同济医科大学学报
同濟醫科大學學報
동제의과대학학보
ACTA UNIVERSITATIS MEDICINAG TONGJI
2000年
5期
388-390
,共3页
段秋红%廖国宁%雷景迈%何善述
段鞦紅%廖國寧%雷景邁%何善述
단추홍%료국저%뢰경매%하선술
低氧症%内皮细胞%平滑肌细胞%1-(2,6-二甲基苯氧基)-2-(3,4-二甲氧基苯乙胺基)丙烷盐酸盐
低氧癥%內皮細胞%平滑肌細胞%1-(2,6-二甲基苯氧基)-2-(3,4-二甲氧基苯乙胺基)丙烷鹽痠鹽
저양증%내피세포%평활기세포%1-(2,6-이갑기분양기)-2-(3,4-이갑양기분을알기)병완염산염
hypoxia%endothelium%DDPH%pulmonary artery smooth muscle cell%proliferation
采用MTT比色、荧光技术和放免技术观察了猪肺动脉低氧内皮细胞条件培养液(HECCM)和1-(2,6-二甲基苯氧基)-2-(3,4-二甲氧基苯乙胺基)丙烷盐酸盐(DDPH)对猪肺动脉平滑肌细胞(PASMCs)增殖、第二信使([Ca2+]1和cAMP)的影响。结果显示:①HECCM促进PASMC增殖,而DDPH可抑制之,抑制率为77.46%。②HECCM升高PASMCs内[Ca2+]i,而DDPH可对抗此作用。③HECCM组PASMCs内cAMP含量明显低于对照组(NECCM组),而HECCM+DDPH组PASMCs内cAMP与NECCM组无显著性差异。
採用MTT比色、熒光技術和放免技術觀察瞭豬肺動脈低氧內皮細胞條件培養液(HECCM)和1-(2,6-二甲基苯氧基)-2-(3,4-二甲氧基苯乙胺基)丙烷鹽痠鹽(DDPH)對豬肺動脈平滑肌細胞(PASMCs)增殖、第二信使([Ca2+]1和cAMP)的影響。結果顯示:①HECCM促進PASMC增殖,而DDPH可抑製之,抑製率為77.46%。②HECCM升高PASMCs內[Ca2+]i,而DDPH可對抗此作用。③HECCM組PASMCs內cAMP含量明顯低于對照組(NECCM組),而HECCM+DDPH組PASMCs內cAMP與NECCM組無顯著性差異。
채용MTT비색、형광기술화방면기술관찰료저폐동맥저양내피세포조건배양액(HECCM)화1-(2,6-이갑기분양기)-2-(3,4-이갑양기분을알기)병완염산염(DDPH)대저폐동맥평활기세포(PASMCs)증식、제이신사([Ca2+]1화cAMP)적영향。결과현시:①HECCM촉진PASMC증식,이DDPH가억제지,억제솔위77.46%。②HECCM승고PASMCs내[Ca2+]i,이DDPH가대항차작용。③HECCM조PASMCs내cAMP함량명현저우대조조(NECCM조),이HECCM+DDPH조PASMCs내cAMP여NECCM조무현저성차이。
By using cell culture, MTT colorimetry, fluorescence and bioluminnescence, and radioimmunoassay techniques, the effects of hypoxial endothelia cell conditioned medium (HECCM) and DDPH on the pulmonary artery smooth muscule cell (PASMC) proliferation and intracellular free calcium and cAMP concentrations were observed. The results showed that DDPH could inhibit PASMC proliferation induced by HECCM with the inhibition ratio being 77.46 %. DDPH could decrease the HECCM-induced elevation of PASMC intracellular free calcium concentration and increase PASMC cAMP level. It was suggested that the mechanism of DDPH inhibiting PASMC proliferation may be contributed to preventing PKC signal pathway, but not excluding other pathway.