肺炎衣原体通过上调酰基辅酶A:胆固醇酰基转移酶1诱导人单核细胞株THP-1源性泡沫细胞形成的实验研究

Objective To investigate the expression changes of acyl-coenzyme A: cholesterol acyhransferase 1 (ACAT1) on Chlamydia pneumoniae (C. pn) induced foam cell formation. Methods Human monocytic cell line (THP-1) was induced into macrophages by 160 nmol/L phorbol myristate acetate (PMA)for 48 h, and were randomly allocated into four groups: negative control group (50 μg/ml LDL for 48 h) ; positive control group (50 μg/ml ox-LDL for48 h) ; C. pn infection group (50 μg/ml LDL plus 1× 105,4×105,5×105and 1×106 IFU C.pn for 48 h or 1×106 IFU C.pn for 0,24,48 and 72h); ACAT inhibitor 58-035 plus C. pn infection group (1, 5, 10 μg/ml ACAT inhibitor 58-035 pretreatment for 1 h,50 μg/ml LDL and 1 × 106 IFU C. pn for 48 h). The mRNA and protein expressions of ACATI were determined by RT-PCR and Western blot, respectively. Lipid droplets in cytoplasm were observed by oil red 0 staining. The contents of intracellular cholesteryl esters were detected by enzyme-fluorescence. Results The mRNA and protein expressions of ACATI were significantly up-regulated in positive control cells compared those in negative control cells and further upregulated by C. pn infection in a time-dependent and concentration-dependent manner (all P ＜ 0.05). There were significantly increases in the accumulation of lipid droplets and the ratio of cholesteryl ester to total cholesterol in positive control cells as compared with negative control cells and these were further aggravated by C. pn (at the concentrations of 5× 105 and 1×106IFU for 48 h) and C. pn infection induced increases in the accumulation of lipid droplets and the ratio of cholesteryl ester to total cholesterol could he significantly attenuated by ACAT inhibitor 58-035 (all P ＜ 0.05). Conclusion Chlamydia pneumoniae induces THP-1-derived foam cell formation by up-regulating the expression of ACATI.     

皮肤淋巴细胞浸润症一例

患者女,75岁.因左侧面部、耳部出现红色斑块,并反复发作半年余就诊.患者半年前无明显诱因,左侧面部出现红色小丘疹,逐渐扩大融合成斑块,并波及耳部,无明显自觉症状,在当地给予抗过敏治疗后不久皮疹消退.     

血管内皮细胞衰老与细胞生物学特征变化

目的探讨血管内皮细胞衰老与细胞生物学特征变化的关系。方法体外培养人脐静脉内皮细胞，通过传代形成细胞的衰老模型。光镜下观察各代细胞的形态结构；流式细胞术检测细胞周期分布和细胞内自发荧光产物的变化；线粒体膜电位特异染色法检测线粒体膜电位的演变。结果随着细胞传代次数的增加，血管内皮细胞结构逐步退化，细胞分裂减缓，细胞周期趋向停滞于G0／G1期。处于G0／G1期的细胞由第2次传代细胞的74．17％增加至第8次传代细胞的88．80％。细胞自发荧光有显著性增加，线粒体膜电位则有显著性降低。结论在血管内皮细胞复制性衰老过程中，伴随着细胞形态退化，细胞周期分布异常，细胞内线粒体功能降低，脂质过氧化反应增强。     

急性心肌梗塞合并传导阻滞82例临床分析

急性心肌梗塞(AMI)合并传导阻滞由于其预后不良,已引起了国内外医务工作者的重视,本文收集我院自1962年6月～1982年6月期间收治的AMI资料较完整的250例,选择其中在发病时或住院过程中并发房室     

神经肽Y、维拉帕米对大鼠心肌细胞肥大的影响

通过测定培养的心肌细胞~3H-leucine(~3H-亮氨酸)掺入率和膜片钳全细胞记录方法记录Ca~(2 )电流(I_(ca)),研究神经肽Y(NPY)、维拉帕米对大鼠心肌细胞肥大的影响。结果:0.1μmol/L NPY促使培养的心肌细胞~3H-leucine掺入率增大,达(136.0±4.4)min~(-1),与对照组(91.0±4.O)min~(-1)相比,差异有显著性意义(p<0.01)。10nmol/L维拉帕米与NPY共同作用于心肌细胞24h,可使NPY促~3H-leucine掺入率增大的作用受到抑制(P<0.01)。NPY可显著增大心肌细胞I_(ca),为(12.0±3.1)pA,与对照组(5.5±2.4)pA比较,差异有显著性意义(P<0.01)。结论:NPY促使培养的心肌细胞蛋白质合成率增大的作用可被维拉帕米阻断,而NPY增加细胞内游离钙,触发心肌蛋白质合成增加,可能是促进心肌肥大的机制之一。     

老年人高血压的诊断与治疗进展

老年人高血压有其独特的临床特点，如单纯收缩期高血压较多见、血压波动范围较大、直立性低血压较多见、并发症多且多种疾病并存，以及可能存在假性高血压等。年龄≥60岁；连续3次非同日测量血压，收缩压≥140 mmHg（1 mmHg＝0.133 kPa)和（或）舒张压≥90 mmHg(老年人单纯收缩期高血压指收缩压≥140 mmHg，舒张压＜90 mmHg）；排除假性和继发性高血压者可诊断为老年人高血压。该病的治疗包括非药物治疗和药物治疗。非药物治疗包括减体重、合理膳食、适当体力活动和运动、保持心理平衡、戒烟等。主要降压药物包括利尿药、β-受体阻滞药、钙拮抗药、ACEI、血管紧张肽Ⅱ（AngⅡ）受体阻滞药和α 受体阻滞药六大类。     

肺炎衣原体通过上调酰基辅酶A:胆固醇酰基转移酶1诱导人单核细胞株THP-1源性泡沫细胞形成的实验研究

Objective To investigate the expression changes of acyl-coenzyme A: cholesterol acyhransferase 1 (ACAT1) on Chlamydia pneumoniae (C. pn) induced foam cell formation. Methods Human monocytic cell line (THP-1) was induced into macrophages by 160 nmol/L phorbol myristate acetate (PMA)for 48 h, and were randomly allocated into four groups: negative control group (50 μg/ml LDL for 48 h) ; positive control group (50 μg/ml ox-LDL for48 h) ; C. pn infection group (50 μg/ml LDL plus 1× 105,4×105,5×105and 1×106 IFU C.pn for 48 h or 1×106 IFU C.pn for 0,24,48 and 72h); ACAT inhibitor 58-035 plus C. pn infection group (1, 5, 10 μg/ml ACAT inhibitor 58-035 pretreatment for 1 h,50 μg/ml LDL and 1 × 106 IFU C. pn for 48 h). The mRNA and protein expressions of ACATI were determined by RT-PCR and Western blot, respectively. Lipid droplets in cytoplasm were observed by oil red 0 staining. The contents of intracellular cholesteryl esters were detected by enzyme-fluorescence. Results The mRNA and protein expressions of ACATI were significantly up-regulated in positive control cells compared those in negative control cells and further upregulated by C. pn infection in a time-dependent and concentration-dependent manner (all P ＜ 0.05). There were significantly increases in the accumulation of lipid droplets and the ratio of cholesteryl ester to total cholesterol in positive control cells as compared with negative control cells and these were further aggravated by C. pn (at the concentrations of 5× 105 and 1×106IFU for 48 h) and C. pn infection induced increases in the accumulation of lipid droplets and the ratio of cholesteryl ester to total cholesterol could he significantly attenuated by ACAT inhibitor 58-035 (all P ＜ 0.05). Conclusion Chlamydia pneumoniae induces THP-1-derived foam cell formation by up-regulating the expression of ACATI.     

肺炎衣原体通过上调酰基辅酶A:胆固醇酰基转移酶1诱导人单核细胞株THP-1源性泡沫细胞形成的实验研究

Objective To investigate the expression changes of acyl-coenzyme A: cholesterol acyhransferase 1 (ACAT1) on Chlamydia pneumoniae (C. pn) induced foam cell formation. Methods Human monocytic cell line (THP-1) was induced into macrophages by 160 nmol/L phorbol myristate acetate (PMA)for 48 h, and were randomly allocated into four groups: negative control group (50 μg/ml LDL for 48 h) ; positive control group (50 μg/ml ox-LDL for48 h) ; C. pn infection group (50 μg/ml LDL plus 1× 105,4×105,5×105and 1×106 IFU C.pn for 48 h or 1×106 IFU C.pn for 0,24,48 and 72h); ACAT inhibitor 58-035 plus C. pn infection group (1, 5, 10 μg/ml ACAT inhibitor 58-035 pretreatment for 1 h,50 μg/ml LDL and 1 × 106 IFU C. pn for 48 h). The mRNA and protein expressions of ACATI were determined by RT-PCR and Western blot, respectively. Lipid droplets in cytoplasm were observed by oil red 0 staining. The contents of intracellular cholesteryl esters were detected by enzyme-fluorescence. Results The mRNA and protein expressions of ACATI were significantly up-regulated in positive control cells compared those in negative control cells and further upregulated by C. pn infection in a time-dependent and concentration-dependent manner (all P ＜ 0.05). There were significantly increases in the accumulation of lipid droplets and the ratio of cholesteryl ester to total cholesterol in positive control cells as compared with negative control cells and these were further aggravated by C. pn (at the concentrations of 5× 105 and 1×106IFU for 48 h) and C. pn infection induced increases in the accumulation of lipid droplets and the ratio of cholesteryl ester to total cholesterol could he significantly attenuated by ACAT inhibitor 58-035 (all P ＜ 0.05). Conclusion Chlamydia pneumoniae induces THP-1-derived foam cell formation by up-regulating the expression of ACATI.     

阿托伐他汀对自发性高血压大鼠血压和心肌血管紧张素Ⅱ1型和2型受体表达的影响

目的　观察阿托伐他汀对自发性高血压大鼠血压和心肌血管紧张素Ⅱ受体 1和血管紧张素Ⅱ受体 2的调节作用。方法　采用免疫组织化学染色法检测心肌血管紧张素Ⅱ受体 1和血管紧张素Ⅱ受体 2蛋白表达 ,原位杂交法测定心肌血管紧张素Ⅱ受体 1和血管紧张素Ⅱ受体 2mRNA表达水平。于给药前和给药后每两周测量大鼠尾动脉收缩压 ,并测定血清总胆固醇、甘油三酯、高密度脂蛋白胆固醇及低密度脂蛋白胆固醇水平。结果　实验前自发性高血压大鼠各组收缩压均显著高于Wistar kyoto大鼠组 (P <0 .0 1)。给药后第 4周和第 6周 ,5 0mg阿托伐他汀组收缩压明显下降 (P <0 .0 1) ,总胆固醇、甘油三酯及低密度脂蛋白胆固醇水平明显降低 (P <0 .0 5 ,P <0 .0 1) ;自发性高血压大鼠对照组心肌血管紧张素Ⅱ受体 1和血管紧张素Ⅱ受体 2蛋白阳性表达及其mRNA表达均明显高于Wistar kyoto大鼠组 (P <0 .0 1) ,6周后 ,5 0mg阿托伐他汀组血管紧张素Ⅱ受体 1蛋白和其mRNA表达明显降低 (P <0 .0 1) ,而血管紧张素Ⅱ受体 2蛋白和其mRNA表达明显高于自发性高血压大鼠对照组 (P <0 .0 1)。结论　阿托伐他汀能降低自发性高血压大鼠的血压 ,并对心肌血管紧张素Ⅱ受体有双重调节作用 ,即使血管紧张素Ⅱ受体 1下调、血管紧张素Ⅱ受体 2上调     

高脂血症患者LDL氧化易感性及调脂药物干预的影响

目的观察高脂血症对LDL氧化易感性的影响以及调脂药物干预后的改变.方法应用短程密度梯度超速离心分离血浆LDL,对11例高甘油三酯血症患者口服微粒化非诺贝特200 mg/d、10例高胆固醇血症患者口服普伐他汀10 mg/d治疗4周前后和6例正常人的LDL在体外以CuCl2诱导氧化,测定LDL开始氧化的迟滞期和氧化速率.结果 (1)LDL氧化的迟滞期,在高甘油三酯血症患者和高胆固醇血症患者均较正常组明显缩短(43.8±11.6,40.8±10.7 vs 70.5±14.6 min, P均<0.01).(2)LDL的氧化速率,在高甘油三酯血症患者和高胆固醇血症患者均较正常组明显增快(0.036±0.004,0.031±0.011 vs 0.020±0.011 O.D./min,P均<0.05).(3)高甘油三酯血症患者给微粒化非诺贝特治疗后LDL氧化的迟滞期显著延长(62.4±5.0 min,P<0.01),氧化速率明显减慢(0.031±0.003 O.D./min,P<0.05).(4)高胆固醇血症患者于普伐他汀治疗后LDL氧化的迟滞期明显延长(58.8±6.1 min,P<0.05),氧化速率无显著性变化(0.025±0.009 O.D./min,P>0.05).结论高甘油三酯血症患者和高胆固醇血症患者LDL氧化易感性增高,微粒化非诺贝特和普伐他汀能够降低高甘油三酯血症患者及高胆固醇血症患者LDL的氧化易感性.