of the association of PrP with GFAP may further provide insight into a potential role of GFAP in the biological function of PrP and the pathogenesis of prion disease.

Animals ; Brain ; metabolism ; Cricetinae ; Gene Deletion ; Glial Fibrillary Acidic Protein ; genetics ; metabolism ; Immunoprecipitation ; Mice ; Prions ; genetics ; metabolism ; Protein Binding ; Recombinant Proteins ; metabolism

Adolescent ; Brain Neoplasms ; metabolism ; pathology ; surgery ; Diagnosis, Differential ; Ependymoma ; metabolism ; pathology ; Ganglioglioma ; metabolism ; pathology ; surgery ; Glial Fibrillary Acidic Protein ; metabolism ; Humans ; Immunohistochemistry ; Male ; Tubulin ; metabolism ; Vimentin ; metabolism

OBJECTIVETo investigate the changes in expression of tumor necrosis factor-alpha (TNF-α) and glial fibrillary acidic protein (GFAP) in rabbits with decompression disease (DCS), and to investigate the functioning mechanism.

METHODSA total of 21 healthy adult rabbits were randomly divided into 3 groups: normal control group, DCS group, and safe relief group, with 7 rabbits in each group. A rabbit DCS model was established by quick decompression. The changes in pathological morphology and mRNA and protein expression of TNF-α and GFAP in the brain and spinal cord of rabbits with DCS were determined by light microscopy, real-time PCR, and immunohistochemistry, respectively.

RESULTSCavity formation was observed in the white matter of spinal cord in DCS group. The mRNA and protein expression of TNF-α and GFAP was significantly higher in the DCS group than in the normal control group and safe relief group (P < 0.01), while no significant differences were observed in the brain (P > 0.05).

CONCLUSIONSpinal cord is the main part of central nervous system injury in DCS. Activation of TNF-α and GFAP genes accompanied by increase in their protein expression can be observed at the early stage of DCS. The astrocytes and TNF-α play important roles in the process of spinal cord injury in DCS.

Animals ; Brain ; metabolism ; Decompression Sickness ; metabolism ; Disease Models, Animal ; Glial Fibrillary Acidic Protein ; metabolism ; Male ; Rabbits ; Spinal Cord ; metabolism ; Tumor Necrosis Factor-alpha ; metabolism

Adult ; Brain Neoplasms ; metabolism ; pathology ; surgery ; Female ; Ganglioglioma ; metabolism ; pathology ; surgery ; Glial Fibrillary Acidic Protein ; metabolism ; Humans ; Magnetic Resonance Imaging ; Phosphopyruvate Hydratase ; metabolism ; Synaptophysin ; metabolism

OBJECTIVETo investigate whether gliosis in the brain tissues of the hamsters infected with various amounts of scrapie strain 263K is correlated with the inoculation doses or the incubation times.

METHODSThe total values of glial fibrillary acidic protein (GFAP) in brains were evaluated by Western Blots and the GFAP-stained cells were detected by immunohistochemistry (IHC). The characteristics of GFAP distributions among various groups were defined by quantitive and statistic analyses.

RESULTSCompared with the brain tissues of normal hamsters, remarkably higher total GFAP levels and more GFAP-stained cells were observed in the brain tissues of infected ones, howbeit, no significant difference was addressed among the infected groups.

CONCLUSIONInoculations of various amounts of scrapie strain 263K into experimental hamsters intracerebrally induced the similar patterns of gliosis in the brains at the clinically terminal stage, regardless of infectious doses and incubation times.

Animals ; Brain ; metabolism ; pathology ; Cricetinae ; Gene Expression ; Glial Fibrillary Acidic Protein ; genetics ; metabolism ; Gliosis ; metabolism ; pathology ; Humans ; PrPSc Proteins ; metabolism ; Prion Diseases ; metabolism ; pathology

OBJECTIVETo determine the effect of willed movement on the expression of glial fibrillary acidic protein (GFAP) and synaptophysin (SYP) in adult rats with cerebral ischemia-reperfusion, and explore the mechanism of willed movement in promoting nerve repair and regeneration.

METHODSAdult rat models of cerebral ischemia-reperfusion injury were established by middle cerebral artery occlusion (MCAO) for 2 h followed by a 24-h reperfusion. The models were then divided randomly into 3 groups, namely the model group, environmental modification (EM) group, and willed movement (WM) group. In each group, neurological deficits were evaluated at 3, 7 and 15 days after reperfusion. Immunohistochemistry and immunofluorescence assay were employed to examine the expression of GFAP and SYP in the brain tissue near the ischemic foci.

RESULTSThe rats in WM group showed lessened neurological deficits at 15 days and lowered expression of GFAP and SYP at 7 and 15 days after reperfusion compared with the model and EM groups (P<0.05). No significant difference was found in the expression of GFAP or SYP between the model group and EM group at any time points.

CONCLUSIONWilled movement can promote the functional recovery of neurological deficits following cerebral ischemia-reperfusion probably in relation to enhanced GFAP and SYP expressions in the ischemic brain tissues.

Animals ; Brain Ischemia ; metabolism ; therapy ; Disease Models, Animal ; Exercise Therapy ; methods ; Glial Fibrillary Acidic Protein ; metabolism ; Male ; Rats ; Rats, Sprague-Dawley ; Reperfusion Injury ; metabolism ; therapy ; Synaptophysin ; metabolism