ABSTRACT
Objective To explore the expression of NT-3 and high-affinity receptors TrkC at mRNA and protein level in the prefrontal cortex of the post stroke depression(PSD)model rats.Methods Open-field method was used to evaluate the behavior.Focal cerebral ischemic rat models were made with thread em-bolization method.PSD rat models were established with comprehensive separately breeding and chronic un-predicted mild stress(CUMS)on this basis.Normal control group,depression group and stroke group were used to compare with PSD group.13 rats were used in each group.At 29th day after the CUMS RT-PCR was employed to detect gene expression of NT-3 and TrkC.The expression of NT-3 and TrkC in positive cells was detected by immunohistochemistry.Results The immunohistochemistry results showed that the number of NT-3 immunopositive cells in PSD group(10.11± 2.89)was lower than that of the normal group(19.00 ± 12.41)(P<0.05).Whereas there was no statistical difference in the other groups(P>0.05).The number of TrkC immunopositive cells in PSD group(19.56±5.66)was less than that of the normal group(25.11±3.95) and stroke group(29.67±7.38).The number of TrkC immunopositive cells in depression group(19.00±5.61)also was lower than that of the normal group(25.11±3.95)and stroke group(29.67±7.38).There was no sta-tistical difference among other groups(P>0.05).RT-PCR results showed that the GAPDH,NT-3 and TrkC mRNA in all of the groups could be detected in the prefrontal cortex of rats.The expression of NT-3 in the prefrontal cortex in the PSD group decreased significantly compared with that of normal control rats(P<0.05).There was no statistical difference in the other groups(P>0.05).The expression of TrkC in the pre-frontal cortex had no statistical difference in all of the groups(P>0.05).Conclusion The down-regulation of NT-3 and TrkC both at mRNA and protein levels in the prefrontal cortex maybe responsible for the pathogen-esis of PSD.
ABSTRACT
Objective To understand the correlation of enterovirus 71 (EV71), P-selectin glycoprotein ligand-1 (PSG L-1), and scavenger receptor B2 (SCARB2) and to explore the possible pathway and mechanismof EV71 infection by observing the expression of EV71, PSG L-1 and SCARB2 in tissues of infants with brain stemencephalitis. Methods T he organs and tissues of infants with EV71-VP1 positivi-ty in their brain stems were chosen. Expression and distribution of EV71-VP1, PSG L-1, and SCARB2 were detected and compared by immunohistochemistry. Results Strong staining of EV71-VP1 was ob-served in the neuron, glial cells, the inflammatory cells of perivascular cuffing, parietal cells of the gas-tric fundus gland while alveolar macrophages, intestinal gland epitheliumcells, mucosa lymphoid nodule and lymphocyte of palatine tonsil showed moderate staining and weak staining were displayed in mesen-teric lymph nodes and lymphocyte of spleen. PSG L-1 expression was detected in parietal cells of the gastric fundus gland, tonsillar crypt squamous epithelium, alveolar macrophages and leukocytes in each tissue. SCARB2 expression was observed in all the above tissues except the intestines and spleen. Con-clusion T he distribution of EV71 correlates with SCARB2 expression. SCARB2 plays an important role in virus infection and replication. Stomach may be an important site for EV71 replication.
ABSTRACT
Current therapies for autoimmune diseases are not cures but merely palliatives, aimed at reducing symptoms. For the most part, these treatments provide nonspecific suppression of the immune system and thus do not distinguish between a pathogenic autoimmune response and a protective immune response. Recently emerging evidence not only has indicated the involvement of members of the TNF receptor/ligand superfamilies but also has revealed exciting innovative strategies for the treatment of autoimmune diseases and other chronic inflammatory diseases without depressing the immune response in general. In this review, we will discuss the regulatory mechanisms of TNF receptor/ligand family members, such as HVEM/ LIGHT, 4-1BB/4-1BBL, and GITR/GITRL that regulate T and B cell functions and participate in the process of inflammatory diseases. We will also discuss how intervening in the costimulatory pathways mediated by these molecules might have some potential as a therapeutic approach to immune disorders.
Subject(s)
Animals , Humans , Apoptosis , Autoimmune Diseases/immunology , B-Lymphocytes/immunology , Dendritic Cells/physiology , Inflammation/immunology , Lymphocyte Activation/immunology , Models, Biological , Receptors, Tumor Necrosis Factor/physiology , T-Lymphocytes/immunology , Tumor Necrosis Factor-alpha/immunologyABSTRACT
Objective To ex pl ore the action of T 3 on neural stem cell (NSC) differentiation and the change of thyroid hormone receptor (TR) mRNA expression during NSC differentiation. Methods Human embryonic brain-derived NSC was suc cessfully expanded into neurospheres with mitogens and identified by immunocytoc hemistry method. T 3 was used to induce the differentiation of NSC. During the NSC differentiation, mRNA expression levels of different TRs were detected by se miquantitative RT-PCR. At the same time the cell types of the differentiated ce lls were identified by immunocytochemistry method. Results After being induced by T 3, NSC could differentiate into neuron, ol igodendrocyte, astrocyte, but myelin basic protein positive cells accounted for 80%. The time sequence expression of different TRs mRNAs existed during NSC diff erentiation. Conclusion T 3 can induce NSC to develop to glial cell and is an important regulator of the oligodendrocyte diffe nrentiation. T 3 exerts distinct effects through time sequence expressions of d ifferent TRs mRNAs.