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Establishment of Myasthenia Gravis Animal Model and the Mechanism of Traditional Chinese Drug Treatment of Myasthenia Gravis

Author: ZhuLiJun
Tutor: JiangXinMei
School: Jilin University
Course: Neurology
Keywords: MG (myasthenia gravis) EAMG (experimental autoimmune myastheia gravis) AchR (acetylcholine receptor) AchR-Ab (acetylcholine receptor antibody) ELISA (enzyme linked immunosorbent assay) NMJ (neuromuscular junction) IL-4(nterleukin-4) TGF-β(transforming growth factor-β) IFN-γ(Interferonγ)
CLC: R-332
Type: PhD thesis
Year: 2011
Downloads: 103
Quote: 0
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Abstract


Objective:To establish experimental autoimmune myasthenia gravis (EAMG) mouse model of muscular strength by observing the experimental drug powder on body weight EAMG mice, clinical symptoms, serum acetylcholine receptor antibody (AchR-Ab), interleukin-4 (IL-4), transforming growth factorβ(TGF-β), interferonγ(INF-γ) and to explore its mechanism of action. Methods:Healthy female mice c57BL/6J, H-2b,3 weeks old, weight 10-13 grams, and 60 were randomly divided into control group (10 rats) and experimental group (50), to pre-CFA and PBS or electric eel acetylcholine receptor antigen to 1:1 volume ratio of the full mix, the control group injected PBS/CFA mixture,0.3 mL, only the experimental group and the CFA subcutaneously nAch mixture,0.3 mL (containing 0.6 mg nAchR)/only at the injection site were the back four points, one point of the root end of the first day to strengthen the immune 30,50,70 d for the model evaluation time. Weight changes in mice, mice with reference to the classic Lennon strength evaluation criteria such as grading evaluation of clinical symptoms, detection of low frequency repetitive electrical stimulation of the sciatic nerve action potential decay rate, enzyme-linked immunosorbent assay (ELISA) serum nAch-Ab level evaluation of results EAMG mouse model was successful. EAMG mice were then randomly divided into five groups of 41, JIQIANGSAN group was fed the way loose, medium and small dose group were given 1.4g/(kg.d),2.8 g/ (kg.d),5.6 g/(kg.d), saline group with the same volume of saline administered continuously for two weeks, the control group was not medicated, hormone group with prednisone 50mg/kg.d, by way of salt dissolved administered orally. Two weeks of continuous administration, recording weight changes of mice in each group and the scoring of clinical symptoms, enzyme-linked immunosorbent assay measured AchR-Ab, IL-4, TGF-β, INF-γ. Results:50 mice in modeling the success of EAMG mice 41. EAMG trend slowed weight gain in mice, appears more obvious symptoms of muscle weakness and muscle fatigue, clinical score (1.63±0.69), with the control group were significantly different (P<0.01); serum AchR-Ab level (60.6±4.76) and the normal group (40.3±3.59) were significantly different (P<0.05); RNS detection of decay rate (18.59±4.83) is also normal (6.25±3.02) were significantly different (P<0.01). After 2 weeks of treatment, compared with the saline group of mice with different doses of JIQIANGSAN and bulk prednisone treatment group mice increased the rate of increase, the clinical symptom score decreased and serum levels of AchR-Ab decreased TGF-lymphocytesβand INF-γlevels, IL-4 levels decreased. JIQIANFSAN bulk to large and medium dose group and the role of prednisone degree of mice significantly, while the dispersion medium and large JIQIANGSAN group and the prednisone dose was no significant difference between groups.Conclusion:(1) In this study, officials from the electric eel electric purified acetylcholine receptor (nAchR) as immunizing susceptible mice (c57BL/6J) induced EAMG in mice and human MG in clinical symptoms, serum AchR-Ab RNS levels and similar changes in other aspects, the initial animal model to determine successfully established EAMG. To further study the pathogenesis of MG muscle strength have been offers casual pharmacodynamic basis for the premise. (2) EAMG effective treatment of JIQIANGSAN, which may be EAMG mice increased the level of TGF-βcells, by inhibiting B, T lymphocyte proliferation and differentiation to inhibit IL-4, IFN-γand other cytokines in excess secretion, thereby reducing the level of serum nAchR-Ab, less nAchR-Ab and the a subunit nAchR MIR in combination to reduce the damage of postsynaptic membrane, so as to improve the role of EAMG symptoms of myasthenia gravis in mice.

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CLC: > Medicine, health > Medical research methods > Experimental medicine, medical experiments > Medical Laboratory Animal Science
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