ABSTRACT
BACKGROUND@#The pathogenesis of multiple sclerosis (MS) is mediated primarily by T cells, but most studies of MS and its animal model, experimental autoimmune encephalomyelitis (EAE), have focused on CD4 T cells. The aims of the current study were to determine the pathological interrelationship between CD4 and CD8 autoreactive T cells in MS/EAE.@*METHODS@#Female C57BL/6 mice (n = 20) were induced by myelin oligodendrocyte glycoprotein (MOG)35-55 peptide. At 14 days after immunization, T cells were isolated from the spleen and purified as CD4 and CD8 T cells by using CD4 and CD8 isolation kits, and then the purity was determined by flow cytometric analysis. These cells were stimulated by MOG35-55 peptide and applied to proliferation assays. The interferon-gamma (IFN-γ) and interleukin (IL)-4 secretion of supernatant of cultured CD4 and CD8 T cells were measured by enzyme-linked immunosorbent assays (ELISA). For adoptive transfer, recipient mice were injected with MOG35-55-specific CD8 or CD4 T cells. EAE clinical course was measured by EAE score at 0-5 scale and spinal cord was examined by staining with hematoxylin and eosin and Luxol fast blue staining.@*RESULTS@#CD8CD3 and CD4CD3 cells were 86% and 94% pure of total CD3 cells after CD8/CD4 bead enrichment, respectively. These cells were stimulated by MOG35-55 peptide and applied to proliferation assays. Although the CD8 T cells had a generally lower response to MOG35-55 than CD4 T cells, the response of CD8 T cells was not always dependent on CD4. CD8 T cell secreted less IFN-γ and IL-4 compared with CD4 T cells. EAE was induced in wildtype B6 naïve mice by adoptive transfer of MOG35-55-specific T cells from B6 active-induced EAE (aEAE) mice. A similar EAE score and slight inflammation and demyelination were found in naive B6 mice after transferring of CD8 T cells from immunized B6 mice compared with transfer of CD4 T cells.@*CONCLUSION@#Our data suggest that CD8 autoreactive T cells in EAE have a lower encephalitogenic function but are unique and independent on pathogenic of EAE rather than their CD4 counterparts.
ABSTRACT
The hotspots and frontiers in studies on medical information education were identified with key words cluster algorithm and burst words detection algorithm by making use of CiteSpaceⅢwith 540 papers on medical in-formation education published in core journals of medical information education from 2007 to 2016 as sample data, which showed that the 7 hotspots and frontiers in studies on medical information education from 2007 to 2016 in medical information education field of China and can thus provide support for keeping abreast of its development trend and working out its development strategies.
ABSTRACT
<p><b>OBJECTIVE</b>To study the influence of modified Shegan Mahuang Decoction (SGMH) on cytokines such as tumor necrosis factor-alpha (TNF-alpha), interleukin (IL)-10 and IL-13 in children suffered from cough and variant asthma (C&VA).</p><p><b>METHODS</b>One hundred and fifty-four children with C&VA were randomly assigned to two groups: 79 in the treatment group were medicated orally with SGMH one dose per day taking in twice; 75 in the control group were medicated with Montelukast once a day in dose of 4 mg for children aged from 2 to 5 years and 5 mg for those from 6 to 14 years, the medication for all was given 4 weeks. Serum contents of cytokines, including TNF-alpha, IL-10 and IL-13, in patients were measured before and after treatment. Besides, serum contents of these cytokines in 45 healthy children were measured for control.</p><p><b>RESULTS</b>Serum levels of TNF-alpha and IL-3 in the treatment group were 2510 +/- 1500 ng/L and 60.76 +/- 23.67 ng/L, and in the control group, 2890 +/- 1410 ng/L and 61.56 +/- 20.37 ng/L, respectively, all were significantly higher than those of healthy (709 +/- 280 ng/L and 39.49 +/- 3.09 ng/L, P < 0.01); but level of IL-10 was significant lower in the two patient groups than that in control (1546 +/- 1434 ng/L and 1823 +/- 1314 ng/L vs 7123 +/- q2641 ng/L, P < 0.01). After treatment, the levels of TNF-alpha and IL-13 decreased and IL-10 increased significantly in the treatment group, and showed significant different to those in the control group respectively (960 +/- 420 ng/L, 43.67 +/- 12.37 ng/L and 6834 +/- 2216 ng/L vs 2610 +/- 1220 ng/L, 50.56 +/-19.56 ng/L and 2529 +/- 1223 ng/L, P < 0.01). Clinical efficacy between groups also showed that the total effective rate in the treatment group was significantly better (86.07% vs. 42.67%, P < 0.01).</p><p><b>CONCLUSION</b>SGMH can regulate the serum levels of TNF-alpha, IL-10 and IL-13, and shows evident clinical effect in treating children's C&VA.</p>
Subject(s)
Adolescent , Child , Child, Preschool , Female , Humans , Infant , Male , Asthma , Blood , Drug Therapy , Cough , Blood , Drug Therapy , Drugs, Chinese Herbal , Therapeutic Uses , Ephedra sinica , Interleukin-10 , Blood , Interleukin-13 , Blood , Interleukin-3 , Blood , Phytotherapy , Tumor Necrosis Factor-alpha , BloodABSTRACT
Objective To investigate the analgesia induced by cobrotoxin (CT) from venom of Naja naja atra, and the effects of atropine and naloxone on the antinociceptive activity of CT in rodent pain models. Methods CT was administered intraperitoneally (33.3, 50, 75 mu g/kg), intra-cerebral venticularly (2.4 mu g/kg) or microinjected into periaqueductal gray (PAG, 1.2 mu g/kg). The antinoCiceptive action was tested using the hot-plate test and the acetic acid writhing test in mice and rats. The involvement of cholinergic system and the opioid system in CT-induced analgesia was examined by pretreatment of animals with atropine (0.5 mg/kg, im or 10 mg/kg, ip) or naloxone (3 mg/kg, ip). The effect of CT on motor activity was tested using the Animex test. Results CT (33.3, 50 and 75 mu g/kg, ip) exhibited a dosedependent analgesic action in mice as determined with hot-plate test and acetic acid writhing test. In the mouse acetic acid writhing test, the intra-cerebral ventricle administration of CT 2.4 mu g/kg (1/23th of a systemic dose) produced marked analgesic effects. Microinjection of CT 1.2 mu g/kg (1/46th of systemic dose) into the PAG also elicited a robust analgesic action in the hot-plate test in rats. Atropine at 0.5 mg/kg (im) or naloxone at 3 mg/kg (ip) failed to block the analgesic effects of CT, but atropine at 10 mg/kg (ip) did antagonize the analgesia mediated by CT in the mouse acetic acid writhing test. At the highest effective dose of antinociception (75 mu g/kg), CT did not change the spontaneous mobility of mice. Conclusion These results suggest that CT from Naja naja atra venom has analgesic effects. Central nervous system may be involved in CT's analgesic effects and the PAG may be the primary central site where CT exerts its effects. The central cholinergic system but not opioid system appears to be involved in the antinociceptive action of CT.
ABSTRACT
Objective To investigate the analgesia induced by receptin (REC), a chemically modified cobratoxin (CTX, a long-chain postsynaptic alpha -neurotoxin from Thailand cobra venom), and the effects of atropine and naloxone on antinociceptive activity of REC in rodent pain models. Methods REC was administered intraperitoneally (5 mg/kg, 7.07 mg/kg, or 10 mg/kg, i.p.) or intra-cerebral venticularly (62.5 mu g/kg, i.c.v.). The antinociceptive action was determined using the hot-plate test, the acetic acid writhing test and tail flick assay in mice and rats. The involvement of cholinergic and the opioid peptidergic systems in REC-induced analgesia were examined by pretreatment of animals with atropine (Atr; 0.5 mg/kg, i.m. or 10 mg/kg, i.p.) or naloxone (Nal; 3 mg/kg, i.p.). The effect of REC on motor activity was tested using the Animex test in mice. Results REC (5 mg/kg, 7.07 mg/kg or 10 mg/kg, i.p.) exhibited a dose-dependent analgesic action in mice as determined with hot-plate test and acetic acid writhing test. The significant analgesia of REC was seen 2 h to 3 h after its administration. In the rat-tail flick assay, the administration of REC at 62.5 mu g/kg (1/160 of systemic dose; i.c.v.) produced marked analgesic effects. Atropine at 0.5 mg/kg (i.m.), 10 mg/kg (i.p.) or naloxone at 3 mg/kg (i.p.) failed to block the analgesic effects of REC. REC at the highest effective dose of 10 mg/kg did not change the spontaneous mobility of mice. Conclusion These results demonstrate that REC has analgesic effect. This activity appears to be mediated through the peripheral nervous system though central nervous system may contribute to REC' s analgesic effects. The central cholinergic system and opioid peptidergic system appear not to be involved in the antinociceptive action of REC.