Enhancement of T Follicular Helper Cell-Mediated Humoral Immunity Reponses During Development of Experimental Autoimmune Myasthenia Gravis.

Myasthenia gravis (MG) is a prototypical antibody-mediated neurological autoimmune disease with the involvement of humoral immune responses in its pathogenesis. T follicular helper (Tfh) cells have been implicated in many autoimmune diseases. However, whether and how Tfh cells are involved in MG remain unclear.

MicroRNA 182 inhibits CD4CD25Foxp3 Treg differentiation in experimental autoimmune encephalomyelitis.

MicroRNA 182 has been found to have a distinct contribution in the clonal expansion of activated- and functioning of specialized-helper T cells. In this study we knocked down microRNA 182 in vivo and induced experimental autoimmune encephalomyelitis (EAE) to determine the influences of microRNA 182 in the Treg cells functional specialization through Foxo1 dependent pathway in the peripheral lymphoid organs. Down-regulation of microRNA 182 significantly increased the proportions of Foxp3 T cells in the peripheral lymph nodes and spleen.

Effect of ginkgolide B on brain metabolism and tissue oxygenation in severe haemorrhagic stroke.

Ginkgolide B, a diterpene, is an herbal constituent isolated from the leaves of Ginkgo biloba tree. The present study demonstrates the effect of ginkgolide B in osmotherapy on brain metabolism and tissue oxygenation. Multimodality monitoring including intracranial pressure (ICP), cerebral perfusion pressure (CPP), partial pressure of brain tissue oxygen (PbtO2), lactate/pyruvate ratio (LPR) and microdialysis were employed to study the effect of ginkgolide B osmotherapy.

Human mesenchymal stem cells increases expression of α-tubulin and angiopoietin 1 and 2 in focal cerebral ischemia and reperfusion.

Angiogenesis is associated with improved neurologic recovery after cerebral ischemia. Human bone marrow mesenchymal stem cells (hMSCs) have been successfully used to treat ischemic stroke and were shown to induce the expression of a number of neurotrophic factors including VEGF, epidermal growth factor (EGF) and basic fibroblast growth factor (bFGF) in a rat middle cerebral artery occlusion (MCAO) ischemia model. In this study, we aimed to understand the mechanism underlying the improvement of neurological function following hMSCs transplantation into MCAO rats.

All-trans-retinoic acid ameliorates experimental allergic encephalomyelitis by affecting dendritic cell and monocyte development.

Experimental allergic encephalomyelitis (EAE) can be induced in animal models by injecting the MOG35-55 peptide subcutaneously. Dendritic cells (DCs) that are located at the immunization site phagocytose the MOG35-55 peptide. These DCs mature and migrate into the nearest draining lymph nodes (dLNs), then present antigen, resulting in the activation of naive T cells.

Effects of IL-17A on the occurrence of lung adenocarcinoma.

The relationship between IL-17A and cancer, whether beneficial or antagonistic, continues to be a controversial issue. In this study, effects of IL-17A on lung adenocarcinoma were investigated using lung cancer cell lines, 95D and 95C. In the presence or absence of IL-17A, cell proliferation and VEGF secretion were detected.

Therapeutic effect of co-transplantation of neuregulin-1-transfected Schwann cells and bone marrow stromal cells on spinal cord hemisection syndrome.

The aim of this present study is to evaluate the therapeutic effect of co-transplantation of neuregulin-1-transfected Schwann cells (SCs) and bone marrow stromal cells (BMSCs) on a rat model of spinal cord hemi-section injuries (Brown-Séquard syndrome), which is relevant to human clinical spinal cord injury. Both in vivo and in vitro data we received demonstrated that co-transplantation BMSCs with NRG1-transfected SCs reduced the size of cystic cavities, promoted axonal regeneration and hind limb functional recovery in comparison with SCs or BMSCs transplantation alone or together, and this treatment could provide important insights into potential therapies of spinal cord hemi-section injuries.

Calcium-sensing receptors regulate cardiomyocyte Ca2+ signaling via the sarcoplasmic reticulum-mitochondrion interface during hypoxia/reoxygenation.

Communication between the SR (sarcoplasmic reticulum, SR) and mitochondria is important for cell survival and apoptosis. The SR supplies Ca2+ directly to mitochondria via inositol 1,4,5-trisphosphate receptors (IP3Rs) at close contacts between the two organelles referred to as mitochondrion-associated ER membrane (MAM). Although it has been demonstrated that CaR (calcium sensing receptor) activation is involved in intracellular calcium overload during hypoxia/reoxygenation (H/Re), the role of CaR activation in the cardiomyocyte apoptotic pathway remains unclear.

The effect of electroacupuncture on T cell responses in rats with experimental autoimmune encephalitis.

Successive electroacupuncture (EA) stimulation on Zusanli ST36 acupoints of rats with experimental autoimmune encephalitis (EAE), which is an inflammatory disease mediated by autoreactive T cells, relieved disease severity, inhibited specific T cell proliferation and rebuilt the CD4+ T cell subset balance. In addition, EA-treated rats had significantly higher ACTH concentrations in vivo compared to untreated EAE rats. These results indicated that EA stimulation could relieve the severity of EAE by restoring balance to the Th1/Th2/Th17/Treg Th cell subset responses by stimulating the hypothalamus to increase ACTH secretion.

MMP-mediated cleavage of beta-dystroglycan in myelin sheath is involved in autoimmune neuritis.

Alpha-/beta-dystroglycans (DG) located at the outmost layer of myelin sheath play a critical role in its formation and stability in the peripheral nerve system. The demyelination of nerve fibers is present in autoimmune neuritis, however, it is not known about the molecular mechanisms underlying this pathological process. In an animal model of experimental autoimmune neuritis, we observed that beta-DG cleavage was associated with the demyelination of peripheral nerves.

IL-17 potentiates neuronal injury induced by oxygen-glucose deprivation and affects neuronal IL-17 receptor expression.

Interleukin-17 (IL-17) is active in a variety of brain injuries, including ischemia. The objective of this study was to test the hypothesis that IL-17 potentiates neuronal injury after stroke. Increased expression of IL-17 and IL-17 receptor (IL-17R) in serum and cortex was evaluated by ELISA, RT-PCR and immunohistochemistry.

A role for the parafascicular thalamic nucleus in the development of morphine dependence and withdrawal.

The parafascicular thalamic nucleus (nPf) is a critical relay in the ascending system that mediates motor control in the central nervous system (CNS). Yet, little is known about whether or not the nPf is involved in the development of morphine dependence and withdrawal. In the present study, kainic acid was used to chemically destroy the nPf in Wistar rats, and morphine dependence and withdrawal models were established.

BM stromal cells ameliorate experimental autoimmune myasthenia gravis by altering the balance of Th cells through the secretion of IDO.

In addition to their capacity to differentiate, BM stromal cells (BMSC) have immunosuppressive qualities that make them strong candidates for use in cell therapy against human autoimmune diseases. We studied the immunoregulatory activities of BMSC on experimental autoimmune myasthenia gravis (EAMG) in vitro and in vivo. Intravenous administration of syngenic BMSC to EAMG-model rats on the day of their second immunization was effective in ameliorating the pathological features of the disease.

Administration of bone marrow stromal cells ameliorates experimental autoimmune myasthenia gravis by altering the balance of Th1/Th2/Th17/Treg cell subsets through the secretion of TGF-beta.

Bone marrow stromal cells (BMSCs) are strong candidates for cell therapy against human autoimmune diseases. Intravenous administration of syngenic BMSCs to EAMG-model rats effectively ameliorated the disease, partially through a TGF-beta-dependent mechanism. The proliferative ability of T or B cells from EAMG rats was inhibited by BMSCs at proper cocultured ratios.

RAGE expression is up-regulated in human cerebral ischemia and pMCAO rats.

To determine whether the receptor for advanced glycation endproducts (RAGE) contributes to cerebral ischemia, we evaluated RAGE expression in human cerebral ischemia and a model of permanent middle cerebral artery occlusion (pMCAO) in rats. Biopsy specimens were obtained from 12 patients with unilateral cerebral infarction. For the pMCAO model, the middle cerebral artery (MCA) of Sprague-Dawley (SD) rats was permanently occluded.

Voriconazole into PLGA nanoparticles: improving agglomeration and antifungal efficacy.

This study is concerned with preparing PLGA nanoparticles loaded with voriconazole (PNLV), investigating the burst release and agglomeration of PNLV, and also evaluating antifungal efficacy of PNLV compared with voriconazole (VRC). The emulsion-solvent evaporation technique for nanoparticles and tests against fungi were completed. The amount of VRC in PNLV with sodium hexametaphosphate was 2.

[Effects of bone marrow mesenchymal stem cells on the proliferation of hepatocytes and cirrhotic fat-storing cells in vitro].

Objective: To investigate the differentiation of bone marrow mesenchymal stem cells (BMSCs) and the effects of BMSCs on the proliferation of cirrhotic fat-storing cells (CFSC) and hepatocytes in vitro.

Methods: BMSCs and hepatocytes were isolated and harvested from the bone marrow and livers of rats. A co-culture system was set up by transwell inserts in which the two chambers were separated by a semipermeable membrane.

[Immunoregulative effect of NK1.1+ cells on the development of experimental autoimmune myasthenia gravis].

Aim: To investigate the effect and immuoregulative mechanisms of NK1.1(+) cells on the development of experimental autoimmune myasthenia gravis (EAMG).

Methods: The NK1.

[Phosphorylation of PKCdelta participates in the toxicity of 6-hydroxydopamine on dopaminergic neuroblastoma cell].

Objective: To investigate the role of phosphorylation of protein kinase C (PKC) delta in the toxicity of 6-hydroxydopamine (6-OHDA) to the death of dopaminergic neurons.

Methods: Human neuroblastoma cells of the line SH-SY5Y were cultured 6-OHDA of the concentrations of 0, 50, 100, 200, and 400 micromol/L was added to observe its toxicity. Rottlerin (PKCdelta inhibitor, 2 micromol/L), bisindolylmaleimide (Bis, general PKC inhibitor, 10 nmol/L), Gö6976 (calcium-dependent PKC inhibitor, 5 nmol/L), and phobol-12-myristate-13-acetate (PMA, PKC activator, 100 nmol/L) were added into the culture fluid of another SH-SY5Y cells respectively, and then (1) culture fluid of equal volume was added for 18 h so as to observe there effects on the survival of the SH-SY5Y cells, or (2) 100 micromol/L 6-OHDA was added to observe the effects of intervention on PKC on the survival of the SH-SY5Y cells by using MTT assay.

[Inhibiton of experimental autoimmune encephalomyelitis in Lewis rats by nasal administration of encephalitogenic MBP peptides: synergistic effects of MBP 68-86 and 87-99].

Aim: To explore the synergistic effect of MBP 68-86 and 87-99, on the inhibition of experimental autoimmune encephalomyelitis (EAE) in Lewis rat by nasal administration.

Methods: Three different MBP peptides(MBP 68-86, 87-99, and the non-encephalitogenic peptide 110-128) were synthesized and administrated nasally to Lewis rat on day-11, -10, -9, -8 and -7 prior to immunization with the guinea pig MBP (gp-MBP)+CFA, which was used to induce EAE. The protective effect on Lewis rat from EAE by the MBP peptides was evaluated.

[Study on therapy of experimental autoimmune neuritis by bone marrow stromal cells].

Aim: To investigate the therapeutic effect of bone marrow stromal cells (BMSCs) transplantation on experimental autoimmune neuritis (EAN) and study the possible mechanism.

Methods: EAN model was established by immunizing Lewis rats with P(0)180-199 peptide and complete Freund's adjuvant (CFA). In the therapy group, BMSCs (2x10(6) cells/rat) were marked with fluorochrome PKH26 and injected into the rats' caudal vein 10 d after immunization.

[Study of mechanism of differentiation of bone stromal stem cells into neurons in vitro].

Aim: To explore the mechanism of differentiation of bone marrow stromal cells (BMSCs) into neurons in different micro-environments in vitro.

Methods: BMSCs were isolated from bone marrow of SD rats and cultured and expanded in vitro. After being identified by immunofluorescence staining, the BMSCs labeled with PKH67 were co-cultured with foetal brain neural cells in the same plate well or in two-layer Petri dish.

Protective effect of M3 receptor on H2O2 -induced apoptosis of rat myocardial cells in vitro.

Aim: To observe the effect of activation of M3 receptor on H2O2 induced apoptosis in cultured rat myocytes and to investigate its possible mechanisms.

Methods: Isolated neonatal cardiomyocytes were cultured. Morphologic changes were observed by microscopy.

[Relationship between M3 receptor and myocyte apoptosis induced by acute myocardial infarction].

Aim: To explore the effects of M3 receptor on myocyte apoptosis induced by acute myocardial infarction in rats.

Methods: Rat model was induced by ligation of the anterior branch of the left coronary artery. All animals were divided into four groups: sham-operated group, occlusion group, choline group (10 mg x kg(-1), iv), and 4DAMP (4-diphenylacetoxy-N-methylpiperidine-methiodide) group (0.

[Expressions of TNF-alpha and IL-1beta in human ischemic brain tissues].

Aim: To detect the expression of TNF-alpha and IL-1beta in human cerebral ischemic tissues.

Methods: 13 cerebral specimens from patients died of cerebral infarction were divided into three groups, <2 d, 3-5 d, and >5d, according to the lasting time of infarctions. The expression of TNF-alpha and IL-1beta in the cerebral ischemic tissues were examined by immnohistochemical staining.