Changes of sleep-disordered breathing after laryngeal surgery in patients with bilateral vocal fold paralysis

中國醫藥大學機構典藏 China Medical University Repository, Taiwan > 公共衛生學院 > 公共衛生學系暨碩博班 > 期刊論文 > Item 310903500/28820

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題名:	Changes of sleep-disordered breathing after laryngeal surgery in patients with bilateral vocal fold paralysis
作者:	Li, HY;Wang, PC;Hsu, CY;Chen, NH;Fang, TJ
貢獻者:	公共衛生學院公衛系;Royal Infirm Edinburgh NHS Trust, Dept Sleep Med, Edinburgh, Midlothian, Scotland;Chang Gung Univ, Chang Gung Mem Hosp, Dept Otolaryngol, Sleep Ctr, Taipei, Taiwan;Cathay Gen Hosp, Dept Otolaryngol, Taipei, Taiwan;China Med Univ, Dept Publ Hlth, Taichung, Taiwan;Taipei City Psychiat Ctr, Dept Neurol, Taipei, Taiwan;Chang Gung Mem Hosp, Dept Pulm & Crit Care Med, Sleep Ctr, Taipei 10591, Taiwan
日期:	2005
上傳時間:	2010-09-24 13:55:39 (UTC+8)
出版者:	SPRINGER
摘要:	Ginsenoside Rh2 (Rh2), a purified ginseng saponin, has been shown to have antiproliferative effects in certain cancer cell types. However, the molecular mechanisms of Rh2 on cell growth and death have not been fully clarified. In this study, the antiproliferative effect of Rh2 in human lung adenocarcinoma A549 cells was investigated. Treatment of A549 cells with 30 mu g/ml Rh2 resulted in G(1) phase arrest, followed by progression to apoptosis. This Rh2-mediated G(1) arrest was accompanied by downregulation of the protein levels and kinase activities of cyclin-D1, cyclin-E and Cdk6, and the upregulation of pRb2/p130. In addition, Rh2-induced apoptosis was confirmed by TUNEL assay and DNA fragmentation analysis. Administration of Rh2 caused an increase in the expression levels of TRAIL-RI (DR4) death receptor but did not alter the levels of other death receptors or Bcl-2 family molecules. Furthermore, the Rh2-induced apoptosis was significantly inhibited by DR4:Fc fusion protein, which inhibits TRAIL-DR4-mediated apoptosis. In addition, caspase-2, caspase-3 and caspase-8 were highly activated upon Rh2 treatment. Inhibitors of caspase-2, caspase-3 and caspase-8 markedly prevented the cell death induced by Rh2. Inhibitor of caspase-8 significantly inhibited the activation of caspase-2, caspase-3 and caspase-8. These observations indicate that multiple G(1)-related cell cycle regulatory proteins are regulated by Rh2 and contribute to Rh2-induced G(1) growth arrest. The increase in the expression level of DR4 death receptor may play a critical role in the initiation of Rh2-triggered apoptosis, and the activation of the caspase-8/caspase-3 cascade acts as the executioner of the Rh2-induced death process.
關聯:	EUROPEAN ARCHIVES OF OTO-RHINO-LARYNGOLOGY 262(4):294-297
顯示於類別:	[公共衛生學系暨碩博班] 期刊論文

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