摘要
目的 研究海洋硫酸多糖 (DPS)对大鼠血管平滑肌细胞 (VSMC)增殖的影响及其作用机制。方法 建立碱性成纤维细胞生长因子 (bFGF)和白介素 1(IL 1)所诱导的VSMC增殖模型 ,以MTT法观察DPS对VSMC增殖的影响 ,分别用Griess重氮化反应法和放免法测定VSMC上清液中一氧化氮 (NO)、血管紧张素II(AngII)和内皮素 1(ET 1)的含量。结果 DPS在 0 0 1- 10 μg·mL-1浓度下 ,对bFGF或IL 1所致的VSMC增殖均有明显抑制作用。DPS呈剂量依赖性增加NO合成及降低AngII和ET 1的生成或释放。 结论 DPS对VSMC增殖有抑制作用 ,其机制可能与增加一氧化氮合成及降低血管紧张素II和内皮素 1的生成或释放有关。
AIM To investigate the inhibitory effects of D polymannuronic sulfate (DPS) on the proliferation of rat vascular smooth muscle cells (VSMC) induced by basic fibroblast growth factor (bFGF) or interleukin 1 (IL 1) and its related mechanisms. METHODS Rat aortic smooth muscle cells pretreated with DPS in concentrations ranging from 0 001 μg·mL -1 up to 100 μg·mL -1 were incubated at 37℃ for 24 h, followed by addition of bFGF (50 ng·mL -1 ) or IL 1 (50 U·mL -1 ) for another 24 h. The effects of DPS on the proliferation of VSMC were evaluated by MTT assays. VSMC were pretreated with DPS in concentrations ranging from 0 001 μg·mL -1 up to 1 μg·mL -1 , followed by addition of L NAME (0 1 μg·mL -1 ) or bFGF (50 ng·mL -1 ) for 24 h. Supernatant nitric oxide (NO) was determined with NO assay kit, while supernatant angiotensin II (Ang II) and endothelin 1 (ET 1) were measured by radioimmunoassay. RESULTS DPS exerted antiproliferative effects at concentrations ranging from 0 01 μg·mL -1 to 10 μg·mL -1 , and its maximal effect was observed at the concentration of 1 μg·mL -1 . Also, the suppressing actions of DPS on the proliferation of VSMC were diminished by increasing the concentrations of bFGF or IL 1. Furthermore, DPS increased NO synthesis and decreased Ang II and ET 1 contents released from VSMC in a concentration dependent manner. CONCLUSION DPS afforded the antiproliferative effects on bFGF or IL 1 treated VSMC and its underlying mechanisms were associated with enhancement of NO synthesis and decrement of Ang II and ET 1 production/release in vitro .
出处
《药学学报》
CAS
CSCD
北大核心
2001年第1期19-24,共6页
Acta Pharmaceutica Sinica
关键词
硫酸多糖
DPS
大鼠
血管平滑肌细胞
细胞增殖
D polymannuronic sulfate
rat vascular smooth muscle cells proliferation
angiotensin II (Ang II)
endothelin 1 (ET 1)
