Effect of Coenzyme Q10 and green tea on plasma and liver lipids, platelet aggregation, TBARS production and erythrocyte Na leak in simvastatin treated hypercholesterolmic rats

This study was conducted to investigate the hypocholesterolemic effect of simvastatin (30 mg/kg BW) and antioxidant effect of coenzyme Q10 (CoQ10, 15 mg/kg BW) or green tea (5%) on erythrocyte Na leak, platelet aggregation and TBARS production in hypercholesterolemic rats treated with statin. Food efficiency ratio (FER, ADG/ADFI) was decreased in statin group and increased in green tea group, and the difference between these two groups was significant (p<0.05). Plasma total cholesterol was somewhat increased in all groups with statin compared with control. Plasma triglyceride was decreased in statin group and increased in groups of CoQ10 and green tea, and the difference between groups of statin and green tea was significant (p<0.05). Liver total cholesterol was not different between the control and statin group, but was significantly decreased in the group with green tea compared with other groups (p<0.05). Liver triglyceride was decreased in groups of statin and green tea compared with the control, and the difference between groups of the control and green tea was significant (p<0.05). Platelet aggregation of both the initial slope and the maximum was not significantly different, but the group with green tea tended to be higher in initial slope and lower in the maximum. Intracellular Na of group with green tea was significantly higher than the control or statin group (p<0.05). Na leak in intact cells was significantly decreased in the statin group compared with the control (p<0.05). Na leak in AAPH treated cells was also significantly reduced in the statin group compared with groups of the control and CoQ10 (p<0.05). TBARS production in platelet rich plasma was significantly decreased in the groups with CoQ10 and green tea compared with the control and statin groups (p<0.05). TBARS of liver was significantly decreased in the group with green tea compared with the statin group (p<0.05). In the present study, even a high dose of statin did not show a cholesterol lowering effect, therefore depletion of CoQ10 following statin treatment in rats is not clear. More clinical studies are needed for therapeutic use of CoQ10 as an antioxidant in prevention of degenerative diseases independent of statin therapy.     

一氧化氮在糖皮质激素性骨质疏松发病中的作用和辛伐他汀对骨代谢的影响

目的探讨一氧化氮(NO)在糖皮质激素性骨质疏松症(GC-OP)发病机制中的作用和辛伐他汀对NO的调控。方法6个月龄SD雄性大鼠随机分为3组,实验组(A)给予辛伐他汀和地塞米松,模型组(B)给予生理盐水和地塞米松,对照组(C)给予生理盐水。8周后观察第3腰椎显微结构、股骨组织形态计量学、腰椎诱生型一氧化氮合酶(i NOS)和内皮细胞型一氧化氮合酶(eNOS)免疫组织化学。结果3组血清NO含量差异无统计学意义(P>0.05)。A组显微结构与C组相似,B组呈骨质疏松表现。3组eNOS表达的平均灰度值与平均积分吸光度分别为(179.08±4.38)与(0.455±0.019)、(169.42±3.00)与(0.401±0.010)、(181.08±2.31)与(0.463±0.150)。A组明显高于B组(P<0.01),与C组差异无统计学意义(P>0.05)。A组的骨体积、类骨质表面、类骨质宽度和成骨表面分别为(53.46±2.49)%、(9.52±1.11)%、(3.25±0.19)μm、(9.20±1.37)%,均比B组(42.48±1.95)%、(7.34±0.66)%、(2.72±0.32)μm、(7.43±0.58)%显著增高(P<0.01),与C组(54.69±1.87)%、(9.44±1.13)%、(3.44±0.28)μm、(9.83±1.06)%差异无统计学意义(P>0.05)。3组骨吸收表面的差异无统计学意义(P>0.05)。结论eNOS依赖性NO的低表达是GC-OP的重要发病机制,辛伐他汀增强eNOS的表达而有效预防该症的发生。     

低分子肝素钙联合辛伐他汀治疗不稳定型心绞痛疗效观察

目的探讨低分子肝素联合辛伐他汀治疗不稳定型心绞痛的疗效。方法将100例不稳定型心绞痛患者随机分为对照组50例和观察组50例。对照组仅采取常规治疗（硝酸酯类、β-受体阻滞剂、钙拮抗剂、阿司匹林等），观察组在常规治疗的基础上加用低分子肝素和辛伐他汀，观察比较各组的疗效。结果观察组总有效率为90．0％，对照组总有效率为60．0％，两组疗效比较差异有显著性意义（P〈0．05）。结论低分子肝素联合辛伐他汀治疗不稳定型心绞痛取得满意的疗效。     

The influence of simvastatin alone or in combination with gemfibrozil on plasma lipids and lipoproteins in patients with type III hyperlipoproteinemia

Summary Nineteen adult patients with type III hyperlipoproteinemia (HLP) and homozygosity for apolipoprotein (apo) E2 were treated with the 3-hydroxy-3-methyl glutaryl coenzyme A (HMG CoA) reductase inhibitor simvastatin (20 or 40 mg per day) alone or in combination with the fibrate derivative gemfibrozil (450 mg per day) during a 30-week outpatient study. With the 20-mg dose (n = 19) the mean plasma cholesterol level decreased from 13.24±8.04 8.04 at baseline to 8.04±4.19 mmol/l (mean reduction 39.3%; P<0.05), and the mean plasma triglyceride level decreased from 13.47±19.22 to 7.84±7.71 mmol/l (–41.8%; NS); this was due to a decrease in very low density lipoprotein (VLDL) cholesterol from 8.95±8.64 to 4.94±4.24mmo1/l (–44.8%; NS), a decrease in low density lipoprotein (LDL) cholesterol from 3.54±0.93to 2.25 ± 0.59 mmol/l (–36.5%; P<0.01), and an increase in high density lipoprotein (HDL) cholesterol from 0.72±0.28 to 0.85±0.34 (+18.1%; NS). Thirteen patients were treated with 40 mg simvastatin per day. Under this regimen there was a further significant decrease in LDL cholesterol from 2.33±0.62 to 1.81±0.49 mmol/l (–22.3%; P<0.01). In six patients who remained hyperlipidemic on monotherapy combination drug therapy with simvastatin (40 mg per day) and gemfibrozil (450 mg per day) was given. Compared to simvastatin alone the addition of gemfibrozil further lowered plasma concentrations of total cholesterol by 14.9%, VLDL cholesterol by 23.5%, and triglycerides by 17.1%, although this was not statistically significant. No patient was discontinued from single or combination drug therapy, and no severe clinical or biochemical side effects were observed. The results of this study demonstrate the usefulness of simvastatin in the therapy of type III HLP and indicate that in individual patients who remain hyperlipidemic on monotherapy combination drug therapy with both of these drugs is effective in further reducing plasma concentrations of total cholesterol, VLDL cholesterol, and triglycerides. Although no patient in this investigation developed myopathy or rhabdomyolysis, combined fibrate-HMG CoA reductase inhibitor treatment should be considered only for severe forms of hyperlipidemia and for patients who do not respond sufficiently to mon-therapy of any of these drugs.Abbreviations Apo Apolipoprotein - CPK creatine phosphokinase - GGT gamma-glutamyl transpeptidase - HDL high density lipoproteins - HLP hyperlipoproteinemia - HMG CoA 3-hydroxy-3-methyl glutaryl coenzyme A - IDL intermediate density lipoproteins - LDL low density lipoproteins - TG triglycerides - VLDL very low density lipoproteins     

含辛伐他汀药物血清对兔血管平滑肌细胞增殖的直接作用及意义

目的 :探讨辛伐他汀对体外培养兔血管平滑肌细胞增殖的影响及意义。方法 :16只雄性新西兰兔随机分为血清对照组和三个不同剂量的辛伐他汀亚组 (每日分别给予辛伐他汀 5mg/kg、10mg/kg、15mg/kg) ,7天后采血并混合每组 4只兔血 ,无菌分离制备三亚组的辛伐他汀含药血清。采用内皮素 1(ET 1)刺激正常喂饲原代培养兔主动脉血管平滑肌细胞的方法 ,建立血管平滑肌细胞增殖模型。采用MTT及3H TdR法检测各组辛伐他汀含药血清对血管平滑肌细胞增殖的作用。结果 :与不含药的正常对照组相比 ,不同亚组辛伐他汀含药血清呈剂量依赖性抑制血管平滑肌细胞增殖 (P <0 .0 1～0 .0 5 )。结论 :兔口服辛伐他汀后的血清具有抑制血管平滑肌细胞增殖的作用     

辛伐他汀治疗混合性高脂血症患者的疗效和耐受性

目的：观察辛伐他汀治疗混合性高脂血症患者的疗效和耐受性。方法;采用开放性、自身对比研究,对１２３例混合性高脂血症患者给予辛伐他汀１０ｍｇ,每晚一次口服,共治疗６周。结果：６周后,血清总胆固醇、低密度脂蛋白胆固醇均较治疗前明显下降（分别降低２３．８％、２９．５％,Ｐ〈０．０５）,血甘油三酯也显著降低（平均降低２７．１％,Ｐ〈０．０５）,高密度脂蛋白胆固醇明显上升（平均升高２３．６％,Ｐ〈０．０５）。未出现严重不良反应。结论：辛伐他汀对混合性高脂血症患者疗效明显,耐受性好。     

沥水调脂胶囊和舒降之片治疗高胆固醇血症的比较研究

目的　评价沥水调脂胶囊和舒降之片治疗高胆固醇血症的疗效与不良反应。方法　 6 6例高胆固醇血症的病人随机分成沥水调脂胶囊组 (A组 )和舒降之组 (B组 ) ;A组 33例给予沥水调脂胶囊 3粒 ,po,tid ,B组 33例给予舒降之 10mg ,po ,qd ;疗程均为 4周。结果　与治疗前相比 ,A组胆固醇 (TC)降低 ,有效率为 90 90 % ,甘油三脂 (TG)降低 ,有效率为 6 9 70 % ;B组TC降低 ,有效率为 93 33% ,TG降低 ,有效率为 5 1 5 1% ;A组和B组疗效间无显著性差异 (P >0 0 5 ) ,不良反应发生率两组间有显著性差异 (3 3%和 12 1% ,P <0 0 1)。结论　沥水调脂胶囊治疗高胆固醇血症与舒降之片相比 ,效果同样明显。     

血脂康辛伐他汀治疗2型糖尿病并血脂异常

目的 比较血脂康与辛伐他汀治疗2型糖尿病（DM）并血脂异常的临床疗效。方法 2型DM并血脂异常患者89例，分A组（血脂康组）及B组（辛伐他汀组）分别测定两组患者服药前及服药后3个月的空腹血糖（FG）、餐后2h血糖（2hPG）、空腹胰岛素（Fins）、血胆固醇（TC）、甘油三脂（TG）、低密度脂蛋白胆固醇（LDL—c）、高密度脂蛋白胆固醇（HDL—C）水平，并进行比较。结果 两组患者的血TC、TG、LDL—C都较服药前降低，HDL—C水平较服药前升高，差异有显著意义。A组空腹血糖、餐后血糖明显较服药前降低，差异有显著意义，B组空腹血糖、餐后血糖较服药前降低，但差异无显著意义。两组的胰岛素敏感指数（IAI）都较服药前提高，但A组较明显（P〈0．05），B组不明显（P〉0．05）。结论 血脂康与辛伐他汀都有明显的调节血脂作用，血脂康还有协助降糖及提高胰岛素敏感性作用。     

辛伐他汀对急性冠脉综合征早期C反应蛋白和血脂的影响

目的　观察急性冠脉综合征的早期应用辛伐他汀后C反应蛋白和血脂的变化。方法　70例急性冠脉综合征患者随机分为对照组(无服用任何调脂药物,34例)和治疗组(辛伐他汀10mg/d ,36例) ,测定治疗前后C反应蛋白和血脂的变化。结果　治疗组治疗5d后C反应蛋白水平下降35 % ,与治疗前比较差异有显著意义(P <0 . 0 5 ) ;治疗4周后TC、LDL C分别下降30 %、4 0 % ,与治疗前比较差异有显著意义;而且随访期间治疗组的心肌梗死发生率、再住院率均明显低于对照组。结论　在急性冠脉综合征早期予以辛伐他汀治疗是可行及有效的,可明显降低血脂和血浆炎症因子的水平,可能有利于动脉粥样斑块的稳定。