Dissertation
Dissertation > Medicine, health > Chinese Medicine > TCM Internal Medicine > Modern medicine, internal diseases

Experimental Study on the Pharmacological Mechanisms on Cellular Immunity of BiQingYin for the Treatment of Rheumatoid Arthritis

Author PangAiMei
Tutor ZhouCuiYing
School Shandong University of Traditional Chinese Medicine
Course Traditional Chinese Medicine
Keywords Bi clean drinking Rheumatoid Arthritis Jurkat cells T cell activation Regulation mechanism
CLC R259
Type PhD thesis
Year 2008
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Objective: To study in rheumatoid arthritis (RA) pathogenesis explore clean drinking anti- RA paralysis cellular immune regulatory mechanism in cellular and molecular level, as Chinese medicine and clinical application of anti- RA further pharmacological studies provide a scientific basis . Methods: Jurkat cells as a model to TGP (TGP), dexamethasone (DEX), methotrexate (MTX) for the control drug , using flow cytometry , MTT, ELISA immunological methods to observe the paralysis clean drinking of Jurkat cell proliferation , differentiation, cycle ; peripheral blood of patients with RA activation of T lymphocytes . Results: Bi clean drinking inhibits proliferation of T lymphocytes , CD69, CD25 expression , decreased production of IL-2 and IFN-γ expression in the model group were significantly different (p lt; 0.01 or p lt; 0.05 ) , and TGP \\ DEX \\ MTX group were no significant differences (p gt; 0.05). Clean drinking can cause paralysis Jurkat cells Gl arrest , Gl phase cell accumulation, can not enter S phase arrest Gl to S phase transformation process , so that the G2 / M phase cells are relatively increased. Conclusion: Bi clean drinking on RA immune regulatory mechanisms may be: by inhibiting the activation of T cells , reduced IL-2 and IFN-γ production indirectly inhibit Th differentiation and proliferation , thereby reducing joint and / or synovial inflammation and hyperplasia , slow down the process of bone destruction ; T cells by blocking the synthesis of energy and raw materials , reduce cell G2 phase transformation to promote the abnormal proliferation of synovial cell apoptosis.

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