【摘要】 目的：研究一氧化氮（ＮＯ） 及一氧化碳（ＣＯ） 对碱性成纤维细胞生长因子（ｂａｓｉｃ ｆｉｂｒｏｂｌａｓｔ ｇｒｏｗｔｈ ｆａｃｔｏｒ，ｂＦＧＦ） 促平滑肌细胞（ｖａｓｃｕｌａｒｓｍｏｏｔｈ ｍｕｓｃｌｅ ｃｅｌｌｓ， ＶＳＭＣ）增殖作用的影响及其机制。方法：以３ＨＴｄＲ参入法测定平滑肌细胞增殖程度，放射活性法测定ＶＳＭＣ内蛋白磷酸化程度、蛋白激酶Ｃ（ｐｒｏｔｅｉｎ ｋｉｎａｓｅ Ｃ，ＰＫＣ） 及丝裂素活化蛋白激酶（ｍｉｔｏｇｅｎａｃｔｉｖａｔｅｄ ｐｒｏｔｅｉｎ ｋｉｎａｓｅ， ＭＡＰＫ）活性。结果：孵育２４ ｈ 后，ｂＦＧＦ刺激的ＶＳＭＣ增殖较对照组增加１．１ 倍（Ｐ＜ ０．０１），细胞内蛋白磷酸化程度增加３８．２％ （Ｐ＜ ０．０１），ＰＫＣ 及ＭＡＰＫ 活性分别增加１．５ 和２ ．５倍（ Ｐ＜ ０．０１）；ＣＯ 前体ｈｅｍｅＬｌｙｓｉｎａｔｅ（ＨＬＬｙｓ） 及ＮＯ 前体ＬＡｒｇｉｎｉｎｅ（ ＬＡｒｇ） 对静止期ＶＳＭＣ 生长无显著影响，亦未引起细胞内蛋白磷酸化、ＰＫＣ及ＭＡＰＫ 活性发生显著改变；５、１０ 、２０ μｍｏｌ·Ｌ－１ ＨＬＬｙｓ 使ｂＦＧＦ刺激的ＶＳＭＣ增殖分别减少４３．４ ％ 、４６．６％ 和４７ ．６％更多还原

【Abstract】 Objective: To investigate the effect of nitric oxide(NO) and carbon monoxide(CO) on proliferation of vascular smooth muscle cells(VSMC) stimulated by basic fibroblast growth factor(bFGF) and their mechanism. Methods: VSMC proliferation was measured by 3H TdR incorporation. Protein phosphorylation, PKC and MAPK activity in VSMC were determined by radioactivity assay. Results: Compared with control, VSMC amplification induced by bFGF was increased by 1.1 fold after 24 h incubation ( P <0.01). Protein phophorylation, PKC and MAPK activities in VSMC were augmented by 38.2%, 1.5 and 2.5 times, respectively ( P <0.01); H L Lys and L Arg had no significant influence on both growth and intracellular protein phosphorylation, PKC and MAPK activities in quiescent VSMC. 5, 10 and 20 μmol·L -1 H L Lys decreased bFGF stimulated VSMC proliferation by 43.4%,46.6% and47.6%,respectively ( P <0.01). Intracellular PKC activities were lowered by 25.6%, 31.8% and 33.9%, respectively ( P <0.01), and MAPK activities were reduced by 15.0%, 25.5% and 40.1%, respectively ( P <0.01); 5, 10 and 20 mmol·L -1 L Arg decreased bFGF stimulated VSMC proliferation by 30.2%, 40.5% and 51.9%, respectively ( P <0.01). Intracellular PKC activities were lowered by 29.8%, 28.9% and 36.6%,respectively ( P <0.01), and MAPK activities were reduced by 19.4%, 32.4% and 44.4%, respectively ( P <0.01). bFGF induced protein phosphorylation in VSMC was inhibited by 10 μmol·L -1 H L Lys and 10 mmol·L -1 L Arg by 31.8% and 37.4%, respectively ( P <0.01). Conclusion: NO and CO may have an inhibitive role against VSMC proliferation caused by bFGF, whose mechanism has a close relationship with inhibition of intracellular protein phosphorylation, PKC and MAPK activities stimulated by bFGF.更多还原