尼古丁对大鼠血管平滑肌细胞增殖和凋亡的影响

目的 探讨尼古丁对大鼠胸主动脉血管平滑肌细胞(VSMCs)增殖和凋亡的影响.方法用终浓度为100 μmol/L的尼古丁作用于体外培养的大鼠VSMCs 24h,不加尼古丁的细胞作为对照组,应用荧光显微镜和扫描电子显微镜观察各组细胞凋亡的形态,BrdU-ELISA和流式细胞术检测各组细胞增殖和凋亡率,进而确定尼古丁对VSM...     

内皮细胞Jagged1下调促进PDGF诱导的大鼠平滑肌细胞增殖迁移

目的： 探讨内皮细胞Jagged1表达对PDGF诱导的大鼠血管平滑肌细胞增殖迁移的调节作用。方法: 分离培养大鼠主动脉内皮和平滑肌细胞,将内皮接种于下室、平滑肌接种于上室建立细胞共培养体系,根据内皮是否行Jagged1小RNA干扰分为对照组、空载体组和Jagged1小RNA干扰组。用Western blotting检测内皮细胞Jagged1的干扰效率。于下室加入PDGF（10 μg/L）干预24 h后分别用［3H］-TdR 掺入和平滑肌迁移计数检测平滑肌细胞增殖迁移能力,用Western blotting检测平滑肌细胞α-SM-actin蛋白表达。结果: 与对照组相比空载体组内皮细胞Jagged1蛋白表达无明显差异,Jagged1小RNA干扰组内皮细胞Jagged1蛋白吸光度相对值明显降低（0.26±0.02 vs 0.67±0.02, P<0.05）;PDGF+空载体组平滑肌［3H］-TdR 掺入量和迁移数与PDGF组相比无明显差异,PDGF+Jagged1小RNA干扰组平滑肌［3H］-TdR 掺入量和迁移数高于PDGF组{［3H］-TdR 掺入(23 074±2 702)counts·min-1·well-1 vs (16 442±1 803)counts·min-1·well-1,n=5,P<0.05;迁移(27±4)cells/field vs (15±3) cells/field, n=5,P<0.05};PDGF+空载体组平滑肌α-SM-actin蛋白表达与PDGF组相比无明显差异,PDGF+Jagged1小RNA干扰组平滑肌α-SM-actin吸光度相对值低于PDGF组（0.25±0.06 vs 0.49±0.04, n=3,P<0.05）。结论: 内皮细胞Jagged1下调促进PDGF诱导的平滑肌细胞增殖迁移,提示血管内皮细胞Jagged1表达在维持平滑肌收缩表型、抑制平滑肌过度增殖迁移中起一定调控作用。     

Induction of endothelin-1 expression by oxidative stress in vascular smooth muscle cells

Atherosclerosis is based on endothelial dysfunction leading to impaired vasomotor function. This is partially due to nitric oxide (NO) depletion caused by oxidative stress. Since the vasoconstrictor endothelin-1 (ET-1) might also be involved in endothelial dysfunction, we investigated whether oxidative stress regulates ET-1 expression in vascular smooth muscle cells (VSMC). Human aortic VSMC were treated with H₂O₂ (200 μM) for up to 8 h. mRNA expression of preproendothelin (prepro-ET) was analyzed by RT-PCR. ET-1 protein and the marker for oxidative stress, 8-isoprostane, were determined by ELISA. Activity of cytosolic phospholipase A2 (cPLA₂) as an indicator of ET-1 autocrine activity was measured photometrically. Stimulation of VSMC with H₂O₂ resulted in increased expression of prepro-ET mRNA after 1 h with a maximum after 6 h (fourfold), similar to treatment with angiotensin II. ET-1 protein was significantly increased by H₂O₂ treatment with a maximum after 8 h (P<.05). This effect was inhibited by the antioxidants resveratrol (100 μM) and quercetin (50 μM). In quiesced VSMC, incubation with H₂O₂-conditioned medium resulted in increased cPLA₂ activity compared to the controls (P<.05). This activity was partially inhibited by the ET_A-receptor antagonist, PD 142893 (10 μM), indicating functional ET-1 in the conditioned medium. The presence of oxidative stress in H₂O₂-treated VSMC was associated by significantly increased formation of 8-isoprostane (P<.05). The data indicate for the first time that oxidative stress increases ET-1 generation and autocrine ET-1 activity in VSMC, a mechanism that might contribute to endothelial dysfunction in atherosclerosis.     

剪切力条件下血管内皮细胞与平滑肌细胞的相互作用

血管内皮细胞(endothelial cells,ECs)与平滑肌细胞(smooth muscle cells,SMCs)是血管壁的主要细胞,它们之间的相互作用在维持血管正常的生理功能以及心血管疾病的发生发展过程中至关重要。为真实模拟ECs与SMCs体内条件下的位置关系与生长状态,人们建立了多种共培养系统。介绍当前几种常用的能够加载流动剪切力的共培养系统,并分别比较其优势与不足;简要总结剪切力条件下ECs与SMCs相互作用对ECs与SMCs表型与分布、SMCs生长与迁移、ECs表面相关黏附分子表达的影响。研究表明,一氧化氮(NO)、细胞因子、microRNA等可以作为信号分子介导ECs与SMCs之间的相互作用。     

Electrical coupling between smooth muscle cells and endothelial cells in pig coronary arteries

 The control of smooth muscle cells by endothelial cells has been well established by the identification of vasoactive factors released by the endothelial cells. In contrast, the possibility that smooth muscle cells influence the endothelial cells has been considered rarely. Some results suggest possible electrical communication between the smooth muscle and the endothelial cells but proof is lacking. We therefore tested for electrotonic conduction of signals from smooth muscle cells to endothelial cells. The endothelium was removed from half of a strip of porcine coronary artery. In a partitioned chamber, rectangular hyperpolarization or depolarization was applied to the de-endothelialized region by field stimulation. The resulting membrane potential changes in the smooth muscle cells spread electrotonically along the media into the area with intact endothelium. We recorded from endothelial cells to determine whether this electrical signal spreads into endothelial cells. Hyperpolarization or depolarization initiated in smooth muscle cells was recorded consistently in endothelial cells. This demonstrates a functional electrotonic propagation from smooth muscle to endothelial cells. Received: 23 May 1996 / Received after revision: 3 September 1996 / Accepted 16 September 1996     

Insulin enhances angiotensin II induced DNA synthesis in vascular smooth muscle cells of the rat

Summary Hypertension has a high prevalence among subjects with decreased insulin sensitivity and/or hyperinsulinemia. Furthermore, angiotensin II plays a pivotal role in the regulation of vascular tone and is known to induce hypertrophy and/or hyperplasia in vascular smooth muscle cells. In the present study, the effect of insulin on angiotensin II induced smooth muscle cell growth (Wistar-Kyoto rat) was investigated. Cell growth was assessed by the measurement of [³H]thymidine incorporation into cell DNA. Insulin in a concentration range of 1.7 × 10^–10–1.7 × 10^–6 M lacked any effect on cell DNA synthesis. However, insulin enhanced the angiotensin 11 induced DNA synthesis in a concentration-dependent manner. This effect was similar in cells with a weak and in cells with a marked response in DNA synthesis to stimulation with 100 nM angiotensin 11. In conclusion, insulin is able to enhance angiotensin 11 induced DNA synthesis and may therefore function as a growth cofactor in vascular smooth muscle cells.Abbreviations AngII angiotensin II - EGF epidermal growth factor - bFGF basic fibroblast growth factor - PDGF-BB platelet-derived growth factor-BB - VSMC vascular smooth muscle cells Dedicated to Prof. Dr. N. Zöllner on the occasion of his 70th birthday     

Stem cell therapy targets the neointimal smooth muscle cells in experimentally induced atherosclerosis: involvement of intracellular adhesion molecule (ICAM) and vascular cell adhesion molecule (VCAM)

Smooth muscle cells (SMCs) are currently considered a central pivotal player in pathogenesis and development of atherosclerotic lesions. As consequence of vascular injury, SMCs migrate from the tunica media into the tunica intima layers where they contribute to neointimal formation by converting into foam cells and producing pro-inflammatory and oxidative stress markers. We targeted the replacement of neointimal SMCs by using the mesenchymal stem cells (MSCs) therapy in experimentally induced atherosclerosis in an attempt to improve the atherosclerotic lesion and its concomitant complications. Rats were divided into 4 groups (n=20). Control group: rats kept on a standard chow diet; atherosclerotic group: rats received the atherogenic diet; stem cells-treated group: rats were injected with CD34⁺ stem cells (6×10⁶ cells in 0.5 mL PBS in rat tail vein) and maintained on the atherogenic diet; and resveratrol-treated group: rats were supplemented orally with resveratrol at a dose level 3 mg/kg per day and the atherogenic diet. After 12 weeks, rats were euthanized, blood samples were collected for separation of serum, and abdominal aortas were excised for further biochemical, molecular, and histopathological investigations. We used resveratrol, the well-established anti-atherosclerotic drug, as a benchmark to assess the efficacy of stem cell therapy. MSCs treatment revealed significant amelioration in both histopathological and biochemical patterns as evidenced by decreased foam cells formation, ICAM-1, VCAM, M-CSF, iNOS, COX-2, and TNF-α. We concluded that MSCs therapy significantly replaced the neointimal SMCs and decreased adhesion molecules as well as the oxidative and inflammatory markers in atherosclerosis.     

过氧化物酶体增殖物激活受体γ对血管平滑肌细胞增殖和动脉粥样硬化形成的影响

目的观察过氧化物酶体增殖物激活受体γ(PPARγ)在动脉粥样硬化形成中的作用,检测其对血管平滑肌细胞(VSMC)增殖的影响,探讨其抗AS的分子机制。方法高脂饮食制作兔动脉粥样硬化模型,石蜡切片HE染色检测AS病变程度。MTT法测定VSMC增殖率,Westernblot检测PPARγ和MMP-9蛋白含量。结果高脂喂养导致兔血清中TC、TG和LDL水平升高,AS斑块形成,吡格列酮可对抗高脂饮食诱导的AS。主动脉粥样斑块中的PPAR-γ蛋白表达较对照组显著增多。吡格列酮可抑制AngⅡ诱导的VSMC增殖,并使高脂喂养的兔主动脉和VSMC中的MMP-9表达减少。结论PPARγ是调节AS的关键分子,被激动剂吡格列酮激活后可能通过下调MMP-9的表达,抑制VSMC的增殖而起到抗AS的作用。     

microRNA-133b在低切应力诱导血管内皮细胞影响血管平滑肌细胞增殖中的作用

目的研究血管内皮细胞(endothelial cells,ECs)直接感受低切应力刺激后分泌类胰岛素生长因子-1(insulinlike growth factor-1,IGF-1)影响血管平滑肌细胞(vascular smooth muscle cells,VSMCs)增殖这一过程中microRNAs(miRs)的作用。方法用平行平板流动腔系统对ECs施加1.5 Pa正常切应力(normal shear stress,NSS)和0.5 Pa低切应力(low shear stress,Low SS),Real-time PCR检测VSMCs的miRs变化。用miRs预测网站预测miR-133b靶基因并验证。Western blotting检测核糖核酸结合蛋白1(polypyrimidine tract binding protein 1,Ptbp1)和N-myc下游调节基因1(N-myc downstream regulated 1,Ndrg1)的蛋白水平变化。Ed U流式检测miR-133b对VSMCs增殖的影响。结果 IGF-1静态刺激后,VSMCs的miR-133b和miR-378a表达上升。Low SS条件下,VSMCs的miR-133b表达显著上升,miR-378a表达无明显变化。下调VSMCs的miR-133b表达,Ptbp1、Ndrg1的mRNA水平均显著升高,上调VSMCs的miR-133b的表达,Ptbp1、Ndrg1的mRNA和蛋白水平显著降低,并且显著促进VSMCs增殖。结论在Low SS条件下ECs分泌IGF-1可能通过调控联合培养VSMCs的miR-133b和靶基因Ptbp1和Ndrg1促进VSMCs增殖。研究结果为心血管疾病治疗提供了一个新的潜在靶标。     

p38促进尼古丁诱导的大鼠血管平滑肌细胞的细胞外基质表达

目的 探讨尼古丁对大鼠胸主动脉血管平滑肌细胞(VSMCs)的细胞外基质(ECM)表达的影响及可能的机制.方法 用终浓度为100μmol/L的尼古丁作用于体外培养的大鼠VSMCs 24 h,以不加尼古丁的细胞为对照组,采用反转录-聚合酶链式反应(RT-PCR)、免疫印迹(Western blotting)方法检测ECM包括Ⅰ型胶原、纤维黏连蛋白和膜受体整合素表达的差异,以及可能参与信号转导的蛋白激酶p38的活性变化.结果 与对照组相比,尼古丁刺激组细胞的两种细胞外基质包括I型胶原和纤维黏连蛋白及膜受体整合素β1的表达均升高,分别为对照组的1.8倍、1.7倍和1.6倍,差异显著(P<0.05);尼古丁刺激组的蛋白激酶p38的活性比对照组高1.95倍,差异极其显著(P<0.01);p38的活性被特异抑制剂SB202190抑制后,尼古丁诱导的I型胶原的表达也随之下降.结论 p38参与尼古丁诱导的细胞外基质的高表达.     

罗格列酮对胰岛素诱导的兔血管平滑肌细胞增殖的影响

目的：观察罗格列酮对胰岛素诱导的兔胸主动脉血管平滑肌细胞增殖的影响。方法:以组织块法原代培养兔胸主动脉血管平滑肌。采用细胞计数法测定细胞增殖，［3H］-TdR掺入法反映细胞DNA累积合成量。用RT-PCR方法测定蛋白激酶C mRNA含量。结果:罗格列酮对正常生长的细胞数目和掺入量无明显影响，与胰岛素组相比，1、5和10 μmol/L罗格列酮减少细胞数目分别为39.8%、46.9%和57.9%（P<0.01）；减少［3H］-TdR掺入量分别为29.6%、43.4%和53.8%（P<0.01）；对胰岛素诱导的a-PKC的表达上调无明显影响。结论:罗格列酮呈剂量依赖性抑制胰岛素诱导的平滑肌细胞的增殖。。     

γ粒子核素支架影响血管平滑肌细胞增殖与凋亡的实验研究

目的： 观察γ粒子钯-103［103Pd］核素支架对损伤血管中膜平滑肌细胞增殖与凋亡的影响。探讨核素支架防治支架内再狭窄的作用机制。方法： 选用雄性新西兰兔50只，随机分为普通支架组及核素支架组，设正常对照。分别于术后3、7、14、28及56 d取材，进行病理形态学、免疫组化（增殖细胞核抗原PCNA）、细胞凋亡(TUNEL)及原位杂交(bcl-2 mRNA及bax mRNA)的观察。结果： ①光镜下发现，核素支架组管腔狭窄程度明显低于普通支架组，术后第56 d最显著（P<0.01）；②免疫组化显示，术后3-28 d核素支架组PCNA表达均低于普通支架组，7 d为表达高峰，16.35%±0.79% vs 24.36%±0.55%(P<0.01)。③ TUNEL法检测发现术后3-28 d，核素支架组的平滑肌细胞凋亡较普通支架组更明显，术后第7 d达峰值，14.72%±0.53% vs 12.42%±1.13%（P<0.01）。④ PCNA阳性率与TUNEL法测得的细胞凋亡阳性率比率PCNA/apoptosis（P〖KG*6〗∶〖KG-*2〗A）显示，核素支架组 P〖KG*6〗∶〖KG-*2〗A 的值在术后3-28 d均显著小于普通支架组(P<0.05)。⑤原位杂交测定凋亡相关基因bcl-2 mRNA及bax mRNA表达并计算其比值显示，普通支架组术后第3、14、28 d均大于对照组(P<0.01)，核素支架组与对照组无显著差异(P>0.05)。术后第3-28 d，核素支架组的比值均小于普通支架组(P<0.05)。结论： γ粒子核素支架通过抑制平滑肌细胞的增殖，促进凋亡，使增殖与凋亡的比率降低，从而减轻再狭窄的程度。     

Isolation and characterization of human smooth muscle cells from umbilical cord vein and their reconstitution in a vascular co-culture model with underlying endothelial cells

Smooth muscle cells have been isolated from human umbilical cord veins, characterized and cultured for the development of an endothelialsmooth muscle cell co-culture system. After harvesting endothelial cells, the umbilical cords were trimmed of amnion, connective tissue and arteries, split into pieces, cut open longitudinally and placed with the luminal surface of the explant down onto a culture plate, without the use of proteolytic enzymes. Adherent primary cells were sequentially passaged and various cytological/biochemical characterizations were performed between passages 2 and 10. Cells stained positive for antibodies against smooth muscle actin, negative for antibodies against factor VIII and displayed typical hill and valley morphology when confluent. Cell proliferation was stimulated and supported in a concentration-dependent manner by both human serum and fetal bovine serum over the range 1%–20%. The use of human serum at concentrations >10% decreased the population doubling time during exponential growth by circa 50%. The cells were also characterized by high seeding efficiencies (>70%) and retained their diploid karyotype for up to 3 months in culture. Endothelial cells and smooth muscle cells prepared from umbilical veins were then seeded at varying densities onto either side of porous tissue culture inserts coated with fibronectin. Utilising the measurement of electrical resistance, the optimal seeding density of 5×10⁴ cells/cm² for each cell type gave maximal resistance across the cell bi-layer already after 24 hours, which remaining essentially unaltered for up to 4 days of culture and which was always substantially higher than the resistance of filters seeded only with endothelial cells on one side. This was not substantially affected either by increasing passage of the HUVSM cells cultured with a fixed passage of endothelial cells, or by varying the donor origin of the endothelial cells. In terms of functionality of the selective permeability of the model, the calcium ionophore ionomycin (25 M), added to the endothelial side of the bi-layer, caused a 30% reduction in the electrical resistance across the co-culture within 60 minutes, with control resistance being re-established within 1 hour of removal of the ionophore by washing. These results clearly indicate that smooth muscle cells and endothelial cells prepared from the same human blood vessel can be reconstituted into a functional vascular model suitable for the study of biochemical, physiological and toxicological phenomena in the human vascular wall.Abbreviations BCA bicinchoninic acid - BSA bovine serum albumin - DMEM DMEM medium supplemented with 4.5 g/l glucose, 100 IU/ml penicillin, 100 g/ml streptomycin and 1.25 g/ml fungizone - DMEM-1 DMEM supplemented with 20% FBS, 300 IU/ml penicillin, 300 g/ml streptomycin and 3.75 mg/ml fungizone - DMEM-2 DMEM supplemented with 20% FBS, 100 IU/ml of penicillin, 100 g/ml of streptomycin and 1.25 g/ml of fungizone - DMSO dimethyl sulfoxide - FBS fetal bovine serum - HPF human pulmonary fibroblasts - HS human serum - HUVE human umbilical vein endothelial - HUVSM human umbilical vein smooth muscle - M199 M199 medium supplemented with 20% HS, 100 IU/ml penicillin, 100 g/ml streptomycin, 1.25 g/ml fungizone and 2 mM L-glutamine - P passage number - PBS phosphate buffered saline - TCA trichloroacetic acid - vwF von Willebrand factor (factor VIII)     

Active cytomegalovirus infection in aortic smooth muscle cells from patients with abdominal aortic aneurysm

Cytomegalovirus (CMV) is associated with atherosclerosis and transplant vascular sclerosis. The aim of this study was to explore the hypothesis that active CMV infection in the vessel wall could be associated with abdominal aortic aneurysm (AAA). We examined the prevalence of CMV in AAA specimens from 22 patients undergoing surgery and, in five cases, characterized the function of smooth muscle cells (SMCs) from the aneurysm in vitro. Twenty-one (95%) of the 22 AAA specimens were CMV positive by a polymerase chain reaction assay, in situ hybridization, or a highly sensitive immunohistochemical staining technique. No positive cells were found in aortas from three CMV-seronegative organ donor cadavers. CMV immediate-early and late antigens were expressed in SMCs in the lesions and were associated with 5-lipoxygenase (5-LO) expression. CMV-positive intimal SMCs migrated 6.6 ± 1.5 times more efficiently than CMV-negative medial SMCs (p < 0.05). In vitro CMV infection of medial SMCs resulted in a 3.2 ± 1.2 times increase in migration (p < 0.05). The intimal migration was significantly inhibited by antibodies against basic fibroblast growth factor (bFGF; p < 0.05) in a dose-dependent fashion. Antibodies against platelet-derived growth factor (PDGF)-AB, insulin-like growth factor 1, vascular endothelial growth factor (VEGF), RANTES, monocyte chemoattractant protein 1 (MCP-1), macrophage inflammatory protein (MIP)-1α, or interleukin-1β did not significantly affect intimal SMC migration. However, intimal and medial SMCs secreted similar amounts of bFGF, MCP-1, MIP-1α, RANTES, PDGF-AB, PDGF-BB, epidermal growth factor, and VEGF. CMV infection in vitro of intimal and medial cells did not result in significant changes of bFGF or MCP-1 secretion. Since CMV infection can affect several functional parameters in SMCs, including several key factors in infected SMCs, our findings provide support for the hypothesis that CMV contributes to the pathogenesis of abdominal aortic aneurysm. Electronic supplementary material  The online version of this article (doi:) contains supplementary material, which is available to authorized users. Sara Gredmark-Russ and Mensur Dzabic contributed equally to this work and share first co-authorship.     

大黄素对人血管平滑肌细胞增殖的影响

目的 观察大黄素对人血管平滑肌细胞周期时相和cyclin D1表达的影响,探讨大黄素抑制平滑肌细胞增殖的作用机制。方法 取对数增长期的平滑肌细胞同步于G0期,药物组:加入含37.5mg·L-1大黄素10％胎牛血清的培养液,对照组:仅加入10％胎牛血清的培养液;作用12、24、36、48 h后分别用流式细胞仪和Westemblot法进行细胞周期时相和cyclin D1表达的测定。结果 与对照组比较,药物组在各相同时间点C0/G1期细胞百分比升高,S期细胞百分比下降,且随着时间的延长差值增大,cyclin D1表达高峰延迟,表达量下调,细胞周期受阻于G0/G1期。结论 大黄素在抑制平滑肌细胞增殖的过程中通过下调,cyclin D1表达,从而阻滞细胞周期进程。     

黄芪多糖对高糖所致血管平滑肌细胞增殖变化的影响

目的: 旨在观察体外高糖环境对大鼠主动脉血管平滑肌细胞(VSMCs)所致的增殖变化以及黄芪对其的影响。方法: 原代培养VSMC,分为正常对照组、25 mmol/L高糖剌激组、高糖剌激加低、中、高浓度黄芪多糖组(终浓度分别为100、200 和400 mg/L)。MTT方法分析细胞增殖率,RT-PCR检测分析MKP-1 mRNA转录及用ELISA法检测炎症因子MCP-1水平。结果: 与对照组相比高糖可以诱导VSMCs增殖(P<0.05),而中、高浓度黄芪多糖可以显著抑制该作用(P<0.05);高糖环境明显下调MKP-1 mRNA表达(P<0.05),但低浓度黄芪多糖可使MKP-1 mRNA上调,恢复到正常水平,在中、高浓度黄芪多糖时可使MKP-1 mRNA上调,显著高于对照组;高糖刺激组可促使VSMCs MCP-1分泌明显升高,低浓度黄芪即可降低高糖诱导MCP-1的水平(P<0.05),在高浓度组最明显。结论: 黄芪多糖防治糖尿病心血管并发症的作用可能与上调MKP-1 mRNA表达、抑制VSMCs增殖和MCP-1分泌相关。     

流感病毒感染致大鼠血管平滑肌细胞功能变化的研究

目的 探讨流感病毒(H1 N1)感染血管平滑肌细胞后,血管平滑肌细胞的数量、增殖率、凋亡率及分泌相关细胞因子的变化,从细胞水平探讨流感病毒感染在动脉粥样硬化形成中的作用以及可能的机制.方法 分别通过细胞计数试验、流式细胞术和酶联免疫吸附试验,检测未感染病毒的细胞(对照组)和病毒感染后细胞(实验组),在不同时段(0h、6h、12h、24h、48 h)血管平滑肌细胞增殖率、凋亡率和分泌IL-6、sFas、血小板衍生生长因子(platelet-derived growth factor,PDGF)的变化情况.结果 实验组0h血管平滑肌细胞增殖率和凋亡率分别为10.39％和0.44％;6 h后细胞增殖率(12.68％)和凋亡率(0.73％)均增加;12 h增殖率达到高峰(18.01％),凋亡率反而降低(0.14％);24 h后增殖率下降(12.89％),凋亡率明显增加(1.09％);48 h增殖率进一步降低(7.07％),凋亡率达到高峰(4.61％).各时期的细胞增殖率和凋亡率与0h比较,差异具有统计学意义(P＜0.05).细胞数量、IL-6、sFas、PDGF均在感染12～18 h达到分泌高峰,随后下降.实验组每个时间点的细胞数量,细胞因子的分泌量与0h比较,差异均有统计学意义(P＜0.05).结论 流感病毒感染血管平滑肌细胞后,使平滑肌细胞增殖、凋亡发生紊乱,由此提示流感病毒感染可能参与动脉粥样硬化的形成和发展,同时细胞因子在其中发挥重要的作用.