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采用碱性成纤维细胞生长因子 (b FGF)诱导的大鼠血管平滑肌细胞 (VSMC)增殖模型 ,对海洋硫酸多糖 DPS抑制 VSMC释放血管紧张素 (Ang )和内皮素 - 1(ET- 1)的机理进行了初步探讨。取生长稳定的 5～ 8代 VSMC,以密度为每孔 5× 10 4 接种在 2 4孔培养板内 ,在含 10 % M199的培养液中 37℃孵育。待细胞贴壁生长稳定后 ,将细胞分为正常对照组 ,b FGF组、DPS组、DPS与 L - NAME联合用药 (DPS+L - NAME)组。DPS组和 DPS+L- NAME组分别在加入含有 DPS(1mg· L-1)的 M199培养液或含有 DPS(1mg· L-1)和一氧化氮合酶抑制剂 (L - NAME,0 .1mg· L-1)的培养液中预孵 2 4 h后 ,正常对照组除外 ,各组均加入含终浓度为 50 mg· L-1的 b FGF继续培养 2 4 h。用均相竞争放射免疫分析法测定 VSMC上清液 Ang 和 ET- 1的含量。结果表明 ,0 .1mg·m L-1的 L- NAME能完全阻断 DPS抑制 VSMC释放 Ang 的作用 ,但对 ET- 1的释放未见明显影响。提示一氧化氮可能介导 DPS抑制 VSMC释放 Ang 的作用 ,对抑制 ET- 1的释放则无介导作用。
The proliferation model of rat vascular smooth muscle cells (VSMC) induced by basic fibroblast growth factor (b FGF) was used to inhibit the release of angiotensin (Ang) and endothelin-1 (ET-1) Mechanism of a preliminary discussion. Five to eight generations of VSMCs with stable growth were inoculated into 2 4-well plates at a density of 5 × 10 4 per well and incubated at 37 ° C in a medium containing 10% M199. Cells were divided into normal control group, bFGF group, DPS group, DPS + L - NAME group (DPS + L - NAME) after stable growth of adherent cells. DPS group and DPS + L-NAME group were cultured in M199 medium containing DPS (1 mg · L -1) or containing DPS (1 mg · L -1) and nitric oxide synthase inhibitor (L - NAME, 1 mg · L-1) for 24 h. Except for the normal control group, bFGF containing 50 mg · L -1 final concentration was added to each group for 24 h. The contents of Ang and ET-1 in supernatant of VSMC were determined by homogeneous competition radioimmunoassay. The results showed that L-NAME at 0. 1 mg · mL -1 could completely block the effect of DPS on the release of Angiotensin Ⅱ from VSMCs, but no significant effect on ET-1 release. It is suggested that nitric oxide may mediate the effect of DPS on inhibiting the release of Angiotensin from VSMC, but not on the inhibition of ET-1 release.