ObjectTo observe the clinical efficacy and safety of the combination therapy of atorvastatin and JiangZhi Decoction (ZJD) for primary hyperlipidemia (Tan Zhuo Zu E Zheng) and to analyze the interactions of drugs in hypolipidemic effect. MethodsA 2*2 factorial design, single-blind, stratified randomized controlled trial according to the level of lipid was conducted. Primary hyperlipidemia (Tan Zhuo Zu E Zheng) patients met the inclusion criteria were divided into 5 groups:ATV 10 mg group (group A), ATV 20 mg group (group B), ATV 10 mg+JZD group (group C), ATV 20 mg+JZD group (group D), JZD group (group E). After two weeks treatment, the efficacy and safety among the 5 groups were compared. ResultsA total of 92 patients were included, of which, 20 were in group A, 25 in group B, 21 in group C, 17 in group D, and 9 in group E. The results showed that:(1) There was no significant difference between group C and group B in the reduction of serum total cholesterol (TC) and low-density lipoprotein cholesterol (LDL-C) (PTC=0.226, PLDL-C=0.818). (2) The results of 2*2 factorial analysis showed that, there was no significant interaction between TCM factor and western medicine factor (PTC=0.605, PLDL-C=0.843). (3) There were no significant differences in safety outcomes among 5 groups (all P values >0.05). ConclusionATV 10 mg+JZD and ATV 20 mg have a similar efficacy in reducing TC and LDL-C. There is no obvious interaction between JZD and ATV in hypolipidemic effect, and the combination therapy of ATV and JZD is safe.
ObjectiveTo investigate the effects and mechanism of atorvastatin in the experimental pulmonary fibrosis. MethodsFifty-four C57BL/6 mice were randomly divided into a control group,a bleomycin group and an atorvastatin group. The mice in the bleomycin group and the atorvastatin group received a single dose intratracheal injection of bleomycin (2.5 mg/kg),while the mice in the control group were injected with isodose physiological saline. The mice in the atorvastatin group were treated with atorvastatin 10 mg·kg-1·d-1 by intragastric administration the day after bleomycin instillation. All groups were sacrificed on the day 3,14 and 28,respectively. HE staining and Masson staining were used to detect the architecture of alveolar and the deposition of cellularity and collagen. RT-PCR and immunohistochemical technology were performed to detect the expression of Krüppel like factor 4 (KLF4). Zymography was used to investigate the activation of matrix metalloproteinase-2(MMP-2). ResultsAfter the treatment of bleomycin,the lung tissues showed acute inflammation on the day 3,the collagen deposition was more obvious and the architecture of alveolar was destroyed on the day 14. The alveolar structure,the inflammation and collagen deposition were attenuated on the day 28 compared with the day 14. Compared with the bleomycin group,the inflammation and the collagen deposition were significantly reduced in the atorvastatin group (P<0.05). Compared with bleomycin group,the expression of KLF4 significantly decreased in the atorvastatin group,although the expression of KLF4 mRNA increased on the day 3 compared with the bleomycin group (0.502±0.261 vs. 0.326±0.164,P<0.05). The expression of KLF4 protein on the day 3 was significantly decreased compared with the bleomycin group (0.048±0.015 vs. 0.130±0.017,P<0.05). After the intervention of bleomycin,the activation of MMP-2 on the day 3 and 14 significantly increased compared with the control group (3.136±1.321 and 3.449±0.356 vs. 0.983±0.147,P<0.05),and significantly decreased after the treatment of atorvastatin (2.191±0.800 and 2.506±0.761). ConclusionAtorvastatin may have anti-inflammation and anti-fibrosis activities in experimental pulmonary fibrosis through KLF4 pathway.
目的:观察阿托伐他汀对抗糖尿病肾病患者肾氧化损伤作用。方法:56例糖尿病肾病患者随即分为对照组和阿托伐他汀组。对照组给予降糖、降压等治疗,阿托伐他汀组则在对照组治疗基础上加用阿托伐他汀10 mg/d,疗程共12周。检测两组患者治疗前后FBG、BUN、Scr、尿微量白蛋白以及血脂、血清SOD和MDA水平。结果:12周后两组患者FBG、BUN、Scr、尿微量白蛋白均较治疗前下降;与治疗前相比,阿托伐他汀组患者血脂水平较治疗前明显改善,同时患者血清SOD活性增,MDA含量下降,二者之间的差异具有显著性意义。结论:阿托伐他汀除具有降血脂作用外,还可改善糖尿病肾病患者的氧化应激状态。
目的：探讨阿托伐他汀治疗高脂血症患者的疗效分析。方法： 对70例确诊高脂血症的患者给予阿托伐他汀10 mg，每日一次，连服3个月，观察观察治疗前后的血脂、肝功能、肾功能,同时观察患者有无不良反应。结果：治疗3个月后,TC、TG、LDL-C均较治疗前显著下降(Plt;0.05),HDL-C较治疗前明显提高(Plt;0.05),TC、TG、LDL-C、HDL-C治疗3个月的总有效率分别是84.28%、74.6%、80%和62.26%,未见明显不良反应。结论：阿托伐他汀治疗高脂血症患者安全有效。
目的 探讨阿托伐他汀钙对颈动脉粥样硬化患者血管内皮的保护作用。 方法 选取2010年10月－2011年8月颈动脉粥样硬化患者80例，随机分为治疗组和对照组。对照组给予阿司匹林肠溶片0.1 g，早饭后口服1次；治疗组在此基础上给予阿托伐他汀钙20 mg，每晚口服1次，10个月为1个疗程。分别在治疗前后进行颈动脉彩色多普勒超声检测颈动脉中膜厚度及颈动脉粥样硬化斑块面积，测定甘油三酯（TG）、总胆固醇（TC）、低密度脂蛋白胆固醇（LDL-C）、高密度脂蛋白胆固醇（HDL-C）、一氧化氮（NO）、血管内皮素-1（ET-1）水平。两组患者在1个疗程治疗结束后停药12周，测定TG、TCH、LDL-C、HDL-C、NO、ET-1水平。 结果 与治疗前比较，治疗组患者的TG、TC、LDL-C、ET-1水平显著降低，HDL-C、NO水平显著升高（P＜0.01）。颈动脉中膜厚度和颈动脉粥样硬化斑块面积明显变小（P＜0.05）。对照组无明显变化。治疗组停药12周后与停药时比较，TG、TC、LDL-C、ET-1水平显著升高，HDL-C、NO水平明显降低（P ＜0.05）。对照组无明显变化。 结论 阿托伐他汀钙能显著改善颈动脉粥样硬化斑块患者的血管内皮功能、血脂水平，稳定颈动脉粥样硬化斑块，促进斑块逆转，且需要长期坚持服用。
ObjectiveTo investigate the effects of migration and expression from chemokine receptor 4 (chemokine receptor-4, CXCR4) of rat bone marrow mesenchymal stem cells (BMSCs) which were pretreated by atorvastatin (ATV) in vitro.MethodsIsolated, cultivated, identified the BMSCs, pretreated P4-P6 of BMSCs with different concentrations of ATV for 12 hours. The experimental group was divided into control group, 0.1 nM/L (group 0.1 nM), 1 nM/L (1 nM group), 10 nM/L (10 nM group), 100 nM/L (100 nM group), 1 000 nM/L (1 000 nM group). The mRNA and protein of CXCR4 were determined by real time-polymerase chain reaction and Western blot. Immunofluoreseence assay were used to detect the expression levels of CXCR4. The migration ability of BMSCs were measured by transwell chamber.ResultsImmunofluoreseence assay showed the protein level of CXCR4 of group 1 nM and 10 nM were significantly higher than the other group. RT-PCR and Western blot showed the protein and mRNA level of CXCR4 in 10 nM was higher than that in group 1 nM. The migration ability of group 10 nM was higher than 1 nM and control group.ConclusionsATV can be dose-dependent promote expression levels of CXCR4 of BMSCs cultivated in vitro.
ObjectivesTo systematically review the influence of nifedipine combined with atorvastatin on hypertension in patients with hypertension.MethodPubMed, EMbase, The Cochrane Library, CBM, CNKI, WanFang Data and VIP databases were electronically searched to collect randomized controlled trials (RCTs) of nifedipine combined with atorvastatin on hypertension in patients with hypertension from inception to November 20th, 2018. Two reviewers independently screened literature, extracted data and assessed the risk of bias of included studies, then, meta-analysis was performed by using Stata 12.0 software.ResultsA total of 17 RCTs involving 1 838 patients were included. The results of meta-analysis indicated that nifedipine combined with atorvastatin was superior to nifedipine alone on SBP (MD=−8.937, 95%CI−11.913 to −5.962, P<0.001), DBP (MD=−3.702, 95%CI−6.626 to −0.778, P=0.013) and total effective rate (RR=1.24, 95%CI 1.07 to 1.44, P=0.003). There was no significant difference between two groups in the incidence of adverse reactions (P>0.05).ConclusionsCurrent evidence shows that nifedipine combined with atorvastatin can significantly improve total effective rate, decrease the level of SBP and DBP, and increasing of dose not increase the incidence of adverse reactions. Due to limited quality and quantity of the included studies, more high quality studies are required to verify above conclusions.
ObjectiveTo observe and analyze the short-term efficacy of different statins on acute myocardial infarction in patients with premature coronary heart disease. MethodWe selected 70 patients with acute myocardial infarction admitted into our hospital for treatment of premature coronary artery disease between January 2012 and June 2013. The patients were randomly divided into experimental group (n=35) and control group (n=35). The experimental group were treated with rosuvastatin, and the control group of patients were given atorvastatin. We observed the rate of overall efficiency within 6 months after treatment, and total cholesterol (TC), triglyceride (TG), low density lipoprotein cholesterol (LDL-C), high density lipoprotein cholesterol (HDL-C), hepersensitive C-reactive protein (hs-CRP), left ventricular ejction fraction (LVEF), and flow-mediated dilation (FMD) were also observed before and after treatment. ResultsThe overall efficacy rate in the experimental group at 6 months was 94.3% and in the control group was 88.6% with no significant difference between each other (P>0.05). TG and FMD of patients in the experimental group at 6 months did not significantly change (P>0.05), while LVEF of the experimental group was significantly higher (P<0.05), and hs-CRP, TC, LDL-C, and HDL-C of the experimental group were significantly lower than the control group (P<0.05). ConclusionsShort-term comprehensive efficacy of rosuvastatin for treatment of premature coronary artery disease in patients with acute myocardial infarction is superior to atorvastatin.
ObjectiveTo investigate whether exosomes derived from atorvastatin (ATV)-pretreated human umbilical cord mesenchymal stem cells (ATV-MSC-EXO) alleviate high glucose-induced injury in human retinal vascular endothelial cells (HREC) via the protein kinase B (AKT)/endothelial nitric oxide synthase (eNOS) signaling pathway. MethodsThe optimal pretreatment concentration of ATV was determined using the cell counting Kit-8 (CCK-8) assay. Exosomes derived from mesenchymal stem cells (MSC-EXO) and ATV-pretreated MSC (ATV-MSC-EXO) were isolated and extracted, and their morphology and surface markers were characterized by transmission electron microscopy, nanoparticle tracking analysis, and Western blotting (WB). The uptake capacity of exosomes by human retinal vascular endothelial cells (HREC) was evaluated using a fluorescence labeling assay. In vitro cultured HREC were divided into the following groups: normal control group (NC group), high glucose group (HG group), high glucose+MSC-EXO group (MSC-EXO group), high glucose+ATV-MSC-EXO group (ATV-MSC-EXO group), high glucose+ATV-MSC-EXO+AKT inhibitor group (ATV-MSC-EXO-MK-2206-2HCL group), and high glucose+ATV-MSC-EXO+eNOS inhibitor group (ATV-MSC-EXO-L-NAME group). Cell proliferation and apoptosis were detected using CCK-8 and flow cytometry, respectively. The protein expression levels of B-cell lymphoma/leukemia-2 (Bcl-2), Bcl-2-associated protein (Bax), and Caspase-3 were measured by WB. In addition, the regulatory effects of ATV-MSC-EXO on the AKT/eNOS signaling pathway and its downstream functional molecules were analyzed by detecting the phosphorylation levels of AKT (P-AKT/AKT) and eNOS (P-eNOS/eNOS) via WB, the mRNA expression levels of AKT and eNOS by quantitative real-time polymerase chain reaction, and the concentrations of nitric oxide (NO) and endothelin-1 (ET-1) using commercial NO and ET-1 assay kits. ResultsThe optimal pretreatment concentration of ATV was 1 μmol/L. ATV-MSC-EXO exhibited similar morphology and particle size to MSC-EXO and were efficiently taken up by HREC. Under high glucose conditions, ATV-MSC-EXO significantly enhanced the viability of HREC (F=83.24, P＜0.000 1) and inhibited apoptosis (F=77.39, P＜0.000 1). WB analysis further confirmed that ATV-MSC-EXO upregulated the expression of the anti-apoptotic protein Bcl-2 (F=53.17), while downregulating the pro-apoptotic proteins Bax (F=36.49) and Caspase-3 (F=60.75) (P＜0.001). In addition, ATV-MSC-EXO markedly increased the protein levels of P-AKT/AKT (F=107.60) and P-eNOS/eNOS (F=38.59), as well as the relative mRNA expression of AKT, eNOS (F=203.60, 315.00; P＜0.000 1). Furthermore, ATV-MSC-EXO promoted NO production (F=407.40) and suppressed the relative expression of ET-1 (F=49.76) (P＜0.000 1). ConclusionATV-MSC-EXO enhances the viability and inhibits apoptosis of HREC under high glucose conditions by activating the AKT/eNOS signaling pathway.