人胰岛素样生长因子Ⅱ反义RNA对肝癌细胞恶性表型的抑制作用

研究人胰岛素样生长因子Ⅱ（ＩＧＦ－Ⅱ）反义ＲＮＡ对肝癌细胞株ＳＭＭＣ－７７２１的抑制效应。方法人ＩＧＦ－ⅡｃＤＮＡ０．１ｋｂ反向插人真核细胞表达载体ｐｃＮＡ３,获得ＩＧＦ－Ⅱ反义ＲＮＡ表达载体ｐＩＧＦ－ⅡＡＳ,将其导人人肝癌细胞株ＳＭＭＣ-７７２１,观察软琼脂培养集落形成的能力。流式细胞仪（ＦＣＭ）测定ｐＩＧＦ－ⅡＡｓ表达ＩＧＦ－Ⅱ反义ＲＮＡ对ＳＭＭＣ-７７２１细胞生长的影响。结果转导人ｐＩＧＦ－ⅡＡｓ的ＳＭＭＣ－７７２１细胞,不能在软琼脂上形成集落,ＦＣＭＭ实导人ＰＩＧＦ－ⅡＡｓ细胞Ｓ期增多,而对照组ＳＭＭＣ－７７２１细胞和带ＤＣＤＮＡ３空载体的ＳＭＭＣ－７７２１细胞则无明显变化．结论ｐＩＧＦ-ⅡＡＳ＆义ＲＮＡ体外可抑制肝癌细胞株ＳＭＭＣ－７７２１的致瘤性。     

反义核苷酸干预血管成形术后平滑肌细胞生长因子基因表达的研究

为了研究反义核苷酸对平滑肌细胞（ＳＭＣ）及生长因子基因表达的影响。本实验对兔髂动脉粥样硬化模型行血管成形术；应用Ｎｏｒｔｈｅｒｎ印迹杂交和ＲＴ－ＰＣＲ方法观察反义核苷酸对体外兔髂动脉ＳＭＣ增殖及转化生长因子－β１（ＴＧＦ－β１）、表皮生长因子受体（ＥＧＦＲ）、碱性成纤维细胞生长因子（ｂＦＧＦ）基因表达的影响。结果表明：反义核苷酸抑制ＳＭＣ增生，并呈浓度依赖性；反义核苷酸抑制ＴＧＦ－β１和ｂＦＧＦｍＲＮＡ表达；阳离子脂质体能明显增强反义核苷酸的上述作用。在培养的兔髂动脉ＳＭＣ中ＥＧＦＲｍＲＮＡ表达阴性。结论：反义核苷酸抑制兔髂动脉ＳＭＣ增生与抑制ＴＧＦ－β１和ｂＦＧＦｍＲＮＡ表达有密切关系。     

肝素干预血管成形术后平滑肌细胞生长因子基因表达的研究

目的探讨肝素影响血管成形术后动脉平滑肌细胞（ＳＭＣ）增生的机理。方法建立兔动脉粥样硬化模型，行血管成形术；观察肝素对体外兔髂动脉ＳＭＣ的增生、细胞周期、转化生长因子－β１（ＴＧＦ－β１）、表皮生长因子受体（ＥＧＦＲ）、碱性成纤维细胞生长因子（ｂＦＧＦ）基因表达等的影响。结果肝素能抑制ＳＭＣ的增生，并具有浓度依赖性和时间依赖性；肝素阻止ＳＭＣ进入Ｓ期，也有浓度依赖性和时间依赖性；肝素能抑制ＴＧＦ－β１和ｂＦＧＦ信使核糖核酸（ｍＲＮＡ）的表达；在培养的兔髂动脉ＳＭＣ中ＥＧＦＲｍＲＮＡ的表达呈阴性。结论肝素抑制培养的兔髂动脉ＳＭＣ的增生与抑制ＴＧＦ－β１和ｂＦＧＦｍＲＮＡ的表达有密切关系。     

细菌脂多糖对小鼠巨噬细胞生长的调节作用

目的研究细菌脂多糖对小鼠巨噬细胞的生长调节作用。方法应用小鼠腹腔渗出性巨噬细胞（ＰＥＭ）和巨噬细胞株Ｊ７７４Ａ．１为靶细胞，测定细菌脂多糖（ＬＰＳ）对Ｍ－ＣＳＦ和ＧＭ－ＣＳＦ刺激的巨噬细胞集落细胞形成的影响，同时用１２５Ⅰ标记的ＧＭ－ＣＳＦ受体结合实验测定了ＬＰＳ对巨噬细胞膜上的ＧＭ－ＣＳＦ受体数目的调节。用反向ＰＣＲ（ＲＴ－ＰＣＲ）法检测ＴＴＧＦ－β１对巨噬细胞产生ＩＦＮ－γ的作用。结果ＬＰＳ单独对巨噬细胞无生长调节作用，但可抑制ＧＭ－ＣＳＦ对巨噬细胞的增殖效应。而在ＴＧＦ－β１同时存在下，ＬＰＳ的抑制效应被消除。ＲＴ－ＰＣＲ证实ＬＰＳ诱生巨噬细胞产生的ＩＦＮ－γ可被ＴＧＦ－β１有效地抑制．而已知ＩＦＮ－γ是强烈的巨噬细胞生长抑制因子。此外，１２５Ⅰ－ＧＭ－ＣＳＦ受体结合实验发现，同ＴＧＦ－β１一样ＬＰＳ增强ＧＭ－ＣＳＦ受体数目的表达。结论ＬＰＳ参与了多种细胞因子对巨噬细胞生长的调节网络，根据存在的细胞因子不同，表现为抑制和增殖的双重作用。     

反义核苷酸干预血管成形术后平滑肌细胞生长因子基因表达…

为了研究反义核苷地平滑肌细胞（ＳＭＣ）及生长因子基因表达的影响。本实验对兔髂动脉粥样硬化模型进行血管成形术；应用Ｎｏｒｔｈｅｒｎ印迹杂交和ＲＴ－ＰＣＲ方法观察反义核苷酸对体外兔髂动脉ＳＭＣ增殖及转化生长因子－β１（ＴＧＦ－β１），表皮生长因子受体（ＥＧＦＲ）、碱改成纤维细胞生长因子基因表达的影响。结果表明：反义核苷酸抑制ＳＭＣ增生、并呈浓度依赖性；反义核苷酸抑制ＴＧＦ－β１和ｂＦＧＦｍＲＮＡ表达；     

对肺动脉平滑肌细胞趋化反应和DNA合成的研究

探讨肺血管平滑肌细胞（ＰＶＳＭＣ）迁移在缺氧性肺血管结构重组中的作用以及缺氧本身对ＰＶＳＭＣ增殖和迁移的影响。方法利用细胞趋化研究方法和３Ｈ－胸腺嘧啶掺入法研究了血小板衍生生长因子（ＰＤＧＦ）对培养的新生小牛肺动脉平滑肌细胞（ＰＡＳＭＣ）趋化反应和ＤＮＡ合成的作用，以及缺氧和心钠素（ＡＮＰ）对ＰＤＧＦ这种作用的影响。结果表明缺氧可促进ＰＤＧＦ诱导的ＰＡＳＭＣ的趋化反应和ＤＮＡ合成，ＡＮＰ可抑制ＰＡＳＭＣ对ＰＤＧＦ的趋化作用，并抑制ＰＡＳＭＣ的ＤＮＡ合成，鸟苷酸环化酶抑制剂美蓝（ＭＢ）可抑制ＡＮＰ的这种抑制作用。结论研究提示ＰＤＧＦ、ＡＮＰ和缺氧本身对ＰＡＳＭＣ的增殖和迁移有重要作用，这可能对缺氧性肺血管结构重组具有重要意义     

血管紧张素II促高血压大鼠血管平滑肌细胞增殖机制的研究

本工作以培养的正常血压ＷＫＹ大鼠主动脉平滑肌细胞（ＡＳＭＣ）为对照，探讨血管紧张素ＩＩ（ＡｎｇＩＩ）对培养的ＳＨＲ ＡＳＭＣ促增殖的机制。结果表明：ＡｎｇＩＩ（１０＾－９￣１０＾－６ｍｏｌ／Ｌ）对ＳＨＲ和ＷＫＹ大鼠的ＡＳＭＣ均有促增殖作用且随剂量增加其作用加强，但对ＳＨＲ ＡＳＭＣ的促增殖效应明显高于ＷＫＹ大鼠。应用碱性成纤维细胞生长因子（ｂＦＧＦ）单克隆抗体（Ａ－ｂＦＧＦ）和反义ｂＦＧＦｍＲ－Ｎ     

自发性高血压大鼠高血压形成前期血管平滑肌细胞增殖和肾素-血管紧张素系统的关系

通过体外培养３周龄自发性高血压大鼠（ＳＨＲ）胸主动脉血管平滑肌细胞（ＡＳＭＣ），探讨ＳＨＲ高血压形成前期ＡＳＭＣ是否存在异常增殖，以及与循环、血管局部血管紧张素Ⅱ（ＡｎｇⅡ）、血管紧张素转换酶（ＡＣＥ）的关系。结果表明：３周龄ＳＨＲＡＳＭＣ肾素－血管紧张素系统（ＲＡＳ）处于高功能状态，合成ＡｎｇⅡ、ＡＣＥ，分泌ＡｎｇⅡ的量比ＷＫＹ高（Ｐ＜０．０５），并呈现异常增殖，３Ｈ－ＴｄＲ参入增加，倍增时间（ＤＴ）缩短（Ｐ＜０．０１）。血管紧张素转换酶抑制剂（ＡＣＥＩ）卡托普利、ＡｎｇⅡ受体拮抗剂Ｓａｒａｌａｓｉｎ长期干预可通过抑制ＳＨＲＡＳＭＣＡｎｇⅡ生成或阻断ＡｎｇⅡ的作用进而抑制其异常增殖。而ＷＫＹ血浆ＡｎｇⅡ、ＡＣＥ活性反比ＳＨＲ高（Ｐ＜０．０１）。说明：血管局部ＲＡＳ处于高功能状态对ＳＨＲ高血压前期ＡＳＭＣ异常增殖起重要作用，而循环ＲＡＳ则不起作用。     

人参皂甙通过GATA转录因子刺激巨核系祖细胞增殖

目的：了解人参皂甙（ＧＳ）对巨核系祖细胞（ＣＦＵ－Ｍｅｇ）的刺激增殖作用，比较ＧＳ与生长因子ＴＰＯ、ＩＬ－３对ＧＡＴＡ转录调控蛋白的诱导作用。方法：正常人和ＩＴＰ患者骨髓ＣＦＵ－Ｍｅｇ培养和ＧＳ刺激试验、电泳带移动阻滞试验（ＥＭＳＡ）、抗体胶移动试验（Ｓｕｐｅｒｓｈｉｆｔ ａｓｓａｙ）和蛋白免疫印迹法（Ｗｅｓｔｅｒｎ Ｂｌｏｔ）。结果：ＧＳ刺激正常ＣＦＵ－Ｍｅｇ增殖，呈剂量依赖的方式，血小板减少性紫癜（ＩＴＰ）患者的ＣＦＵ－Ｍｅｇ也对ＧＳ敏感。ＧＳ、ＴＰＯ和ＩＬ－３均能诱导生长因子依赖ＭＯ７ｅ细胞核内ＧＡＴＡ蛋白与ＤＮＡ结合的活性及使ＧＡＴＡ－２蛋白含量增加。ＧＳ＋ＴＰＯ或ＧＳ＋ＩＬ－３可协同地诱导ＧＡＴＡ蛋白活性进一步增高。结论：ＧＳ能够通过类生长因子和增强生长因子作用而刺激ＣＦＵ－Ｍｅｇ增殖，ＧＡＴＡ族转录因子，主要是ＧＡＴＡ－２参与造血细胞对ＧＳ反应的信号传递途径。     

高血压病人白细胞流变性与细胞粘附分子表达的变化

目的探讨白细胞流变性和细胞粘附分子（ＣＡＭＳ）表达与高血压发生及病情严重程度的关系。方法采用红细胞变形能力测定仪、体外血栓血小板粘附两用仪和酶联免疫吸附法（ＥＬＩＳＡ），检测１４９例高血压病人和１１０例健康人外周血白细胞变形能力（ＬＤ）、白细胞粘附功能（ＬＡＦ）、白细胞ＣＤ１８表达及血清可溶性细胞间粘附分子－１（ｓＩＣＡＭ－１）浓度的变化。结果高血压病人白细胞滤过指数（ＬＦＩ）、白细胞粘附率（ＬＡＲ）、白细胞ＣＤ１８表达和ｓＩＣＡＭ－１浓度均明显增高，与对照组比较差异有极显著性（Ｐ＜０．００１），三期病人各指标之间比较差异也具有极显著性（Ｐ＜０．００１），且以第３期病人各指标增高最明显。高血压病人ＬＡＲ与ＬＦＩ呈正相关（ｒ＝０．５７９，Ｐ＜０．００１）；ＬＡＲ和ＬＦＩ与白细胞ＣＤ１８表达和ｓＩＣＡＭ－１浓度呈正相关（ｒ＝０．６６２～０．８０４，Ｐ＜０．００１）。结论ＬＤ降低、ＬＡＦ及白细胞ＣＤ１８表达和ｓＩＣＡＭ－１浓度增高参与高血压的发生，且与病情严重程度有密切关系。     

氧化LDL和抗氧化剂对大鼠主动脉平滑肌细胞产生二酰基甘油的影响

目的研究ＯＸ－ＬＤＬ及抗氧化剂对平滑肌细胞信号转导的影响。方法采用薄层层析、放射自显影及放射酶标法分离、检测细胞中ＤＡＧ含量。结果ＯＸ－ＬＤＬ刺激平滑肌细胞产生ＤＡＧ具有双时相性变化,并且随浓度增加而增加。抗氧化剂ＶｉｔＥ明显抑制平滑肌细胞产生ＤＡＧ。结论ＯＸ－ＬＤＬ能明显刺激ＤＡＧ的生成,抗氧化剂ＶｉｔＥ显著抑制平滑肌细胞ＤＡＧ的形成,并且具有浓度依赖效应。     

Effect of Dexamethasone on Bovine Airway Smooth Muscle Cell Proliferation

Airway smooth muscle proliferation is a key component of airway wall remodelling that occurs as a consequence of inflammation in asthma. Studies were conducted to examine the effect of dexamethasone on airway smooth muscle cell (ASMC) proliferation in vitro. Dexamethasone (25-250 nM) significantly inhibited DNA synthesis and cell division induced by β-hexosaminidase A (Hex A, 50 nM) in bovine ASMC. The inhibitory effect of dexamethasone on DNA synthesis was variable depending on the growth factors: significant effect was observed on Hex A and insulin; no significant effect was observed on epidermal growth factor and fetal bovine serum.     

L苯丙氨酸抑制自发性高血压大鼠心肌成纤维细胞增殖

目的旨在观察Ｌ－苯丙氨酸对自发性高血压大鼠心肌成纤维细胞的增殖作用的影响。方法取１天龄自发性高血压大鼠心脏组织培养心肌成纤维细胞,分别以不同浓度的Ｌ－苯丙氨酸、酪氨酸和组氨酸干预一定时间后,利用３Ｈ－胸腺嘧啶掺入技术和细胞计数测定各不同浓度的氨基酸对心肌成纤维细胞ＤＮＡ合成和细胞增殖数目的影响。结果随着Ｌ－苯丙氨酸浓度的增加,心肌成纤维细胞的ＤＮＡ合成量减少,细胞增殖数目减低。而Ｌ－酪氨酸和组氨酸随着浓度的增加对心肌成纤维细胞ＤＮＡ的合成量和细胞增殖数目无影响。结论Ｌ－苯丙氨酸可以特异性地抑制ＳＨＲ心肌成纤维细胞的增殖。     

异搏定、尼卡地平对原发性高血压患者离体血管平滑肌细胞内钙的干预研究

作者采用原发性高血压患者的离体动脉血管 ,并分离、培养动脉平滑肌细胞 ,观察了异搏定、尼卡地平对人动脉平滑肌细胞内钙的影响。由于原发性高血压患者动脉血管平滑肌细胞内钙的跨膜流动和细胞内释放机制尚不清楚 ,作者试图得到异搏定、尼卡地平对人离体动脉平滑肌细胞内钙释放和转运的直接证据。结果如下 :(1)原发性高血压患者动脉平滑肌细胞内总钙比正常血压组高 ,并与细胞内游离钙明显相关 ;(2 )两个钙通道拮抗剂均能显著减少两组的细胞内钙。异搏定显著减少4 5Ca2 的跨膜内流 ,尼卡地平主要是阻止细胞内钙的释放     

Platelets stimulate airway smooth muscle cell proliferation through mechanisms involving 5-lipoxygenase and reactive oxygen species

Continuous recruitment and inappropriate activity of platelets in the airways may contribute to airway remodeling, a characteristic feature of inflammatory airway diseases that includes increased proliferation of the smooth muscle. The aim of the present investigation was to examine the effect of platelets on proliferation of airway smooth muscle cells (ASMC) in culture and to determine the possible role of 5-lipoxygenase (5-LOX) and reactive oxygen species (ROS) in this context. ASMC obtained from guinea pigs were cultured and co-incubated with washed platelets for 24 hours. Thereafter, the proliferation was measured with the MTS-assay; the results were also verified by using thymidine incorporation, DNA measurements and manual counting. The interaction between platelets and ASMC was visualized with fluorescence microscopy. We found that platelets bind to the ASMC and the presence of platelets caused a significant dose-dependent increase in ASMC proliferation. Co-incubation of ASMC with platelets also increased ROS-production, detected by the fluorescent probe DCFDA. Furthermore, the platelet-induced proliferation was reduced in the presence of the NADPH-oxidase inhibitors DPI and apocynin. A possible role of 5-LOX in platelet-induced proliferation and ROS-generation was evaluated by using the 5-LOX inhibitor AA-861 and the PLA(2)-inhibitor ATK. The results showed that inhibition of these enzymes significantly reduced the platelet-induced proliferation. Moreover, Western blot analysis revealed that the ASMC but not the platelets express 5-LOX. In addition, our experiments revealed that the presence of AA-861 and ATK significantly inhibited the ROS-production generated upon co-incubation of platelets and ASMC. In conclusion, we show that platelets have a marked capacity to induce ASMC proliferation. Furthermore, our study indicates that the interaction between platelets and ASMC leads to activation of 5-LOX in the ASMC followed by an increased ROS-production, events resulting in enhanced ASMC proliferation. The new findings are of importance in understanding possible mechanisms contributing to airway remodeling.     

血小板衍生生长因子—BB对血管内皮细胞、平滑肌细胞及成纤维细胞增殖的影响

目的 观察血小板衍生生长因子—BB对培养的人血管内皮细胞、兔平滑肌细胞和人成纤维细胞增殖的影响。方法 采用培养的人脐静脉血管内皮细胞、兔动脉血管平滑肌细胞和人血管成纤维细胞，应用^3H—TdR掺入方法，观察血小板衍生生长因子—BB对三种细胞DNA合成的影响。结果 血小板衍生生长因子—BB可促进处于静止状态的三种细胞DNA的合成，并呈现出明显的浓度依赖关系，在30ng／ml的浓度时成纤维细胞DNA的合成达到高峰，在40ng／ml的浓度时内皮细胞、平滑肌细胞DNA的合成达到高峰。成纤维细胞、平滑肌细胞分别在PDCF-BB作用24h和36h年到DNA合成的高峰，内皮细胞在48h时DNA合成量最高。结论 血小板衍生生长因子—BB可明显促进培养的人脐静脉血管内皮细胞、兔动脉血管平滑肌细胞和人血管成纤维细胞的增殖。     

Heterogeneity in the response of vascular smooth muscle to heparin: altered signaling in heparin-resistant cells

OBJECTIVE: Vascular smooth muscle cells show phenotypic heterogeneity in vivo that affects the extent to which they respond to the antimitogenic effects of heparin. In vitro, heparin-resistant cells are readily selected. This study was undertaken to determine whether differences in the antiproliferative response to heparin involve differences in activity of heparin-sensitive signal transduction pathways. METHODS: Rat thoracic aorta smooth muscle cells (ASMC) at early passage together with two established vascular smooth muscle lines, PAC-1 and A10, were examined before and after selection for growth in the presence of heparin (10 micrograms/ml). Cells were rendered quiescent and then stimulated with serum. RESULTS: The three cell types showed different sensitivities to the antimitogenic effects of heparin. With respect to [3H]thymidine incorporation, A10 cells were insensitive to 1 microgram/ml heparin whereas PAC-1 cells responded down to 0.05 microgram/ml and ASMC were of intermediate sensitivity. ASMC and PAC-1 cells but not A10 showed a decrease in c-fos mRNA in response to 1 microgram/ml heparin, and a decrease in the c-Fos content of AP-1 DNA binding activity. None of the cells had decreased c-jun mRNA in the presence of heparin. Although induction of c-fos by serum is thought to signal through the Erk mitogen activated protein kinase family, Erk activity was decreased more by 1 microgram/ml heparin in A10 cells than in PAC-1 or ASMC. When cells were selected by growth in the presence of 10 micrograms/ml heparin, A10 cells were unaffected but PAC-1 and ASMC showed a blunted effect of heparin on serum stimulation. In contrast to A10 and their controls not exposed to continuous heparin, heparin-selected PAC-1 and ASMC showed a diminished ability to induce c-fos in response to serum. CONCLUSIONS: Smooth muscle cell lines show different responses to the antimitogenic effects of heparin that correlate with the heparin sensitivity of c-Fos/c-Jun expression. Although Erk is implicated in c-fos induction, cells comparatively resistant to heparin still show heparin-dependent inhibition of Erk activation, suggesting that other pathways may be more important for heparin resistance. Furthermore, cells selected for heparin resistance may develop c-fos-independent pathways for proliferation.     

脐动脉平滑肌细胞体外培养方法的改进

目的:建立并优化的人脐动脉血管平滑肌细胞(VSMCs)的体外培养方法。方法:人脐动脉VSMCs的体外原代培养应用优化的组织块贴壁法进行。在分别应用传统细胞培养法和优化后细胞培养法贴壁培养提取的原代细胞10 d后,计数6孔板每孔细胞数目,并做统计比较分析相同时间内原代细胞的数量。以抗α-平滑肌肌动蛋白(α-SMA)抗体和抗CD31抗体进行免疫荧光染色和倒置相差显微镜观察鉴定培养的细胞。结果:与传统细胞培养法相比,在相同的时间周期内优化实验方法后培养的原代细胞数量较传统多,我们可以在较短时间内得到实验所需的细胞量,因此优化后可缩短细胞的培养周期。原代和传代培养的脐动脉VSMCs生长良好,细胞经冻存、复苏后状态依然良好。光镜下细胞呈典型的"峰-谷"样生长,细胞多为长梭形,具有VSMCs的特征,且传代培养至第7代,细胞生长特性不变。经抗α-SMA、CD31抗体进行免疫荧光染色鉴定证实为VSMCs。结论:优化的组织块贴壁法可缩短原代人脐动脉VSMCs的培养周期,且细胞的生物学特性较稳定,为与平滑肌相关的疾病进展及心血管生长发育的研究奠定了实验基础。     

Human airway smooth muscle cells express eotaxin in response to signaling following mast cell contact

BACKGROUND: Asthma is a chronic inflammatory disease of the airways. Mast-cell (MC)-derived cytokines may mediate both airway inflammation and remodeling. It has also been shown that airway smooth muscle cells (ASMC) can be a source of proinflammatory cytokines. In the human airways, MC-ASMC cell interactions may have pivotal effects on modulating inflammation. OBJECTIVES: We wanted to know whether the production of eotaxin, an important proinflammatory cytokine, through a cell-to-cell contact mechanism of human ASMC activation by MC was mediated by p38 MAPK. METHODS: We cocultured normal humanASMC with a human MC line (HMC-1) and assayed for the production of eotaxin. RESULTS: When cultured together, human ASMC and HMC-1 contact induced eotaxin secretion. Separation of HMC-1 and human ASMC by a porous membrane inhibited this induction. Coculturing of human ASMC with HMC-1 induced increased expression of eotaxin gene mRNA. HMC-1-derived cellular membranes caused an increase in eotaxin production in human ASMC. Activation of p38 MAPK was also seen in cocultures by Western blot, whereas eotaxin production in cocultures was significantly inhibited by the p38 inhibitor SB203580. CONCLUSION: These novel studies reveal the importance of cell-to-cell interactions in the complex milieu of airway inflammation.     

L-精氨酸对哮喘大鼠气道平滑肌细胞增殖的影响

目的 观察L-精氨酸（L-Arg）对哮喘气道重构大鼠气道平滑肌细胞（ASMC）的细胞周期分布及细胞周期调节蛋白（CCRP）表达水平的影响,探讨L-Arg体内干预哮喘大鼠ASMC增殖的可能作用机制。方法实验分成对照组、哮喘组、L-Arg组,建立大鼠哮喘气道重构模型,检测血清NO2^-／NO3^-含量、肺内支气管内管壁和平滑肌层厚度及ASMC核数、ASMC的细胞周期分布以及ASMC内细胞周期素E（cyclin E）、cyclinA、cyclinB、蛋白27^kip1（P27^kip1）的表达。结果 哮喘组大鼠支气管内管壁、平滑肌层的厚度和ASMC数目显著大于对照组（P〈0．05）;L-Arg组大鼠支气管内管壁的厚度、平滑肌层的厚度和ASMC数目显著小于哮喘组（P〈0．05）。哮喘组血清一氧化氮（nitricoxide,NO）水平显著低于对照组（P〈0．05）;L-Arg组血清NO水平显著高于哮喘组（P〈0．01）。哮喘组G0／G1期ASMC比例及P27^kip1表达水平显著低于对照组（P〈0．01）,G2／M＋S期ASMC比例及cyclinE、cyclinA和cyclinB表达水平显著高于对照组（P〈0．01）;L-Arg组G0／G1期ASMC比例及P27^kip1表达水平显著高于哮喘组（P〈0．05）,G2／M＋S期ASMC比例及cyclinE和cyclinA表达水平显著低于哮喘组（P〈0．05）。结论 L-Arg通过调控CCRP的表达水平阻滞细胞从G1期进入S期而抑制哮喘ASMC的增殖。