多廿醇对高脂血症大鼠血清胆固醇水平的影响

目的观察多廿醇对高脂血症大鼠的降胆固醇作用并探讨其作用机制。方法大鼠分为正常对照组、多廿醇4mg.kg-1预防组、高脂模型组、多廿醇4,6和8mg.kg-1治疗组和洛伐他汀阳性对照组;后5组大鼠在实验前4周给予高脂饲料制备高脂大鼠模型,从第5周开始,除正常对照和高脂模型组外,各给药组ig给予不同浓度的多廿醇或洛伐他汀,每天1次,连续6周。多廿醇预防组喂饲高脂饲料的同时ig多廿醇,每天1次,连续10周。用全自动生化分析仪测定血清总胆固醇(TC)、甘油三酯(TG)、低密度脂蛋白胆固醇(LDL-C)和高密度脂蛋白胆固醇(HDL-C)水平,并测定粪便总胆汁酸(FBA)排出量,紫外分光速率法测定肝脏微粒体3-羟基-3-甲基戊二酸单酰辅酶A(HMG-CoA)还原酶活性,荧光配体标记法测定外周血淋巴细胞低密度脂蛋白受体(LDL-R)活性。结果与高脂模型组比较,多廿醇预防组、多廿醇治疗组和洛伐他汀阳性对照组大鼠血清TC含量明显下降(39.1%～46.4%),LDL-C含量明显下降(66.6%～80.7%),粪便FBA明显升高(9.7%～19.0%),肝脏微粒体HMG-CoA还原酶活性明显下降(13.8%～23.6%),外周血淋巴细胞LDL-R活性升高(27.5%～129.6%);多廿醇预防组、多廿醇8mg.kg-1组和洛伐他汀组HDL-C水平明显升高(12.2%～16.7%);洛伐他汀组TG水平明显下降。结论多廿醇具有明显降低胆固醇的作用,其机制包括增加胆汁酸的排泄、抑制胆固醇合成限速酶HMG-CoA还原酶活性和促进低密度脂蛋白受体活性的表达。     

多廿醇对高脂血症大鼠脂蛋白代谢关键酶活性的影响

目的:研究多廿醇的降胆固醇作用及其酶学机制。方法:将大鼠随机分为对照组、多廿醇(4.0mg·kg-1·d-1)预防组、多廿醇低、中、高剂量(4.0、6.0、8.0mg·kg-1·d-1)组、阳性药洛伐他汀组和高脂模型组(后5组先行高脂造模4周),灌胃给药6周后采集血液,测定血清中总胆固醇(TC)、甘油三酯(TG)、低密度脂蛋白胆固醇(LDL-C)、高密度脂蛋白胆固醇(HDL-C)含量;称量大鼠体质量、肝重,计算肝脏系数;测定血清卵磷脂胆固醇酰基转移酶(LCAT)、肝脏脂蛋白脂酶(LPL)和肝脂酶(HL)活性。结果:多廿醇各组能明显降低高脂模型大鼠TC39.1%～43.3%(P<0.01)、LDL-C66.6%～80.7%(P<0.01)、肝脏系数11.1%～11.8%(P<0.01);高剂量组升高HDL-C14.0%(P<0.05),中、高剂量组LCAT活性分别升高41.9%、44.3%(P<0.01),HL活性分别升高20.0%(P<0.05)、28.0%(P<0.01)。结论:多廿醇对高脂模型大鼠具有明显降胆固醇作用,其作用可能与升高脂蛋白代谢关键酶的活性有关。     

丹皮酚体内外抗人食管癌Eca-109细胞增殖及诱导凋亡的作用

目的研究丹皮酚(paeonol,Pae)在体内外对人食管癌细胞Eca-109的抑瘤作用及其对细胞凋亡的影响。方法采用噻唑蓝(MTT)体外试验法和灌胃给药体内抗肿瘤试验。光镜及电镜观察各组的肿瘤组织的形态学变化。应用末端脱氧核苷酸转移酶介导的缺口末端标记(TUNEL)法测定细胞凋亡指数。结果丹皮酚在体外对Eca-109细胞有明显的细胞毒作用,半数抑制浓度(IC50)为0.342mmol·L-1;体内灌胃给予丹皮酚25、50、100和200mg·kg-1对裸鼠移植人食管癌Eca-109的抑制率分别为10.67%、23.54%、27.91%和34.46%;顺铂5mg·kg-1组抑瘤率为58.71%;丹皮酚在100mg·kg-1剂量下与顺铂5mg·kg-1联合用药抑制率为77.91%。光镜下用药组可见较多凋亡的肿瘤细胞。透射电镜下可见肿瘤细胞核染色质浓缩边聚、胞质浓缩、核碎裂以及凋亡小体形成等典型的凋亡表现。用药组凋亡指数较对照组明显增加。结论丹皮酚在体内外具有抑制人食管癌Eca-109细胞增殖及诱导其凋亡作用。     

多廿醇降胆固醇及抗氧化作用的实验研究

目的 观察多廿醇对高脂血症大鼠的降胆固醇和抗氧化作用.方法 将大鼠随机分为正常对照组、多廿醇预防组和高脂造模组.多廿醇预防组喂饲高脂饲料的同时给予多廿醇灌胃10周;高脂造模组先给予高脂饲料4周制备大鼠高脂血症模型,再按照总胆固醇水平分为多廿醇低、中、高剂量组和阳性药物洛伐他汀对照组,灌胃给予相应药物6周后采血,测定血清中总胆固醇(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,并计算LDL-C/HDL-C、TG/HDL-C比值和动脉硬化指数(AI);测定血清中丙二醛(MDA)含量,超氧化物歧化酶(SOD)和谷胱甘肽过氧化物酶(GSH-Px)活性.结果 与高脂模型组比较,多廿醇预防组、多廿醇低、中、高剂量组和阳性对照组大鼠的血清中TC、LDL-C含量显著性下降(P＜0.01);阳性对照组大鼠的血清中TG水平显著性降低(P＜0.05);多廿醇预防组、多廿醇高剂量组和阳性对照组大鼠血清中HDL-C水平显著性升高(P＜0.05);多廿醇预防组,多廿醇低、中、高剂量组和阳性对照组LDL-C/HDL-C比值显著性下降(P＜0.01);AI显著性下降(P＜0.01);血清中MDA含量显著性下降(P＜0.05或P＜0.01);多廿醇中、高剂最组和阳性对照组的血清中SOD活性显著性升高(P＜0.05或P＜0.01);多廿醇中和高剂量组的血清中GSH-Px活性显著性升高(P＜0.01).结论 多廿醇对高脂血症模型大鼠具有明显降胆固醇的作用,且可增强机体的抗氧化作用.     

20(S)-原人参二醇对SMMC-7721细胞体内外作用的研究

目的观察不同剂量的20(S)-原人参二醇(Protopanaxadiol,PPD)在体内外对人肝癌细胞株SMMC-7721抗肿瘤作用。方法建立人肝癌裸鼠皮下移植瘤模型,观察20(S)-原人参二醇的肿瘤抑制作用。MTT比色法检测20(S)-原人参二醇对SMMC-7721细胞的增殖抑制作用,Ho-echst33342核染色观察细胞凋亡形态学改变,采用FITC-An-nexinⅤ/PI双染流式细胞术分析凋亡情况,同时检测Caspase-3活性。结果在体内,PPD可抑制SMMC-7721细胞裸鼠异种移植瘤生长;在体外,PPD对SMMC-7721细胞的增殖具有明显的抑制及诱导其凋亡作用,呈时间和剂量依赖性,Hoechst33342核染色可见凋亡小体,同时伴有Caspase-3活性的增加。结论20(S)-原人参二醇在体内外均可抑制SMMC-7721细胞增殖,并诱导其凋亡,其机制可能通过活化Caspase-3诱导细胞凋亡而发挥抗肿瘤作用。     

氯化两面针碱体外和体内的抗肿瘤作用

目的观察氯化两面针碱(NC)的抗肿瘤作用。方法采用MTT法观察NC体外对肿瘤细胞存活的影响。移植性S180肉瘤模型小鼠,ip给予NC,每天1次,共10d,测瘤重,计算抑瘤率,并在电镜下观察移植瘤细胞的超微结构。腹水型H22肝癌模型小鼠,sc给予NC,每天1次,共10d,观察小鼠的存活时间,计算生命延长率。结果体外给予NC0.625,1.25,2.5,5.0和10.0mg·L-1可浓度依赖性地降低人鼻咽癌细胞CNE1、人肺癌细胞SPC-A-1和人乳腺癌细胞MDA-MB-231等9种肿瘤细胞的存活率,作用48h平均IC50为(3.33±0.28)mg·L-1。体内给予NC2.5,5.0和10.0mg·kg-1对小鼠S180肉瘤的抑瘤率分别为1.95%,27.3%和42.9%,对腹水型H22肝癌小鼠的生命延长率分别为35.7%,71.4%和85.7%。电镜下可见NC10.0mg·kg-1组S180移植瘤细胞核染色质浓缩并边缘化,核碎裂,胞浆空泡化明显。结论NC体内外应用均具有明显的抗肿瘤作用。     

多廿烷醇与普伐他汀治疗高脂血症的疗效和安全性

目的评价多廿烷醇治疗高脂血症,特别是高胆固醇血症的疗效和安全性。方法多甘烷醇组(试验组,多廿烷醇10mg·d~(-1))和普伐他汀组(对照组,普伐他汀10 mg·d~(-1))各119例。进行随机、双盲、双模拟、阳性药物平行对照试验。观察2组降脂疗效和不良反应发生情况。结果经过12 wk治疗,多廿烷醇组总胆固醇(TC)、低密度脂蛋白胆固醇(LDL)、TC-高密度脂蛋白胆固醇(HDL-C)/ HDL-C、载脂蛋白B_(100)(Apo B_(100))、脂蛋白(Lpa)治疗前分别为(6.6±s0.7)、(4.0±0.6)、(0.10±0.03)、(3.3±0.5)mmol·L~(-1)、(260±184)mg·L~(-1),治疗后分别为(6.0±1.3)、(3.5±0.8)、(O.09±0.04)、(2.7±0.8)mmol·L~(-1)、(130±130)mg·L~(-1),治疗后各指标较治疗前均有非常显著差异(P<0.01)。普伐他汀组TC、LDL-C、TC-HDL-C/HDL-C、Apo B_(100)、Lpa治疗前分别为(6.7±0.8)、(4.1±0.7)、(0.10±0.03)、(3.4±0.5)mmol·L~(-1)、(279±240)mg·L~(-1),治疗后分别为(6.0±1.3)、(3.5±0.9)、(0.09±0.03)、(2.8±0.8)mmol·L~(-1)、(182±213)mg·L~(-1),治疗后各指标较治疗前均有非常显著差异(P<0.01)。但2组相比较,调脂作用相似,无显著差异(P>0.05)。不良反应方面,多廿烷醇组(9.2%)明显少于普伐他汀组(18.5%),2组有显著差异(P<0.05)。不良反应大多较轻微,不需停药能自行缓解。结论多廿烷醇10 mg·d~(-1)降脂效果与普伐他汀10 mg·d~(-1)的疗效相当,均能明显降低TC、LDL-C、TC-HDL-C/ HDL-C、Apo B_(100)、Lpa。多廿烷醇的安全性优于普伐他汀,不良反应轻微,耐受性好。     

异十三基二乙胺体内外抗肿瘤作用研究

目的:探讨异十三基二乙胺(D-108)体内外抗肿瘤作用。方法:应用台盼蓝排染法、MTT法检测D-108对多种体外培养肿瘤细胞、人牙龈成纤维细胞(HGF)及Beagle犬骨髓基质干细胞(MSC)的细胞毒作用;Bliss法观察小鼠灌胃(i.g.)D-108急性毒性实验;在可耐受剂量下观察D-108对小鼠移植性实体瘤U14的抑制率。Giemsa染色法观察在D-108影响下,HL60细胞的形态学变化。结果:D-108对肿瘤细胞的体外细胞毒作用(IC50:0.22~2.19mg·L-1)强于HGF及MSC(IC50分别为5.55、3.57mg·L-1)。LD50为36.49mg·kg-1(i.g.)。D-108有效抑制U14在小鼠体内的生长,100mg·kg-1·d-1i.g.瘤质量抑制率为45.27%。HL60细胞经D-108处理后呈典型凋亡形态学改变。结论:D-108有较强的体内外抗肿瘤活性且毒性较小,并能诱导HL60细胞凋亡。     

鲜壁虎醇提物与水提物体内、外对肿瘤活性的影响

目的:研究鲜壁虎水提物与醇提物体内、外的抗肿瘤活性。方法:体外采取MTT法测定鲜壁虎水提物、醇提物对BEL-7402细胞和HepG2细胞生长的抑制作用。体内复制移植瘤小鼠H22模型,给药后计算抑瘤率、胸腺指数和脾脏指数。结果:0.0625mg·mL-1壁虎水提物对HepG2细胞生长有显著抑制作用(P<0.05),1.0000、0.2500、0.0625mg·mL-1壁虎水提物对BEL-7402细胞的生长均有显著抑制作用(P<0.05)。1.0000、0.2500、0.0625mg·mL-1壁虎醇提物对2种细胞有促进增殖的趋势。1.0000、0.2500、0.0625mg·mL-1壁虎水提物与1.0000、0.0625mg·mL-1壁虎醇提物均可显著抑制H22荷瘤小鼠肿瘤生长活性(P<0.05)。结论:鲜壁虎水提物体外有抑制肿瘤细胞生长的作用,醇提物有促进细胞增殖的趋势。鲜壁虎水提物、醇提物体内均有抗肿瘤活性,水提物抑瘤率高于醇提物。     

尿多酸肽对人肝癌细胞Smmu7721体内体外抑制作用

目的 :研究由人尿提取的尿多酸肽 (uroacitide)对人肝癌细胞的体内体外抑制作用。方法 :体外实验 ,以四唑盐(MTT)比色法测定培养板中加入尿多酸肽后 ,人肝癌细胞Smmu772 137℃ 5 %CO2 培养箱培养 72h的生物活性 ;体内抑瘤实验为裸鼠皮下接种人肝癌细胞Smmu 772 1,待肿瘤生长后 ,连续每天ip尿多酸肽 10天 ,观察其抑制作用。结果 :体外实验 ,尿多酸肽剂量为 0 0 3～ 2 0 0mg·mL- 1 ,对人肝癌细胞Smmu 772 1的IC5 0 为 0 35～ 0 49mg·mL- 1 ;体内实验 ,尿多酸肽剂量 5 0 0～ 2 0 0 0mg·kg- 1 ,对裸鼠接种人肝癌细胞Smmu 772 1的抑瘤率在 38 9%～ 6 7 9%。结论 :尿多酸肽对人肝癌细胞Smmu772 1体内体外均有显著的抑制作用。     

Effects of policosanol treatment on the susceptibility of low density lipoprotein (LDL) isolated from healthy volunteers to oxidative modification in vitro

AIMS: The aim of this study was to investigate the effect of policosanol on the susceptibility of LDL-C to in vitro lipid peroxidation in human healthy volunteers. METHODS: The effect of policosanol (5 and 10 mg day(-1) on LDL-C oxidation was studied in a double-blind, randomized, placebo-controlled trial conducted in 69 subjects. LDL-C samples isolated at baseline and after 8 weeks were subjected to in vitro tests of LDL-C oxidation. We tested the susceptibility of LDL-C to lipid peroxidation in a cell-free system by the addition of copper ions as well as in a more physiological system, macrophage-mediated oxidation. RESULTS: At baseline all groups were well matched regarding all variables. After 8 weeks of therapy policosanol administered at 5 and 10 mg, significantly and in a dose-dependent manner increased the lag phase of conjugated diene generation (mean +/- s.d.) from 83.79+/-29.16 min to 94.90+/-25.50 min (5 mg day(-1)) and from 82.74+/-17.16 min to 129.89+/-35.71 min (10 mg day(-1)), while in the placebo group LDL-C oxidation did not change significantly. Policosanol (10 mg day(-1)), but not placebo, significantly decreased the rate of conjugated diene generation. Comparison with placebo after therapy also showed significant differences. Macrophage mediated-oxidation was also inhibited by policosanol as evident by measuring thiobarbituric acid reactive substances (TBARS). Policosanol (10 mg day(-1)) significantly lowered malondialdehyde (MDA) generation from 8.50+/-0.91 to 5.76+/- 1.01 nmol mg(-1) protein. Comparison with placebo after 5 and 10 mg day(-1) showed significant differences. Policosanol significantly lowered total cholesterol by 10.5% (5 mg day(-1)) and 12.4% (10 mg day(-1)) and LDL-C by 16.7% and 20.2%, respectively. Also, policosanol (10 mg day(-1)) increased HDL-C by 15.2%. Five subjects withdrew from the study, none because of adverse experiences. No clinical or blood biochemical drug-related disturbances were found. CONCLUSIONS: The present study demonstrated that policosanol administered within its therapeutic dosage for lowering cholesterol (5 and 10 mg day(-1)), decreased the susceptibility of LDL-C to lipid peroxidation in vitro.     

Comparative study of the efficacy and tolerability of policosanol and lovastatin in patients with hypercholesterolemia and noninsulin dependent diabetes mellitus

This randomized, double-blind study was undertaken to compare the efficacy and tolerability of policosanol (10 mg/day) and lovastatin (20 mg/day) in patients with hypercholesterolemia and noninsulin dependent diabetes mellitus. After 6 weeks on a lipid lowering diet, 53 patients were randomized to receive either policosanol or lovastatin tablets that were taken o.i.d. for 12 weeks under double-blind conditions. Both groups were similar at randomization. Policosanol significantly (p < 0.001) lowered low-density lipoprotein (LDL)-cholesterol (20.4%), total cholesterol (14.2%) and the ratio of LDL-cholesterol to high-density lipoprotein (HDL)-cholesterol (23.7%). Lovastatin significantly (p < 0.01) lowered LDL-cholesterol (16.8%), total cholesterol (14.0%) and the ratio (p < 0.05) of LDL-cholesterol to HDL-cholesterol (14.9%). Triglyceride levels did not significantly change after therapy. Policosanol, but not lovastatin, significantly increased (p < 0.01) levels of HDL-cholesterol (7.5%). Comparison between groups showed that changes in HDL-cholesterol induced by policosanol were significantly greater (p < 0.01) than those induced by lovastatin. Both treatments were safe and well tolerated. Lovastatin moderately but significantly (p < 0.05) increased levels of aspartate aminotransferase, creatine phosphokinase and alkaline phosphatase. Adverse reactions were more frequent in the lovastatin group (p < 0.01) than in the policosanol group. In conclusion, policosanol administered at 10 mg/day produces more advantageous changes in HDL-cholesterol and has a better safety and tolerability profile than lovastatin 20 mg/day.     

Effects of policosanol and pravastatin on lipid profile, platelet aggregation and endothelemia in older hypercholesterolemic patients

This randomized, double-blind study was undertaken to compare the effects of policosanol and pravastatin administered at 10 mg/day on lipid profile, platelet aggregation and endothelemia in older patients with type II hypercholesterolemia and high coronary risk. After 6 weeks on a lipid-lowering diet, patients with low-density lipoprotein (LDL) cholesterol levels > 3.4 mmol/l were randomized to receive, under double-blind conditions, policosanol or pravastatin 10 mg tablets that were taken with the evening meal for 8 weeks. Policosanol significantly (p < 0.00001) lowered LDL-cholesterol (19.3%), total cholesterol (13.9%) and the ratios of LDL-cholesterol/high-density lipoprotein (HDL)-cholesterol (28.3%) and total cholesterol/HDL-cholesterol (24.4%). Pravastatin significantly (p < 0.00001) lowered LDL-cholesterol (15.6%), total cholesterol (11.8%) and the ratios (p < 0.0001) of LDL-cholesterol/HDL-cholesterol (18.9%) and total cholesterol/HDL-cholesterol (15.7%). Policosanol, but not pravastatin, significantly increased (p < 0.001) levels of HDL-cholesterol (18.4%) and reduced (p < 0.01) triglycerides (14.1%). Policosanol was more effective (p < 0.05) than pravastatin in inhibiting platelet aggregation induced by all agonists and it significantly reduced (p < 0.0001) platelet aggregation induced by arachidonic acid at 1.5 and 3 mmol/l by 42.2% and 69.5%, respectively, platelet aggregation induced by collagen 0.5 microgram/ml (p < 0.05) (16.6%) and that induced by adenosine diphosphate 1 mumol/l (p < 0.01) (20.3%). Pravastatin significantly reduced (p < 0.001) (27%) only platelet aggregation induced by arachidonic acid 3 mmol/l. Both drugs significantly decreased (p < 0.00001) endothelemia levels but final values were significantly lower (p < 0.001) in the policosanol than in the pravastatin group. Both treatments were safe and well tolerated. Pravastatin significantly (p < 0.01) increased serum levels of alanine amine transferase but individual values remained within normal. Two patients on pravastatin discontinued the study because of adverse experiences (myocardial infarction and jaundice, respectively). In conclusion, the effects of policosanol (10 mg/day) on lipid profile, platelet aggregation and endothelemia in older patients with type II hypercholesterolemia and high coronary risk are more favorable than those induced by the same doses of pravastatin.     

Comparison of the efficacy,safety and tolerability of original policosanol versus other mixtures of higher aliphatic primary alcohols in patients with type II hypercholesterolemia

This randomized, double-blind study was undertaken to compare the efficacy and tolerability of policosanol and Octa-60 in patients with type II hypercholesterolemia. After 4 weeks on a diet, 110 patients were randomized to policosanol or Octa-60 5 mg tablets once a day for 5 weeks. The dose was then doubled to 10 mg/day for the next 5 weeks. Policosanol 5 and 10 mg/day significantly lowered low-density lipoprotein-cholesterol (LDL-C) (p<0.0001 and p<0.00001), the main efficacy variable, by 18.6% and 30.2%, while Octa-60 significantly reduced (p<0.05) LDL-C by 10.0% at study completion only. The frequency of policosanol patients reaching reductions of LDL-C > or = 15% after 5 mg/day (37/55; 67.3%) and 10 mg/day (47/55; 88.7%) was greater (p<0.01 and p<0.01) than in the Octa-60 group, which was 5/55 (9.1%) and 20/55 (36.4%). Likewise, the frequency of patients reaching LDL-C values of <3.4 mmol/l at study completion was greater (p<0.001) in the policosanol group (39/55, 70.9%) than in the Octa-60 group (6/55, 10.9%). Policosanol 5 and 10 mg/day significantly lowered (p<0.00001) total cholesterol (TC) (13.4% and 20.4%), LDL-C/high-density lipoprotein-cholesterol (HDL-C) (22.1% and 37.0%) and TC/HDL-C (17.2% and 28.2%). Octa-60 at 10 mg/day lowered (p<0.05) TC (8.7%), LDL-C/HDL-C (12.6%) and TC/HDL-C (9.4%). HDL-C was increased (p<0.001 and 0.0001) by policosanol 5 and 10 mg/day (5.6% and 12.5%) but was unchanged by Octa-60. In both groups, triglycerides remained unchanged. Both treatments were safe and well tolerated. Octa-60, but not policosanol, significantly increased glucose and alanine aminotransferase, but individual values were within the normal range. Four patients (two from each group) discontinued the trial, but only one (in the Octa-60 group) did so because of an adverse event (AE) (skin rash). Overall, three patients (all from the Octa-60 group) reported AEs. In conclusion, original policosanol at 5 and 10 mg/day, but not Octa 60, was effective in patients with type II hypercholesterolemia. Thus, policosanol reached the efficacy criterion for LDL-C reduction in both steps, while Octa-60 failed to reach this goal. In addition, policosanol was better tolerated than Octa-60.     

Comparison of the efficacy and tolerability of policosanol with atorvastatin in elderly patients with type II hypercholesterolaemia

BACKGROUND: Hypercholesterolaemia is a risk factor for coronary heart disease (CHD). Clinical studies have shown that lowering elevated serum total cholesterol (TC) levels, and particularly low density lipoprotein-cholesterol (LDL-C) levels, reduces the frequency of coronary morbidity and deaths, whereas high serum levels of high density lipoprotein-cholesterol (HDL-C) protect against CHD. Policosanol is a cholesterol-lowering drug purified from sugar cane wax with a therapeutic dosage range from 5-20 mg/day. Atorvastatin is an HMG-CoA reductase inhibitor which across its dosage range (10-80 mg/day) has shown significantly greater lipid-lowering effects than all previously marketed statins. OBJECTIVE: This study was undertaken to compare the efficacy and tolerability of policosanol with atorvastatin in older patients with type II hypercholesterolaemia. PATIENTS AND METHODS: This randomised, single-blind, parallel-group study was conducted in older patients (60-80 years) with type II hypercholesterolaemia. After 4 weeks on a cholesterol-lowering diet, 75 patients were randomised to policosanol or atorvastatin 10mg tablets taken once daily with the evening meal for 8 weeks. An interim and final check-up were performed at 4 and 8 weeks, respectively, after treatment was initiated. RESULTS: At 4 (p < 0.0001) and 8 (p < 0.00001) weeks, policosanol 10 mg/day significantly lowered serum LDL-C levels by 17.5 and 23.1%, respectively compared with baseline; corresponding values for atorvastatin were 28.4 and 29.8%. At study completion, policosanol significantly (p < 0.0001) reduced serum TC (16.4%), LDL-C/HDL-C ratio (25.5%) and TC/HDL-C ratio (19.3%), as well as (p < 0.001) triglyceride levels (15.4%). Atorvastatin significantly (p < 0.0001) decreased serum TC (22.6%), LDL-C/HDL-C (26.2%) and TC/HDL-C (19.8%) ratios, as well as (p < 0.001) triglyceride levels (15.5%). Atorvastatin was significantly more effective than policosanol in reducing LDL-C and TC, but similar in reducing both atherogenic ratios and triglyceride levels. Policosanol, but not atorvastatin, significantly (p < 0.05) increased serum HDL-C levels by 5.3%. Both treatments were well tolerated. At study completion, atorvastatin mildly, but significantly (p < 0.05) increased creatine phosphokinase (CPK) and creatinine, whereas policosanol significantly reduced AST and glucose (p < 0.01) and CPK (p < 0.05) levels. All individual values, however, remained within normal limits. Three atorvastatin but no policosanol patients withdrew from the study because of adverse events: muscle cramps (1 patient), gastritis (1 patient) and uncontrolled hypertension, abdominal pain and myalgia (1 patient). Overall, no policosanol and seven atorvastatin patients (18.9%) reported a total of nine mild or moderate adverse events during the study (p < 0.01). CONCLUSIONS: This study shows that policosanol (10 mg/day) administered for 8 weeks was less effective than atorvastatin (10 mg/day) in reducing serum LDL-C and TC levels in older patients with type II hypercholesterolaemia. Policosanol, but not atorvastatin, however, significantly increased serum HDL-C levels, whereas both drugs similarly reduced atherogenic ratios and serum triglycerides. Policosanol was better tolerated than atorvastatin as revealed by patient withdrawal analysis and overall frequency of adverse events. Nevertheless, further studies must be conducted in larger sample sizes and using dose-titration methods to achieve target lipid levels in order to reach wider conclusions.     

Effects of policosanol and lovastatin on lipid profile and lipid peroxidation in patients with dyslipidemia associated with type 2 diabetes mellitus

In this pilot, randomized, double-blind study, we compared the effects of policosanol and lovastatin on lipid profile and lipid peroxidation in patients with dyslipidemia and type 2 diabetes mellitus. After 4 weeks on a cholesterol-lowering diet, 36 patients were randomized to policosanol (10 mg/day) or lovastatin (20 mg/day) tablets o.i.d. for 8 weeks. Policosanol significantly (p < 0.001) lowered serum low-density lipoprotein-cholesterol (LDL-C) (29.9%), total cholesterol (21.1%), triglycerides (13.6%) and the LDL-C/high-density lipoprotein-cholesterol (HDL-C) (36.7%) and total cholesterol/HDL-C (28.9%) ratios and significantly (p < 0.01) increased HDL-C (12.5%). Lovastatin significantly (p < 0.001) lowered LDL-C (25%), total cholesterol (18%), triglycerides (10.9%) and the LDL-C/HDL-C (30.4%) and total cholesterol/HDL-C ratios (23.9%) and significantly (p < 0.01) raised HDL-C (8.3%). Policosanol was more effective (p < 0.05) than lovastatin in reducing both ratios and in increasing (p < 0.05) HDL-C. Policosanol, but not lovastatin, significantly raised the lag time (20.9%) of Cu+2-induced LDL peroxidation and total plasma antioxidant activity (24.2%) (p < 0.05). Both policosanol and lovastatin significantly decreased the propagation rate (41.9% and 41.6% respectively, p < 0.001), maximal diene production (8.3% and 5.7%) and plasma levels of thiobarbituric acid reactive substances (9.7% and 11.5%, p < 0.001). Both treatments were well tolerated. Only one patient in the lovastatin group withdrew from the trial due to adverse events. In conclusion, policosanol and lovastatin administered short term to patients with dyslipidemia secondary to type 2 diabetes were effective in lowering cholesterol and in inhibiting the extent of lipid peroxidation. Policosanol (10 mg/day) was slightly more effective than lovastatin (20 mg/day) in reducing the LDL-C/HDL-C and total cholesterol/HDL-C ratios, in increasing HDL-C levels and in preventing LDL oxidation. Nevertheless, since this was a pilot study, further clinical studies performed in larger sample sizes of diabetic patients are needed for definitive conclusions.     

Effect of Policosanol on Lipofundin-induced Atherosclerotic Lesions in Rats

Policosanol is a mixture of higher aliphatic alcohols isolated from sugar cane wax, showing cholesterol-lowering effects and preventing the development of lipofundin-induced lesions in New Zealand rabbits. This study was conducted to determine whether policosanol orally administered to rats also protects against the development of lipofundin-induced atherosclerotic lesions. Fifty four male Wistar rats were randomly distributed amongst a negative control group, a positive control group intravenously injected with lipofundin for eight days, and four experimental groups also injected with lipofundin, but orally receiving policosanol at 0·5, 2·5, 5 and 25 mg kg^?1, respectively. Policosanol treatment was orally administered once-a-day for eight days, while control groups similarly received equivalent amounts of vehicle. A significant reduction of the atherosclerotic lesions in the treated animals was observed. It is concluded that policosanol has a protective effect on lipofundin-induced aortic lesions in Wistar rats.     

Effect of Policosanol on Isoprenaline-induced Myocardial Necrosis in Rats

Abstract— Policosanol is a mixture of higher aliphatic primary alcohols isolated from sugar cane (Saccharum officinarum L.) and octacosanol represents its main component. This study was conducted to examine the effects of policosanol on myocardial necrosis induced by subcutaneous injection of isoprenaline in rats. A significant reduction (P < 0·01) of infarct size, polymorphonuclear cells and mast cells was observed in animals treated with policosanol at 5 or 25 mg kg^?1, while animals receiving only acetysalicylic acid pretreatment showed a significant decrease in the infarct area (P < 0·05). No significant differences in polymorphonuclear and mast cells were obtained when compared with positive control data. It is concluded that policosanol delays the evolution of infarction, showing a protective effect on the myocardial necrosis induced by isoprenaline in this experimental model.