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Xie J.,Yangtze River Shipping General Hospital | Lin Y.K.,Guangxi Medical University | Wang K.,Yangtze River Shipping General Hospital | Che B.,Yangtze River Shipping General Hospital | And 4 more authors.
Genetics and Molecular Research | Year: 2014

This study investigated the induced immune tolerance of autoantigen dendritic cells (imDCs) in homogenic lupus mice to support the use of dendritic cell treatment against autoimmune diseases, such as systemic lupus erythematosus. A lupus mouse was used to model based on in vitro cell culture. An immunohistochemistry assay was used to assess CD8+, CD4+ cell ratio in mouse spleen cells. The ratio of CD4+CD25+ cells in mouse spleen lymphocytes was detected by flow cytometry, whereas the kidney was directly measured by immunofluorescence. After the injection of mouse antigen loaded bone marrow-derived antigen imDCs with a homogenetic background, mouse nucleoprotein immune with a homogenetic background was carried out. The results were compared against the simple mouse nucleoprotein immune model with a homogenic background. The 24-h urine protein, serum antinuclear antibody and anti-ds-DNA antibodies of the simple mouse model were lower compared to group S1. The CD4+CD25+ cell percentage of spleen was higher in the simple mouse model compared to group S1. In the spleen, the number of lymphocyte CD8+ cells declined, whereas the number of CD4+ cells increased. In conclusion, after autoantigen uptake, imDCs are able to induce immune tolerance to the antigen by reinfusion, which appears to prevent or mitigate systemic lupus erythematosus-like illness. © FUNPEC-RP.

PubMed | Wuhan University of Science and Technology, University of Science and Technology of China and Yangtze River Shipping General Hospital
Type: | Journal: European journal of pharmacology | Year: 2015

Baicalin has been shown to provide the neuroprotective effect by alleviating cerebral ischemia injury. However, littles known about the underlying mechanism. Here, a cerebral artery occlusion (MACO)/reperfusion rat model and rat primary cortical neuron culture exposed to hydrogen peroxide (H2O2) were established to evaluate the effect of baicalin on ischemia-induced neuronal apoptosis. We found baicalin can significantly less neurological deficit and reduced infarct volume in vivo. And it efficiently inhibited neuronal apoptosis in vivo and vitro, which was especially characterized by the enhancing of transcription and expression of myeloid cell leukemia-1 (MCL-1) and B-cell lymphoma-2 (BCL-2) in a dose-dependent manner. Furthermore, Baicalin markedly increased myocardin-related transcription factor-A (MRTF-A) level either in ischemic hemisphere or in primary cortical neuron cultures, whiles the anti-apoptosis effect of baicalin was significantly inhibited by transfected with the small interfering RNA of MRTF-A (MRTF-A siRNA) in primary cortical neuron cultures. The luciferase assays also indicated baicalin enhanced the transactivity of MCL-1 and BCL-2 promoter by activating the key CArG box (CC [A/T] 6GG) element, which was reduced by MRTF-A siRNA, suggesting MRTF-A may participate the anti-apoptosis effect of baicalin, and MRTF-A was involved in the transcriptional activity of MCL-1 and BCL-2 that was induced by baicalin. LY294002 (phosphatidylinositol-3 kinase (PI3K) inhibitor) and PD98059 (extracellular signal regulates kinase-1/2 (ERK1/2) inhibitor) obviously reduced baicalin-induced MRTF-A expression and transactivity and expression of MCL-1 and BCL-2, which further abolished the anti-apoptotic effect of baicalin on neuronal apoptosis. Taken together, our data provided the evidence demonstrating the neuroprotective effect of baicalin partially due to MRTF-A-mediated transactivity and expression of MCL-1 and BCL-2 by triggering the CArG box, which might be controlled by the activation of PI3K and ERK1/2.

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