Relationship between expression of type Ⅲ collagen and phenotype of vascular smooth muscle cells in neointimal of stented coronary artery

Objective To investigate the secretive features of type Ⅲ collagen in restenosis of the stented coronary artery and the relationship between the expression of type Ⅲ collagen and vascular smooth muscle cells (VSMCs). Methods An animal model of restenosis was established by implanting oversized tantalum stents into the coronary arteries in 26 dogs. At the 7th, 14th and 28th days after implantation, the stented coronaries were harvested. Transmission electronic microscopy and immunohistochemistry were employed to investigate the features of type Ⅲ collagen secretion and VSMCs’ phenotype. The expression of type Ⅲ collagen was quantified and compared for the three stages. Results Migration and proliferation of VSMCs were the main features at the 7th day after injury. At the 14th day, proliferation of VSMCs reached the peak while much more secretion of collagen was noticeable. VSMCs began to transform from the synthetic phenotype to the contractile phenotype at the 28th day, when a great quantity of collagen was also secreted. The quantity of secreted type Ⅲ collagen was greater at the 14th and 28th day than that at the 7th day (P<0.05). The stain density of type Ⅲ collagen was positively correlated to neointimal thickness at both of 14th and 28th day. Conclusion The pathological bases of restenosis are variant in different period of restenosis formation. Type Ⅲ collagen may play an important role in the late stage of restenosis after coronary stenting.     

EXPRESSION OF TISSUE-TYPE PLASMINOGEN ACTIVATOR IN SMOOTH MUSCLE CELLS OF INJURED ILIAC ARTERIES IN RABBITS

In this experiment, expression of tissue-type plasminogen activator (t-PA) in smooth muscle cells(SMCs) was measured at different iutervals after the arterial injury. In the normal lilac arteries, only low levels of t-PA activity were estimated, t-PA activity in extracts of the iliac arteries increased significantly at the 4th day after the injury, equivalent to the process that SMCs migrated from the media to the intima,and the t-PA activity was then decreased approximately to the normal level at the 7th day. Coexistent to the above data, results from in situ hybridization showed that the expression of t-PA mRNA in the intimaas well as media increased also significantly nr the 4th day after the arterial injury, and at the 7th day, t-PA mRNA was detected only in those SMCs locating closely adjacent to the internal elastic lamina. These results suggest that t-PA might play an important role in SMC migration following endothelial injury, and antagcaaism of t-PA expression and/or activity within the vessel wall might be helpful in intervening the devnlopment of restenosis following angioplasty.     

Effects of magnesium sulfate on neuron apoptosis and expression of caspase- 3， bax and bcl-2 after cerebral ischemia-reperfusion injury

Objective To investigate the effects of magnesium sulfate on neuron apoptosis and the expressions of caspase-3,bax and bcl-2 after cerebral ischemia-reperfusion injury. Methods Thirty-six gerbils were randomly divided into three groups: Sham-operation group (So, n=12), ischemia-reperfusion group (I-R, n=12) and magnesium sulfate group (Ms, n=12). The neuron apoptosis was detected by the terminal deoxynucleotidyl transferase (TdT)-mediated dUTP-fluorescence nick end labeling (TUNEL stain), and the protein expressions of caspase-3, bax and bcl-2 were detected by immunohistochemisty stain.Results Apoptotic neurons and the expressions of caspase-3 and bax were significantly increased in I-R and Ms groups, compared with those in So group. Apoptotic neurons and the expressions of bax and caspase-3 in Ms group were significantly less than those in I-R group. There was no significant difference in the expression of bcl-2 among three groups.Conclusions Magnesium sulfate decreases neuron apoptosis after cerebral ischemia-reperfusion injury, which may be related with the suppressed expressions of caspase-3 and bax.     

The Role of NF-kB and I-kB in Intimal Proliferation Following Balloon Catheter-induced Injury in the Rat Carotid Artery

The aim of our study was to gain insight into the molecular and cellular mechanisms of post-angioplasty restenosis using balloon catheter-induced injury model in the rat carotid artery. SD rats were subjected balloon catheterization at one side carotid artery as study group and another side as control group. Six rats were killed on the 6 h, and 3rd, 7th, 14th, 28th day after balloon-induced injury respectively. The intimal thickness and the expression of NF-κB and I-κB were detected by HE-staining, gel electrophoretic mobility shift assay （EMSA） and Western-blot methods. The results showed that： （1） The thickening of intima was observed on the 3rd day after balloon-induced injury, and it became more significant on the 7th, 14th and 28th day. The area ratio of intima/media was increased significantly （P〈0.05）; （2） The expression of NF-κB was not detectable in the control group, however, in study group, the expression of NF-κB was detected on the 6th h after balloon-induced injury, reached the peak on the 14th day, and on 28th day, strong expression of NF-κB was observed; （3） The expression of I-κB protein was reduced after balloon-induced injury, and there were significant differences between the study group and the control group （P〈0.05）. It was concluded that the alteration of NF-κB/I-κB system might play an important role in aberrant proliferation within the intima and vascular remodeling following vascular injury. To block NF-κB activation and its role in arterial restenosis initiation may potentially provide a novel therapeutic tool for the treatment and prevention of arterial restenosis.     

Experimental Study of Adenovirus Vector Mediated-hVEGF165 Gene on Prevention of Restenosis after Angioplasty

This study evaluated the effects of adenovirus vector mediated human vascular endotheli-al growth factor-165 (hVEGF165) gene on prevention of restenosis after angioplasty. Rabbit models of bilateral carotid artery injury were established by balloon denudation. The recombinant adenovi-ruses containing hVEGF165 cDNA was directly injected into left side of the injured carotid arteries.On day 3 and week 3 after transfection the expression of VEGF was observed by RT-PCR and im-munohistochemistry. The thrombokinesis, reendothelialization (rET) and intimal hyperplasia in ca-rotid arteries were evaluated by computerized image analysis system 3 weeks after gene transfer,The changes in the VEGF gene-treated side were compared with the control side. Our results showed that 3 days and 3 weeks after hVEGF165 gene transfer the VEGF mRNA and antigen ex-pression were detected in vivo. 3 weeks after the transfer, the carotid artery rET was markedly better in the VEGF gene-treated group compared with the control. The thrombokinesis, intima are-a/media area (I/M), maximal intimal and medial thicknesses (ITmax and MTmax) demonstrated a statistically significant decrease in arteries treated with VEGF gene as compared with the control group. It is concluded that VEGF gene transfer could be achieved by intra-arterial injection of re-combinant adenoviruses. It might accelerate the restoration of endothelial integrity, inhibit throm-bokinesis and attenuate intimal hyperplasia in the injured arteries after VEGF gene transfer. This procedure could be useful in preventing restenosis after angioplasty.     

INHIBITORY EFFECT OF FLUVASTATIN ON AORTIC INTIMAL THICKENING IN NORMOCHOLESTEROLEMIC RABBITS

Objective, The anti-atherosclerotic effect of fluvastatin at doses insufficient to lower serum cholesterol on the catheter-induced intimal thickening and possible mechanism were investigated in abdominal aorta of rabbits. Methods. Fifty-six rabbits were randomly divided into eight groups( n = 7, each). Fluvastatin was given mixed with food at daily dose of 8mg/kg starting 5 days before catheterization. Light microscope, immanohistochemistry, transmis-sion electron microscope and RT-PCR assay were applied to assess vascular smooth muscle cell (VSMC) proliferation and apoptosis, as well as oncogene expression in vascular wall. Results. At day 10 and day 15 after catheter induced denudation intima/media( I/M) thickness ratio was obviously higher, and also the percentage of PCNA-positive cells and TUNEL-positive cells in media was significantly higher compared with controls. The intimal hyperplasia was mostly composed of α-SM-actin-pesitive cells. In rabbits given flu-vastatin I/M ratio and the percentage of these positive cells significantly decreased compared with those without fluvas-tatin.The overexpression of proto-oncogene H-ras mRNA and decreased expression of anti-oncogene p53 mRNA were found after vascular injury, whereas fluvastatin significantly reduced H-ras mRNA and increased p53 mRNA expres-sion. Conclusion. Proliferation of VSMC in the media and the migration to the intima can be inhibited, and apoptosis of VSMC be induced by short-term use of fluvastatin after balloon catheter denudation, independent of serum lipid change. The underlying mechanism is presumably associated With the influence of fluvastatin on oncogene expression in the injured vascular Wall.     

CHANGES OF IMMUNE FUNCTIONS AFTER RADIATION, BURNS AND COMBINED RADIATION-BURN INJURY IN RATS

The changes ot several immune functions were observed in rats after they were inflicted with 6 Gy gamma rays irradiation, 15% TBSA full thickness hrun and the combination of the 2 injuries. It was found that the ftmcldons of thymocytes and epienocytes suffered the most severe suppressinn in the 24th to 72nd hour after radiation injury and began to recover on the 7th day. In the rats with burn injury, the suppression on thymocytes and splenocytes were significantly less severe than that after radiation and recovered more rapidly. The effects of combined rediation-bura injury showed several characteristics. The suppression on the thymocytes was more severe with slower recovery as compared with that after single radiation injury only. The suppression on the splenocytes as a whole was similar to that after single radiation injury, but in the early stage after combined injury, the suppression was far more severe than that after radiation. Escharectccny and skin grafting on the burn wounds on the lst day after combined injury could accelerate the recovery on both the thymocytes and eplenocytes. Our findings indicated that the severity of the suppression on the immune functions due to combined radiadon-burrt injury might depend on the size of the burn wounds.     

The Expression of Cyclins in Neurons of Rats after Focal Cerebral Ischemia

The change of the expression of Cyclins in neurons of rats after focal cerebral ischemia was investigated. Ischemia was induced by temporary middle cerebral artery occlusion （MCAO）. The experimental rats induced by MCAO were sacrificed on 7th and 14th day after reperfusion. The brain was taken out at 7th and 14th day after injury, and the expression of Cyclin D1, E, A and B1 in neurons of cerebral cortex or hippocampal CA1 region was detected by immunofluorescence and confocal microscope. The results showed that after MCAO, in the ipsilateral CA1 subfield of hippocampus the expression of Cyclin D1, E, A and B1 in neurons was significantly gradually up-regulated at 7th and 14th day after reperfusion （P〈0.05） as compared with that in control group. In the ipsilateral cerebral cortex the expression of Cyclin D1 and B1 in neurons was notably gradually down-regulated at 7th and 14th day, and that of Cyclin E and A was significantly up-regulated at 14th day after reperfusion as compared with that in control group （all P〈0.05）. It was concluded that there was a differential sensitivity among neurons from different brain regions to ischemic injury. But all of them re-enter into cell cycle after MCAO.     

Rhubarb extracts in treating complications of severe cerebral injury

Objective To investigate the therapeutic effects of the Chinese medicinal herb, Rhubarb, on severe brain injury.Methods Rhubarb extracts in ethyl alcohol and water were used to treat 20 patients with severe cerebral injury complicated by hyperthermia, renal failure, hemorrhage in the upper digestive tract, and increased intracranial pressure.Vital signs, variations of Glasgow coma scale (GCS) and intracranial pressure (ICP) of the patients were observed.The degree of hemorrhage in the digestive tract and the change in creatinine value were also observed.Other 20 patients served as controls.Results The result of the treatment group was more marked than that of the control group.Three days after administration of the rhubarb extract, the body temperature decreased by 1.1℃, ICP by 0.4kPa (1mmHg=0.1333kPa) on average, and the incidence of hemorrhage in the digestive tract by 30%.The volume of hemorrhage of the digestive tract decreased by 700±250ml, and the time for turning occult blood to negative by 10%.Conclusion The Chinese medical herb, rhubarb, has multiple therapeutic effects on severe brain injury.     

An experimental study of endovascular brachytherapy using liquid32P filled balloon catheter

Objective To observe the effect of endovascular brachytherapy on the prevention of restenosis after interveneional therapy and to investigate its possible mechanisms. Methods In the balloon injuried rabbit model,pathological sections of iliac arteries were observed and the changes of vascular histomorphology were estimated by computer analysis of photomicrograms. Using immunohistochemical techniques, proliferating cell nuclear antigen （PCNA） was quantified to assess the proliferation of vascular smooth muscle cells. Results After rabbit iliac arteries were injured by balloon overstretch angioplasty, neointima were shown to be less proliferative in the irradiated group than in the control group, from PCNA scores. The formation of neointima was suppressed with the external elastic laminar area increasing and without the luminal area decreasing in the irradiation group. Conclusion Endovascular brachytherapy using a liquid (32)P filled balloon catheter system could prevent restenosis possibly by inhibiting the formation of neointima and improving positive vascular remodeling.     

EXPRESSION OF TISSUE－TYPE PLASMINOGENACTIVATOR IN SMOOTH MUSCLE CELLS OF INJUREDILIAC ARTERIES IN RABBITS

ＥＸＰＲＥＳＳＩＯＮＯＦＴＩＳＳＵＥ－ＴＹＰＥＰＬＡＳＭＩＮＯＧＥＮＡＣＴＩＶＡＴＯＲＩＮＳＭＯＯＴＨＭＵＳＣＬＥＣＥＬＬＳＯＦＩＮＪＵＲＥＤＩＬＩＡＣ　ＡＲＴＥＲＩＥＳＩＮＲＡＢＢＩＴＳＭａＸｉａｏｌｉ；（马晓莉），ＨｕａｎｇＷｅｎｙｉｎｇ；（黄文...     

血管内放射对猪受损髂动脉平滑肌细胞增殖与凋亡的影响

目的 :观察血管内放射照射对猪髂动脉球囊损伤后血管新生内膜平滑肌细胞(SMC)增殖与凋亡的影响。方法 :2 7头小型猪分为 3组 ,所有猪行髂动脉球囊过大扩张 ,通过后装装置将 1 0Gy和 2 0Gy的192 Ir放射源分别置于 9只猪受损髂动脉部位 ,其他 9只猪的受损髂动脉作为对照。每组的 9头猪分别术后 3天、1 0天和 2 8天分 3次处死。用增殖细胞核抗原(PCNA)和三磷酸脱氧尿嘧啶缺口末端标记法 (TUNEL)法检测内膜SMC增殖和凋亡情况。结果 :代表血管内膜增殖的PCNA指数在 1 0天和 2 8天宰杀的猪中 ,放射治疗组明显低于对照组。术后 1 0天内膜SMC凋亡在对照组和 1 0Gy、2 0Gy组的值分别为 :(1 85± 0 49) %比 (2 2 7± 0 49) %(P >0 0 5)和 (1 85± 0 49) %比 (2 53± 0 45) %(P <0 0 5) ;术后 2 8天上述值分别为(1 61± 0 3 5) %比 (3 1 1± 0 51 ) %(P <0 0 5)和 (1 61± 0 3 5) %比 (7 0 5± 1 82 ) %(P <0 0 5) ;2 8天时 2 0Gy组的内膜SMC凋亡明显高于 1 0Gy组 (7 0 5± 1 82 ) %比 (3 1 1± 0 51 ) %(P <0 0 5)。相同的放射剂量时 ,2 8天宰杀猪的髂动脉SMC凋亡高于 1 0天宰杀猪的量。结论 :血管内γ射线照射能抑制小型猪球囊损伤髂动脉内膜SMC增殖和刺激SMC凋     

Restenosis after balloon angioplasty: role of platelets, thrombosis and smooth muscle cells proliferation]

Iliac atherosclerosis was produced in 50 New Zealand rabbits and followed by balloon angioplasty (BA) for the study of the mechanism of restenosis after BA. 41 rabbits undergoing successful dilatation were randomly grouped and killed at 30 min, 24 h, one and four weeks after BA, respectively. Histomorphological results showed that platelets adhered to the angioplastic areas 30 min after BA. At 24 h, a large quantity of platelets adhered to or aggregated at the areas to form a dense carpet of platelets and large or small thrombi, even a totally obstructive luman. At the 4th week, organized mural thrombi in lumen produced restenosis. There were plenty of foam cells and less smooth muscle cells (SMCs) in the vessel wall of atherosclerotic rabbits before BA. One week after BA, SMCs proliferated increasingly and migrated into the intima from the media at the second week. At the fourth week, SMCs proliferated markedly in the intima, forming new atherosclerotic plaque, which resulted in thickening of vessel wall and restenosis of originally angioplastic sites.     

大鼠胸主动脉血管成形术后管壁ICAM-1的表达

目的　研究血管成形术后再狭窄形成的机制。方法　 30只大鼠随机分为假手术组和球囊损伤组 ,在术后 1,3,7,14d分别处死动物 (n =6 ) ,光学显微镜检测HE染色的主动脉壁横切面的病理改变 ,免疫组化染色检测细胞间黏附分子 - 1的表达 ,并应用计算机图像分析系统进行分析。结果　球囊损伤组主动脉壁中膜和新生内膜细胞间黏附分子 - 1有高度表达。结论　细胞间黏附分子 - 1参与了血管成形术后再狭窄的发生、发展过程。     

病毒载体对大鼠移植静脉的影响

目的探讨腺病毒载体转染后对大鼠移植静脉的影响。方法选用Wistar大鼠间置移植颈静脉于同侧颈总动脉,术后移植静脉行HE染色和VG染色,观测血管内膜厚度。应用免疫组织化学染色,观察血管内膜平滑肌细胞（SMC）内增殖细胞核抗原（PCNA）表达及增殖情况。于倒置荧光显微镜,以紫外光激发观察测定腺病毒转染率。逆转录聚合酶链反应（RT-PCR）及Western蛋白印迹检测细胞间黏附分子-1（ICAM-1）、血管细胞黏附分子-1（VCAM-1）水平。结果术后3d,GFP表达较高;术后10d,GFP表达有所下降;术后30d,GFP几乎没有表达。移植术后10d试验组及对照组可见明显内膜增生。移植术后30d试验组及对照组内膜增生减轻。试验组及对照组与正常非移植静脉相比,内膜增生明显（P〈0．05）,试验组较对照组内膜增生稍明显,但差异无统计学意义。实验中正常静脉平滑肌细胞PCNA阳性细胞极少,对照组与试验组术后10d,内膜与中膜SMC的PCNA阳性细胞增多,增殖达到高峰。术后30d中膜SMC的PCNA阳性细胞明显减少。试验组及对照组与正常非移植静脉相比,PCNA阳性细胞增高明显（P〈0．05）。试验组较对照组PCNA阳性细胞稍多,但差异无统计学意义。正常静脉ICAM-1、VCAM-1的mRNA和蛋白表达很少,对照组移植后3d部分细胞即出现阳性表达,10d表达最强,30d仍较高。与正常静脉组比较,差异有统计学意义（P〈0．05）。试验组较对照组表达更高,但与对照组比较,差异无统计学意义。结论腺病毒载体能高效地进行体内基因转移,作用时间短暂。腺病毒载体促进移植静脉的血管内SMC活化、增多、血管内膜增生、ICAM-1、VCAM-1的表达的增加,腺病毒转染到移植静脉血管壁后产生炎症、内膜增生等效果,混淆了目的基因的效果。     

球囊损伤术建立血管再狭窄鼠模型

目的 建立大鼠颈动脉球囊损伤血管再狭窄模型,观察损伤血管的组织形态学变化.方法 雄性Wistar大鼠36只,随机分为假手术组（对照组）、损伤后1d组、损伤后3d组、损伤后7d组、损伤后14 d组、损伤后28 d组,每组6只.除假手术组其余各组均利用PTCA球囊导管损伤颈动脉建立血管再狭窄模型,用光学显微镜观察损伤后不同时间血管的形态学变化.结果 球囊导管损伤术使颈动脉内皮剥脱、VSMC增殖、迁移、新生内膜增生,导致管腔狭窄.损伤后7d,内膜开始增生,14 d内膜增生最显著,28 d达到最大.结论 利用PTCA球囊导管成功建立血管再狭窄鼠模型,方法科学,能满足研究血管损伤后再狭窄的需要.     

Effects of granulocyte colony-stimulating factor on repair of injured canine arteries

Background Endothelial progenitor cells （EPCs） derived from bone marrow may differentiate into endothelial cells and participate in endothelial repair. These cells can be mobilized into peripheral blood by cytokines, including granulocyte colony-stimulating factor （G-CSF）. In the present study, we investigated the effects of G-CSF on neointimal formation and restenosis in a canine model of arterial balloon injury.
Methods Sixteen male beagle dogs were injected subcutaneously with 20 μg·kg^-1·d^-1 recombinant human G-CSF （n=8） or normal saline （n=8） for 1 week. On the fifth day of treatment, the dogs underwent renal arterial angioplasty. At 8 weeks after arterial balloon injury, angiographic observations were made and injured arteries were processed for morphometric analysis of neointimal formation.
Results Peripheral white blood cell counts were increased by 3.34-fold compared to baseline on the fifth day of administration of G-CSF. Angiographies revealed that one stenosis had occurred among the eight injured renal arteries from dogs treated with G-CSF, whereas all injured renal arteries from dogs treated with normal saline remained patent. The mean extent of stenosis among injured arteries was 18.3%±17.9% in the G-CSF treated group compared to 12.5%±7.6% in the saline treated control group （P=0.10）. G-CSF treatment slightly increased neointimal thickness （0.42±0.15 mm vs 0.25±0.06 mm, P=-0.08） with an intima to media ratio of 0.83±0.49 vs 0.54±0.18 （P=0.11）.
Conclusions G-CSF treatment does not attenuate neointimal hyperplasia and restenosis formation in a canine model of renal arterial injury, suggesting that the therapeutic strategy for preventing restenosis by stem cell mobilization should be investigated further.     

水溶性壳聚糖对腹主动脉球囊损伤大鼠血管狭窄的抑制作用

[摘 要］ 目的:探讨水溶性壳聚糖（WSC）在血管狭窄方面的作用,阐明WSC对大鼠腹主动脉球囊损伤的影响,为开发防治血管狭窄的高效低不良反应药物提供实验依据。方法：75 只雄性 SD大鼠随机分 5 组：50、100和 200 mg/kg 的WSC 组、模型组和对照组（假手术组）,每组15只。采用球囊损伤大鼠腹主动脉内膜方法制备血管狭窄模型,对照组仅分离结扎右髂总动脉。造模后WSC各组经大鼠尾静脉分别注射50、100 和 200 mg/kg浓度的 WSC;模型组和对照组注射生理盐水,每次0.4 mL,每天1次。每组按 7、14 和 21 d 3个时点随机选取 5 只大鼠处死,常规HE染色制作病理切片,观察各组大鼠血管损伤形态,计算相对管腔面积,比较 WSC 对血管狭窄的抑制作用。结果：普通光学显微镜观察,对照组大鼠腹主动脉结构完整,中膜血管平滑肌细胞排列整齐。模型组大鼠在第7天时腹主动脉血管内膜增生明显;第14天时可见内膜、中膜明显增厚,管壁局限性隆起;第21天内膜增厚,以平滑肌细胞为主,中膜细胞排列紊乱,有假腔形成。与模型组比较,实验组第7天时内膜增生明显减轻,以100 和 200 mg/kg WSC组为最好;第14天时可见内膜、中膜增厚均不明显,但200 mg/kgWSC组仍可见大量排列紊乱的血管平滑肌细胞;第21天时各浓度的WSC组均表现正常,其中以200 mg/kg WSC组更为明显。管腔相对面积比较,对照组大鼠管腔面积随术后时间变化不明显（P>0.05）;模型组大鼠管腔面积在第7、14 和 21天时均减小,与对照组比较差异有统计学意义（P<0.01）。50 mg/kgWSC 组大鼠在第 14 天和第21天时,管腔面积有一定的增加,但与对照组比较差异有统计学意义（P<0.01）;100 mg/kg WSC组大鼠的管腔面积明显大于 50 mg/kg WSC 组,其中在第14 天和第21天时的管腔面积与对照组比较差异有统计学意义（P<0.05）;200 mg/kg WSC 组的管腔面积在多于 14 d时为最大,与对照组相比较差异无统计学意义（P>0.05）。各实验组不同天数之间比较差异均无统计学意义（P>0.05）。结论：WSC对大鼠腹主动脉球囊损伤后的血管狭窄有明显抑制作用,其中以200mg/kg浓度的 WSC作用14 d以上为抑制作用最强。     

通心络对犬血管成形术后细胞凋亡及C-MYC和C-FOS基因表达的影响

目的观察通心络对犬血管成形术后细胞凋亡及C-MYC和C-FOS基因表达的影响。方法24只犬建立股动脉血管成形术后血管内膜损伤模型,随机分成单纯手术对照组、通心络治疗组,每组12只,再按取材时间不同(14d和30d),随机分成2个亚组,每组6只,取损伤后血管进行光镜观察、原位细胞凋亡标记实验(TUNEL)以及C-MYC、C-FOSmRNA原位杂交实验。结果光镜下显示血管内膜增生,治疗组管腔狭窄程度明显小于对照组;TUNEL显示,治疗组凋亡细胞阳性表达强于对照组(P<0.05),以14d最为显著;C-MYC、C-FOSmRNA原位杂交实验亦显示,对照组的细胞阳性表达强于治疗组(P<0.05),以14d最为显著。结论C-MYC、C-FOS基因参与了对血管内膜细胞的调节;通心络具有促进内膜细胞凋亡及下调C-MYC、C-FOS基因表达的作用,可减轻再狭窄程度。