Shulan Yuan, Yanping Wang, Xiaohe Chen, Yi Song, Yan Yang
{"title":"[丹参酮ⅱA诱导鼻咽癌细胞株凋亡及其分子机制研究]。","authors":"Shulan Yuan, Yanping Wang, Xiaohe Chen, Yi Song, Yan Yang","doi":"","DOIUrl":null,"url":null,"abstract":"<p><strong>Objective: </strong>To assess effect of Tanshinone II A on the apoptosis of human nasopharyngeal carcinoma (NPC) cell line CNE-1 and inquire into the mechanism there in involved.</p><p><strong>Methods: </strong>The CNE-1 cells cultured in vitro were treated with 0.5 microgram/ml Tanshinone II A for 4 days. The morphology of the cells was observed by microscopy. The cell growth and proliferation were measured by cell counting. The DNA break was examined by gel electrophoresis. The cell cycle, apoptosis index (AI) and the expression of apoptosis associated gene were analysed by flow cytometry.</p><p><strong>Results: </strong>0.5 microgram/ml Tanshinone II A could induce the apoptosis of CNE-1 cells. In the treatment group, the morphologic characteristics of apoptotic cells were observed, the DNA of cells presented \"ladder\" break, the cell growth and proliferation were inhibited obviously, and the AI was 16.9% (the AI of control group was 6.4%). The cells were arrested in G0/G1 phase and cellular DNA synthesis was inhibited. The expressions of apoptosis associated gene fas, bax, p53 and p21 were up-regulated; the expression of bcl-2 was down-regulated.</p><p><strong>Conclusion: </strong>Tanshinone II A can induce apoptosis of human nasopharyngeal carcinoma cells. Its molecular mechanism may relate to modulation of the apoptosis associated gene expression.</p>","PeriodicalId":13173,"journal":{"name":"Hua xi yi ke da xue xue bao = Journal of West China University of Medical Sciences = Huaxi yike daxue xuebao","volume":"33 1","pages":"84-6, 90"},"PeriodicalIF":0.0000,"publicationDate":"2002-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"[A study on apoptosis of nasopharyngeal carcinoma cell line induced by Tanshinone II A and its molecular mechanism].\",\"authors\":\"Shulan Yuan, Yanping Wang, Xiaohe Chen, Yi Song, Yan Yang\",\"doi\":\"\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><strong>Objective: </strong>To assess effect of Tanshinone II A on the apoptosis of human nasopharyngeal carcinoma (NPC) cell line CNE-1 and inquire into the mechanism there in involved.</p><p><strong>Methods: </strong>The CNE-1 cells cultured in vitro were treated with 0.5 microgram/ml Tanshinone II A for 4 days. The morphology of the cells was observed by microscopy. The cell growth and proliferation were measured by cell counting. The DNA break was examined by gel electrophoresis. The cell cycle, apoptosis index (AI) and the expression of apoptosis associated gene were analysed by flow cytometry.</p><p><strong>Results: </strong>0.5 microgram/ml Tanshinone II A could induce the apoptosis of CNE-1 cells. In the treatment group, the morphologic characteristics of apoptotic cells were observed, the DNA of cells presented \\\"ladder\\\" break, the cell growth and proliferation were inhibited obviously, and the AI was 16.9% (the AI of control group was 6.4%). The cells were arrested in G0/G1 phase and cellular DNA synthesis was inhibited. The expressions of apoptosis associated gene fas, bax, p53 and p21 were up-regulated; the expression of bcl-2 was down-regulated.</p><p><strong>Conclusion: </strong>Tanshinone II A can induce apoptosis of human nasopharyngeal carcinoma cells. Its molecular mechanism may relate to modulation of the apoptosis associated gene expression.</p>\",\"PeriodicalId\":13173,\"journal\":{\"name\":\"Hua xi yi ke da xue xue bao = Journal of West China University of Medical Sciences = Huaxi yike daxue xuebao\",\"volume\":\"33 1\",\"pages\":\"84-6, 90\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2002-01-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Hua xi yi ke da xue xue bao = Journal of West China University of Medical Sciences = Huaxi yike daxue xuebao\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Hua xi yi ke da xue xue bao = Journal of West China University of Medical Sciences = Huaxi yike daxue xuebao","FirstCategoryId":"1085","ListUrlMain":"","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
[A study on apoptosis of nasopharyngeal carcinoma cell line induced by Tanshinone II A and its molecular mechanism].
Objective: To assess effect of Tanshinone II A on the apoptosis of human nasopharyngeal carcinoma (NPC) cell line CNE-1 and inquire into the mechanism there in involved.
Methods: The CNE-1 cells cultured in vitro were treated with 0.5 microgram/ml Tanshinone II A for 4 days. The morphology of the cells was observed by microscopy. The cell growth and proliferation were measured by cell counting. The DNA break was examined by gel electrophoresis. The cell cycle, apoptosis index (AI) and the expression of apoptosis associated gene were analysed by flow cytometry.
Results: 0.5 microgram/ml Tanshinone II A could induce the apoptosis of CNE-1 cells. In the treatment group, the morphologic characteristics of apoptotic cells were observed, the DNA of cells presented "ladder" break, the cell growth and proliferation were inhibited obviously, and the AI was 16.9% (the AI of control group was 6.4%). The cells were arrested in G0/G1 phase and cellular DNA synthesis was inhibited. The expressions of apoptosis associated gene fas, bax, p53 and p21 were up-regulated; the expression of bcl-2 was down-regulated.
Conclusion: Tanshinone II A can induce apoptosis of human nasopharyngeal carcinoma cells. Its molecular mechanism may relate to modulation of the apoptosis associated gene expression.