大黄素对肾小球系膜细胞c—myc原癌基因表达的影响

观察大黄素对肾小素系膜细胞ｃ－ｍｙｃｍＲＮＡ表达的影响，探讨大黄素抑制ＭＣ生长的分子机理。网筛法分离大鼠肾小球，培养肾小球ＭＣ。ＡＧＰＣ一步法提取细胞总ＲＮＡ，ｃ－ｍｙｃｍＲＮＡ水平用斑点杂交法测定，以显著斑点最大的ＲＮＡ稀释度表示ｍＲＮＡ水平。     

蝮蛇抗栓酶对兔血管损伤后血管平滑肌细胞C—myc原癌基因表达的影响

目的：探讨蜊蛇抗栓酶抑制血管再狭窄的作用机制。对临床应用提供理论依据。为再狭窄的防治寻找治疗药物。方法：建立兔髂动脉再狭窄模型。用自行设计、全盛的C-myccDNA探针和原位杂交技术观察血管内膜C-mycmRNA的表达与内膜血管平滑细胞（cscularsmooth muscle cells,vSMCs)增殖和内膜形成的关系。结果：C-mycmRNA表达于动脉受损后1周即达高峰并分布于增生的内膜全层,平均阳性细胞个数为29.23.min^-2,蜊蛇抗栓酶1周时对C-mycmRNA的表达有明显的抑制作用,平均阳性细胞个数为10.73.mm^-2。结论：抑制C-myc基因的表达可能减少或阻止内明显病变的形成,有利于血管再狭窄的防治,研究显示蜊蛇抗栓酶对防治再狭窄有效。     

c—myc基因在食管异型增生组织和鳞癌中的表达及其意义

本研究通过单克隆抗体免疫组化LSAB法检测c-myc基因在正常食管粘膜(EM)、食管异型增生(EED)和食管鳞癌(SCCE)中表达的变化,目的是了解c-myc基因在食管癌发生和发展中的作用,及对临床的意义。 材料与方法 一、材料和试剂 1.选择35例食管癌术后标本,取EM10块(远癌5cra以外)、EED和SCCE各35块(分别取自癌旁0.5～1.0cm和癌中心)。标本用10％福尔马林固定和石蜡包埋,并记录年龄、发生部位、原发瘤大小、淋巴结状态、组织分化和PT参数,同时按1987年国际食管癌分期标准进行TNM分期。2.c-myc癌基因蛋白鼠抗人单抗NM-0409购于美国Novacastra(胞浆和核旁染色),LSAB试剂盒为美国Zymed公司生产。     

普罗布考预防经皮冠状动脉球囊成形术和经皮冠状动脉介入治疗术后再狭窄的研究进展

普罗布考（丙丁酚,probucol）是1977年首先在美国上市的一种降脂药,后在英、法、德、日等十几个国家相继上市,国内直在最近几年才开始使用,具有抗术后冠状再狭窄、调脂和抗氧化等作用。动物实验表明,普罗布考可减低动脉壁破损后内膜增生。在临床试验中,MVP（Multivitam ins and ProbucolTrial）试验显示,     

K—ras和C—myc在肺癌中表达的意义

目的：探讨原发性肺癌中K—ras和c—myc的表达与肺癌发生发展之间的关系。方法：应用免疫组化法测定53例肺癌标本及19例正常人的肺组织中K—ras和c-myc的表达。结果：肺癌细胞中K—ras和c—myc的阳性表达率明显高于正常人肺组P〈0．01）；K-ras和c—myc在不同病理类型（确切p=1），和不同大小的肺癌组（P〉0．05）之间的差异无显著性；在三组不同分化程度的肺癌组间的阳性表达率差异有显著性（P〈0.05）；K—ras和c—myc在淋巴结有转移组的阳性表达率明显高于无转移组，差别有显著意义（P〈0．05）。结论：K—ras和c—myc蛋白的过度表达参与了人肺细胞癌的发生发展过程。     

小檗碱对局灶性脑缺血大鼠原癌基因c—fos表达的影响

目的：研究大鼠局灶性脑缺血过程中c-fos mRNA表达的动态变化，并观察小檗碱（Ber）对其作用。方法：运用斑点杂交技术，观察Ber对局灶性脑缺血再灌注大鼠大脑皮质及海马组织c-fos mRNA表达的影响。结果：大鼠局灶性脑缺血2h再灌注0．5－4h，脑皮质及海马组织c-fos mRNA出现一过性高表达，2h达高峰，分别为对照组的4．5和4．7倍。Ber 20mg/(kg·d)ip显抑制大鼠脑缺血诱导的c-fos高表达，降低病灶侧海马和皮层组织水、钙含量。结论：脑缺血过程中c-fos原癌基因呈现一过性高表达，Ber可降低c-fos mRNA水平，该作用可能是其抗脑缺血机理之一。     

甲状旁腺激素、1，25（OH）2D3对鼠心肌细胞c—myc基因表达的影响

目的　研究不同浓度水平的甲状旁腺激素 (PTH)和 1,2 5 (OH) 2 D3 对新生大鼠心肌细胞c mycmRNA表达的影响。 方法　采用新生大鼠心肌细胞原代培养和逆转录多聚酶链反应 (RT PCR)技术 ,比较正常对照组、不同浓度PTH组和 1,2 5 (OH) 2 D3 组心肌细胞c mycmRNA表达程度。结果　 (1)高浓度PTH组 (10 -8M )心肌细胞c mycmRNA表达较正常对照组和低浓度PTH组(10 -10 M)明显增高 (分别为 1 84± 0 38、0 11± 0 16和 0 10± 0 14,P <0 0 1) ,而后两组之间没有差异 (P >0 0 5 ) ;(2 )两种浓度 1,2 5 (OH) 2 D3 组心肌细胞均未见c mycmRNA表达。 结论　高浓度PTH明显刺激心肌细胞c mycmRNA表达 ,1,2 5 (OH) 2 D3 能抑制c mycmRNA表达     

川芎嗪对球囊损伤后大鼠血管新生内膜增生的影响

目的探讨川芎嗪对大鼠颈总动脉球囊损伤后新生内膜增生的影响及其机制。方法 SD雄性大鼠32只,随机分为假手术组、模型组、川芎嗪高剂量组(60mg·kg~(-1)·d~(-1))和低剂量组(30mg·kg~(-1)·d~(-1))。用球囊导管损伤术建立大鼠颈总动脉内膜增生模型,测量给药14d后颈总动脉内膜面积(NIA)及内膜面积/中膜面积(NIA/MA),免疫组化法检测该动脉增殖细胞核抗原(PCNA)的表达,real-time RT-PCR法测定内皮型一氧化氮合酶(Nos3)和原癌基因c-Myc的mRNA表达,并检测血浆中超氧化物歧化酶(SOD)活性、丙二醛(MDA)以及环磷酸腺苷(cAMP)和环磷酸鸟苷(cGMP)的含量。结果川芎嗪高、低剂量组均能明显减少球囊损伤后大鼠颈总动脉的NIA及NIA/MA(P<0.05),并使PCNA蛋白质表达降低(P<0.01);显著升高球囊损伤大鼠血浆SOD活性和cAMP及cGMP的含量,而降低血浆MDA水平(均P<0.01);川芎嗪高剂量组还能上调Nos3 mRNA表达,而使c-Myc mRNA的表达降低(均P<0.05)。结论川芎嗪能抑制球囊损伤所致血管内膜异常增生,该作用可能与其抗氧化和促进环核苷酸生成有关。     

雷帕霉素抑制增生内膜中基质细胞衍生因子-1的表达

目的：进一步探讨雷帕霉素抗血管内再狭窄的分子机制。方法：球囊拉伤大鼠颈总动脉建立血管内膜增生的动物模型,口服雷帕霉素（25mg/kg）,4周后处死动物。HE染色观测血管病变,免疫组化检测增生内膜中基质细胞衍生因子-1（SDF-1）的表达,小室迁移系统观察SDF-1对平滑肌细胞迁移的影响。结果：球囊拉伤明显诱导血管内膜增生,增生内膜中有明显的SDF-1的表达,雷帕霉素能显著下调增生内膜中SDF-1的表达,而SDF-1浓度依赖性地诱导平滑肌细胞的迁移。结论：雷帕霉素可能通过下调SDF-1的表达从而抑制血管再狭窄。     

经皮冠状动脉腔内成形术后应用降压药对肾功能的影响

目的 评估经皮冠状动脉腔内成形术后应用抗高血压药对患者肾功能损伤的影响.方法 回顾分析2020年1月至2020年12月在南京鼓楼医院心血管内科行经皮冠状动脉腔内成形术治疗并且规律服用抗高血压药物的患者,共193例.根据用药种类不同分为4组:血管紧张素转化酶抑制剂/血管紧张素受体拮抗剂(ACEI/ARB)组、β受体阻滞剂...     

丙丁酚对高脂血症小鼠表达C反应蛋白的影响

目的观察丙丁酚对高脂高胆固醇饲养的高脂血症小鼠体内C反应蛋白（CRP）活性及表达的影响，探讨丙丁酚的作用机制。方法以高脂高胆周醇饲料饲喂小鼠，制作高脂血症模型。HE染色观察小鼠肝脏病变情况；采用相关检测试剂盒测定小鼠血脂水平、血浆中CRP和谷胱甘肽S转移酶的活性；采用逆转录聚合酶链式反应（RT—PCR）检测小鼠肝脏CRP mRNA的表达。结果高脂高胆固醇饮食显著增加C57BL／6J和apoE^./.小鼠血脂水平（P〈0．05），而丙丁酚则可降低高脂血症小鼠血脂水平（P〈0．05）。高脂组小鼠肝脏结构比较紊乱，脂肪空泡明显。与高脂组比较，经丙丁酚处理后，小鼠肝脏的脂肪空泡明显减少，并且其血浆中CRP的水平也下降（P〈0．05）。结论丙丁酚可以减轻高脂高胆固醇饲料诱导的高脂血症小鼠的CRP的水平，对肝脏产生抗炎性的保护作用。     

Effect of nilvadipine on balloon catheterization-induced intimal thickening of the coronary artery in miniature pigs.

The effect of nilvadipine on balloon catheterization-induced intimal thickening of the coronary artery was examined in miniature pigs. A diffuse intimal thickening was observed in vehicle-treated controls 6 weeks after balloon catheterization. The histologic features of the intimal thickening resembled those of early atherosclerotic lesions and restenosis after percutaneous transluminal coronary angioplasty (PTCA). Nilvadipine given in a daily dose of 10 mg/kg (subcutaneously, s.c.) for 6 weeks significantly inhibited intimal thickening. The ratio of the cross-sectional area of the intima to the cross-sectional area of the media was significantly reduced by 62% in nilvadipine-treated animals. These results suggest that nilvadipine may prevent or exert beneficial effects on coronary arterial injuries such as atherosclerosis and restenosis after PTCA.     

Effect of nicotine on the intimal hyperplasia after endothelial removal of the rabbit carotid artery

• 1.1. The present experiments were designed to investigate the effect of long-term oral nicotine (10mg/200m1/kg/day for 7 weeks) on the intimal hyperplasia after endothelial removal of the rabbit carotid artery.
• 2.2. The plasma concentrations of nicotine were determined to be 11.7–12.5ng/ml during the term of administration and corresponded to the plasma levels in human smokers.
• 3.3. Six weeks after the endothelial removal, light microscopy revealed a marked intimal hyperplasia. Administration of nicotine tended to accelerate the intimal hyperplasia, which was estimated by comparing the histological findings, DNA content and wet weight of the vessel wall.
• 4.4. Acetylcholine- and A23187-induced endothelium-dependent relaxations were greatly impaired in the hyperplastic artery strips. The impairment of relaxations tended to be accelerated in the nicotine group. Sodium nitroprusside-induced relaxation was not different between the control and the hyperplastic artery strips and remained unaffected in the nicotine group.
• 5.5. The concentrations of endogenous nitric oxide (NO) synthesis inhibitors, N^G-monomethyl-l-arginine (l-NMMA) and asymmetrical N^G,N^G-dimethyl-l-arginine (ADMA) were significantly more increased in the regenerated endothelial cells compared with those in the control endothelial cells. The concentrations of l-NMMA and ADMA in the regenerated endothelial cells were significantly increased by as much as 1.3×10⁻⁶ and 5.6×10⁻⁷M, respectively, in the nicotine group.
• 6.6. Immunoreactive endothelin-1 was significantly increased in the hyperplastic vessel wall (2.4 times that of the control) in 6 weeks. Administration of nicotine tended to increase the level.
• 7.7. It seems possible to assume from these results that, although, under the present experimental conditions, nicotine exhibited a tendency to accelerate the intimal hyperplasia after endothelial removal, the longer exposure to nicotine or a higher dose of the agent or both would significantly accelerate the intimal hyperplasia through the enhanced impairment of endothelium-derived relaxing factor/ NO production, which might be brought about by the enhanced increases in L-NMMA and ADMA concentrations, and the enhanced increase in endothelin-1 in the vessel wall.

     

碘帕醇对糖尿病患者肾脏功能的影响

目的 探讨不同剂量碘帕醇对糖尿病患者肾功能的影响.方法 入选148例行冠状动脉造影或经皮冠状动脉介入(PCI)治疗的糖尿病患者,根据对比剂的使用量,分为低剂量组(＜100 ml),中剂量组(100～200 ml)和高剂量组(＞200 ml).术前及术后72 h检测患者血清肌酐浓度;分析不同剂量对比剂对血清肌酐水平、估测肌酐清除率(eGFR)的影响及年龄、性别和eGFR、低密度脂蛋白、血压水平等因素对对比剂肾病(CIN)发生率的影响.结果 术后各组间的肌酐浓度、eGFR差异无统计学意义(P＞0.05);术后肌酐水平在中、高剂量组明显高于术前[分别(96.4±21.8)μmol/L比(87.5±21.8)μmol/L,(100.8±23.9)μmol/L比(88.1±19.9)μmol/L,均P＜0.05],各组eGFR同术前相比差异无统计学意义(P＞0.05).低eGFR及女性患者CIN 发生率明显高于eGFR正常和男性患者(均P＜0.05).结论 在特定的糖尿病患者中使用较大剂量的碘帕醇是安全的.

Abstract：

Objective To determine the effects of the volume of contrast media and risk factors on kidney function in diabetic patients undergoing elective cardiac catheterization or percutaneous coronary intervention (PCI). Methods Totally 148 consecutive diabetic patients undergoing elective cardiac catheterization or PCI were divided into three groups; low dose (＜100 ml), middle dose (100-200 ml) and high dose group (＞200 ml). Serum creatinine and estimated glomerular filtration rate(eGFR) at baseline and after 72 hours of the procedure were measured. The incidence of CIN and the effect of variables on rate of CIN were evaluated. Results There were no significant differences on serum creatinine level and eGFR among groups after cardiac catheterization or PCI. Compared with the preoperative, the levels of serum creatinine in middle dose and high dose group were higher after the procedure [(96.4±21.8)μmol/L vs (87. 5 ±21. 8)μmol/L, (100. 8 ±23. 9) μmol/L vs (88.1 ± 19.9) μmol/L, P＜ 0.05]. The increase of serum creatinine in high dose group were significantly higher than in low dose and middle dose groups. There was no significant difference on eGFR and on the incidence of CIN among groups after cardiac catheterization or PCI. CIN developed more frequently after PCI in female or lower eGFR patients. Conclusion It is safe for some diabetic patients to use large dose of contrast media.     

Ultrasound microbubble-carried PNA targeting to c-myc mRNA inhibits the proliferation of rabbit iliac arterious smooth muscle cells and intimal hyperplasia

Objective: To elucidate the transfected effect of albumin ultrasound microbubbles carrying peptide nucleic acids (PNAs) against c-myc gene to the vascular walls and their effect on the intimal proliferation induced by vascular denudation.

Methods: A rabbit iliac artery intimal proliferation model was constructed and PNA against c-myc mRNA was designed and synthesized and was added to albumin solution before ultrasound microbubbles were prepared and encapsulated in matrix of albumin. The ultrasound microbubbles carrying PNA were transfected to intima under ultrasound exposure. The transfected effect was identified by a histochemical method and the expression of c-myc was detected by in situ hybridization. The proliferation of intimal smooth muscle cells was estimated by the expression of proliferative cell nuclear antigen (PCNA) of them. The intimal area and thickness were judged morphologically for intimal hyperplasia.

Results: The ultrasound microbubbles with PNA were successfully prepared and c-myc PNA was transfected to vascular intimal cells. The expression of c-myc and PCNA by intimal vascular smooth muscle cells (vSMCs) was inhibited significantly and the intimal thickness and area were reduced remarkably.

Conclusion: Transfection of c-myc PNA could inhibit proliferartion of vSMCs and intima in the rabbit iliac artery intimal proliferation model and the targeted transfection of albumin ultrasound microbubbles carrying PNA offers a feasible way to facilitate its access to specific cells in vivo and produce bioavailability.     

栉孔扇贝裙边糖胺聚糖对增殖的血管平滑肌细胞 c-myc和TNF-αmRNA水平的影响

目的 观察栉孔扇贝(Chlamys farreri)裙边糖胺聚糖(SS-GAG)对体外培养的血管平滑肌细胞(VSMC)内原癌基因c-myc mRNA、肿瘤坏死因子(TNF-α)mRNA水平的影响,以探讨SS-GAG抗动脉粥样硬化(AS)的作用机理.方法建立碱性成纤维细胞生长因子(bFGF)诱导的平滑肌细胞增殖模型,采用非同位素原位杂交方法测定SS-GAG对增殖的VSMC内c-mycmRNA、TNFαmRNA水平的影响.结果低、高剂量SS-GAG组c-myc、TNF-αmRNA水平明显低于模型组(P<0.01).结论 SS-GAG对bFGF诱导增殖的VSMC内c-myc,TNF-α基因的表达均有抑制作用,且随着SS-GAG浓度的升高押制作用增强.     

Neutrophil accumulation promotes intimal hyperplasia after photochemically induced arterial injury in mice

The role of leukocytes in the pathogenesis of coronary arterial disease has become a focus for clinical research. The aim of this study was to determine whether neutrophil accumulation would participate in the development of intimal hyperplasia after endothelial injury in mice, and whether d-myo-inositol hexakisphosphate (phytic acid) which inhibits the binding of L- and P-selectin to sialyl Lewis^X could inhibit the development of intimal hyperplasia. Endothelial injury was inflicted in one femoral artery via the photochemical reaction between systemically injected rose bengal and transillumination with green light (wavelength: 540 nm). Scanning electron microscopic observation at 3 days after the injury showed an increase in the number of leukocytes adhering to the injury site. Histological observation at 21 days showed that in the neutropenia group administered anti-neutrophil antibody and in the phytic acid-treated group the progression of intimal hyperplasia was significantly attenuated by comparison with the corresponding control groups.

These results suggest that neutrophil accumulation contributes to the initiation and/or development of intimal hyperplasia and L- and/or P-selectin may participate in their mechanisms.