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。     

普罗布考对冠状动脉球囊损伤后管壁原癌基因c—myc表达的影响

目的通过建立猪冠状动脉球囊损伤模型 ,观察普罗布考对血管内膜增生及管壁原癌基因c-myc表达的影响.方法选用雌性New Yorkshire良种猪19头,随机分为2组,对照组1 1头,普罗布考组8头,均行冠状动脉球囊扩张术,术后喂饲6周,重复冠状动脉造影后处死动物.普罗布考组于术前4周给予普罗布考1g,bid ,至实验结束.常规病理制片,观察形态学变化,采用RT-PCR的方法检测c-myc mRNA的表达强度.结果对照组损伤动脉内膜可见大量平滑肌细胞增生,呈偏心性增厚 ,普罗布考组内膜增厚程度明显减低.对照组c-myc mRNA相对表达强度为(2.73±0.51) ,明显高于正常动脉[(0.82±0.09),P<0.05],普罗布考组c-myc mRNA相对表达强度为(1.44±0.25),较对照组减弱(P<0.05),但仍高于正常动脉(P<0.05).结论普罗布考具有抑制冠状动脉球囊损伤后c-myc表达和内膜增生的作用.     

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。     

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。     

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。     

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。     

右美沙芬对局灶脑缺血所致的c—fos蛋白表达的抑制作用

观察右美沙芬对局灶脑血所致的ｃ－ｆｏｓ蛋白表达的作用。     

Modulation of adrenergic receptors during left ventricular hypertrophy development and after regression by captopril.

The objective of this study was to analyze adrenergic receptors during cardiac hypertrophy development, after establishment of cardiac hypertrophy and after regression of cardiac hypertrophy by an angiotensin-converting enzyme inhibitor. Left ventricular hypertrophy (LVH) was induced by abdominal aortic stenosis. After surgery, plasma norepinephrine concentrations (PNE) and left ventricular adrenergic receptors from rat hearts subjected to aortic stenosis were assessed during cardiac hypertrophy development (at 3, 7, 15, and 30 days of aortic stenosis), once cardiac hypertrophy had been established (7 and 14 weeks after the stenosis) and after regression of cardiac hypertrophy by an antihypertensive dose (200 mg/kg/day) of captopril. The presence of LVH was observed from day 7 after stenosis. PNE had significantly increased after 15 days but returned to control values 30 days after surgery. The density of alpha1-adrenoceptors was found to decrease with development of hypertrophy. Once hypertrophy had been established, 7 weeks from stenosis, PNE was not different from control; however, the density of alpha1-adrenoceptors continued to diminish, whereas PNE and the density of beta-adrenoceptors were no different from control values. Fourteen weeks after stenosis, a significant decrease in PNE was recorded, and no change in alpha1- but an increase in beta-adrenoceptors was observed. LVH was reversed by treatment with captopril; PNE was similar in control and stenosed treated animals. The density of alpha1-adrenoceptors was decreased when compared with control animals, and no change in the density of beta-adrenoceptors was observed with treatment. In conclusion, a decrease of alpha1-adrenoceptors was associated with LVH development and earlier stages of established cardiac hypertrophy. Later stages of established cardiac hypertrophy were characterized by no change in alpha1- and an increase in beta-adrenoceptors. Treatment with captopril induced LVH regression and decreased the number of alpha1-adrenoceptors without any change in beta-adrenoceptors.     

卡托普利早期治疗自发性高血压大鼠抑制左室肥厚和c-myc表达而不影响c-fos表达(英文)

目的:探讨早期卡托普利治疗抑制左室肥厚的机制.方法:♂SHR宫内期给药(100 mg·kg~(-1)·d~(-1))到16周,40周处死,测定收缩压,左室重与体重比,左室c-myc和c-fos表达量(Northern杂交).结果:治疗明显降低血压,停药后24周,仍维持较低血压(20.9±1.2vs对照SHR 28.3±1.3 kPa,P<0.01)并抑制左室肥厚,心肌c-myc表达明显减少(0.57±0.13 vs对照SHR 2.07±0.16,c-myc mRNA/18S rRNA,P<0.01),c-fos表达无变化.结论:卡托普利持久地阻止高血压形成,抑制左室肥厚.后者可能是抑制c-myc表达结果,治疗不改变c-fos表达.     

卡托普利对实验大鼠左室肥厚的干预作用

目的观察卡托普利逆转压力负荷增加大鼠左室肥厚的作用。方法采用腹主动脉狭窄所致压力负荷增加大鼠左室肥厚模型,将雄性SD大鼠36只随机分为假手术组、模型组、卡托普利组,观察用药4周后左室重量指数（LVMI）、左室心肌病理形态HE染色、左室心肌细胞超微结构等指标的改变。结果模型组LVMI明显高于假手术组（P〈0．01）,卡托普利组（2．32±0．35）明显低于模型组（2．98±0．36）,P〈0．01;左室心肌病理形态HE染色、左室心肌细胞超微结构的改变与LVMI的改变基本一致。结论卡托普利具有逆转心肌肥厚的作用。     

不同剂量卡托普利对自发性高血压大鼠左心室肥厚逆转作用比较

观察了小剂量卡托普利（Ｃａｐ）是否能在血压无明显下降情况下逆转自发性高血压大鼠（ＳＨＲ）的左心室肥厚。已有左心室肥厚的ＳＨＲ经Ｃａｐ２０ｍｇ·ｋｇ￣（－１）·ｄ￣（－１）治疗２４ｗｋ后血压仍维持在给药前水平，左心室重和体重的比值轻度下降，Ｃａｐ５０ｍｇ·ｋｇ￣（－１）·ｄ￣（－１）治疗２４ｗｋ后血压，左心室重和体重的比值均低于给药前水平，但仍未达正常水平。两种剂量的Ｃａｐ对心肌内去甲肾上腺素和羟脯氨酸含量及血小板内游离钙离子的影响基本相同。长期小剂量Ｃａｐ治疗即使在血压没有明显下降情况下仍能防止左心室肥厚发展，甚至还有轻度逆转ＳＨＲ的左心室肥厚和减少心脏胶原的作用。大剂量Ｃａｐ除减少心脏胶原外，还有明显的逆转左心室肥厚的作用，Ｃａｐ的降压和逆转左心室肥厚作用有相关性。     

Comparative effects of irbesartan versus amlodipine on left ventricular mass index in hypertensive patients with left ventricular hypertrophy

The aim of this study was to comparatively assess the effects of irbesartan and amlodipine monotherapies on left ventricular mass index (LVMI) in patients with mild to moderate untreated hypertension and echocardiographically determined left ventricular hypertrophy (LVH). Sixty hypertensive patients (35 men, 25 women; mean age, 52.8 years +/- 12.6) with diastolic blood pressure (BP) > or = 100 mm Hg were randomized to irbesartan 150 mg once daily or amlodipine 5 mg once daily for a 4-week titration period. Dosage of both drugs was increased to irbesartan 300 mg once daily or amlodipine 10 mg once daily in case of sitting diastolic BP still >90 mm Hg after the first 2 weeks of treatment. Dosage doubling was necessary in more than 50% of patients in both treatment groups. After the titration period, only the responders (sitting diastolic BP < or = 90 mm Hg) entered a 5-month maintenance period. After 3 months, echocardiographically estimated LVMI decreased by 23.2% in the irbesartan-treated patients and 11.4% in the amlodipine-treated patients, with an adjusted mean difference of 11.8% in favor of irbesartan (P < 0.0001). After 6 months, it decreased by 24.7% in the irbesartan-treated patients and 13.0% in the amlodipine-treated patients, with an adjusted mean difference of 11.6% in favor of irbesartan (P < 0.0001).     

氯沙坦治疗高血压病伴左室肥厚患者的疗效观察

目的观察氯沙坦对高血压病伴左室肥厚患者降压及左室肥厚的治疗效果。方法高血压病伴左室肥厚患者60例,随机分为氯沙坦组（30例）和卡托普利组（30例）,用药前及用药后3个月测量血压和计算患者左室质量指数。结果2组用药后血压和左室质量指数均比用药前有显著的下降（P〈0.01）,但组间差异无统计学意义（P〉0.05）。结论氯沙坦可有效降低高血压病伴左室肥厚患者的血压,逆转左心室肥厚。     

Regression of left ventricular hypertrophy on long-term treatment with captopril of severe hypertensives refractory to standard triple treatment

Ten patients (mean age 53 years; range 37-65 years) with hypertension refractory to standard triple treatment were selected for measurement of blood pressure and echocardiographic evaluation of the left ventricular dimensions before and after 3, 6 and 12 months of captopril therapy. In each patient the dose of captopril was titrated to a maximum of 150 mg t.d.s. (range 25 to 150 mg t.d.s.) with a therapeutic goal of less than or equal to 90 mm Hg diastolic blood pressure. Most patients had added diuretic therapy. Four patients were unable to complete the study, two because of insufficient response to captopril therapy, and two because of side-effects (skin rash and cough). A significant fall in blood pressure was seen after three months of treatment and a reduced blood pressure was still maintained after 12 months. Over the same period, the average number of drugs was reduced from 3.6 to 2.1 per patient. A gradual reduction of septal and posterior wall thickness were noted, from 12.8 and 11.5 mm to 10.0 and 8.5 mm, respectively, after 12 months. Calculated left ventricular muscle mass was insignificantly reduced from 281 to 243 g after 12 months. The present study suggests that in hypertension resistant to conventional multiple therapy, captopril can reduce the blood pressure, and, in the long run it can also induce reversal of left ventricular wall thickening without causing deterioration of left ventricular function.     

依那普利对高血压病患者左室结构及功能影响

为了探讨依那普利对高血压病患者左室结构及功能的影响 ,观察了 2 8例 期高血压病患者口服依那普利平均 2 2个月后左室结构及功能改变。结果显示 ,依那普利长期治疗可有效降压 ,并同时逆转左室肥厚 ,改善左室舒张功能     

苯那普利对高血压病左室肥厚及室性心律失常的影响

目的探讨血管紧张素转换酶(AEC_I)苯那普利对高血压病左室肥厚(LVH)和室性心律失常(VA)的影响。方法采用超声检查和动态心电图监测56例高血压病患者服用苯那普利前和后6个月的心脏形态和心律失常变化。结果检测的27例LVH患者VA发生率明显高于无LVH者(77.7 %对34.5 %) ,尤以复杂型VA多见(48.2 %对10.4 %) ;治疗6个月后 ,IVS、LVPW、LA和LVMI显著消退 ,VA发生率亦明显降低。结论高血压伴LVH时VA和复杂型VA发生率显著增多 ;苯那普利对高血压病的LVH有明显消退作用 ,VA亦随之减少