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標題: Molecular mechanism of T cell activation modulated by honeybee venom polypeptide, melittin
作者: Chiang, Chih-Hong
關鍵字:;蜜蜂蜂毒;melittin;concanavalin A;NF-kB;activated protein-1;Na+/K+ ATPase;ouabain
出版社: 昆蟲學系所
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Honeybee (Apis mellifera) venom (BV) has been used for a long history in the treatment of rheumatoid diseases in Asia. However, some adverse effects induced by BV had also been reported, indicating a controversial role of BV in the therapies of rheumatoid diseases. In this study, the effect of melittin (the major component of BV) on the activation of human lymphocyte SUP-T1 cells was examined. Our results showed that melittin significantly inhibited the concanavalin A (Con A)-induced SUP-T1 cells proliferation. The melittin-mediated antiproliferative effect was accompanied by the IkB-a

蜜蜂 (Apis mellifera)蜂毒被運用在風濕性疾病的治療上,在亞洲已行之有年,但也有許多蜂毒成份對人體產生毒害的相關文獻報導。因此,蜂毒是否可用於風濕性疾病之治療上仍有爭議之處,究竟蜂毒或其成份分子對免疫系統之活化是抑制或促進,至今尚無定論。有鑑於此,本論文之試驗探討蜜蜂蜂毒主要成份-melittin對T細胞活性之調控及可能之分子機轉。試驗結果發現melittin能抑制由concanavalin A (Con A)所誘發的T細胞增生。然而抑制細胞增生的現象伴隨產生IkB-a的降解、NF-kB p65次單元體的核轉移與c-Jun N-terminal kinase (JNK)的磷酸化。由gel electrophoretic mobility shift assay (EMSA)的結果也發現melittin確實會增加NF-kB及activated protein-1 (AP-1)與DNA結合的能力。此外,melittin會促使受Con A所刺激活化的T細胞,分泌更高量的發炎相關細胞素。然而使用Na+/K+ ATPase的抑制劑-ouabain處理T細胞後,可以阻絕部份的melittin進入細胞,並可減緩melittin所造成的生物功能。綜合本試驗結果,推測melittin可能藉由與Na+/K+ ATPase作用後進入細胞,活化NF-kB與JNK調控之AP-1路徑,進而增加發炎相關細胞素的產生。因此,對於蜂毒應用於風濕性疾病的治療,未來需更多的研究證據來驗證其對免疫系統之作用,釐清其對人體確實的功用或不良之副作用。
其他識別: U0005-2407200818184200
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