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1.
目的:探讨非诺贝特(fenofibrate)对血管紧张素Ⅱ(AngⅡ)诱导的肥大心肌细胞的抑制作用及对FoxO1表达的影响。方法:首先采用AngⅡ诱导心肌细胞肥大,将细胞分为三组:对照组:未给予任何干预;心肌细胞肥大组:AngⅡ(10-7mol/L)刺激细胞;治疗组:先给予fenofibrate(10-5mol/L),30min后AngⅡ(10-7mol/L)刺激细胞。应用蛋白免疫印迹法(western-blotting)和实时定量PCR法(real time PCR)检测各组细胞中转录因子FoxO1的蛋白质及mRNA含量,心肌细胞肥大的判断使用脑钠肽(brain natriuret icpepide BNP)。结果:心肌细胞肥大组的FoxO1表达较对照组明显降低,而治疗组的FoxO1表达较心肌肥大组明显升高。结论:非诺贝特可能通过上调FoxO1表达,从而抑制心肌细胞肥大。  相似文献   
2.
摘要 目的:分析熊去氧胆酸联合非诺贝特对原发性胆汁性胆管炎无熊去氧胆酸生化反应的临床疗效及安全性。方法:151例原发性胆汁性胆管炎无熊去氧胆酸患者按随机数表法分为73例对照组和78例研究组。对照组在常规治疗基础上给予安慰剂联合熊去氧胆酸治疗,研究组在常规基础上给予非诺贝特联合熊去氧胆酸治疗,两组均持续治疗12个月。比较两组临床疗效,肝功能,血脂指标,肝纤维化指标,免疫球蛋白G(IgG)、免疫球蛋白M(IgM),瘙痒及乏力评分,不良反应发生情况。结果:治疗后,研究组总有效率高于对照组,比较差异有统计学意义(P<0.05)。治疗后,两组肝功能指标均降低,研究组低于对照组,比较有统计学意义(P<0.05)。治疗后,两组总胆固醇(TC)、甘油三酯(TG)均降低,研究组低于对照组,比较有统计学意义(P<0.05),两组治疗前后低密度脂蛋白胆固醇(LDL-C)、高密度脂蛋白胆固醇(HDL-C)比较无统计学意义(P>0.05)。治疗后,两组肝纤维化指标均降低,研究组低于对照组,比较有统计学意义(P<0.05)。治疗后,两组IgG、IgM均降低,研究组低于对照组,比较有统计学意义(P<0.05)。治疗后,两组瘙痒、乏力评分均降低,研究组低于对照组,比较有统计学意义(P<0.05)。两组不良反应发生率比较差异无统计学意义(P>0.05)。结论:熊去氧胆酸联合非诺贝特对原发性胆汁性胆管炎无熊去氧胆酸生化反应的疗效较好,能够改善肝功能,且未明显增加药物不良反应。  相似文献   
3.
摘要 目的:探讨乙酰辅酶A羧化酶抑制剂(MK-4074)联合非诺贝特对小鼠非酒精性脂肪肝(NAFLD)的脂质含量以及肝功能的改善效果。方法:20只C57BL/6小鼠给予60%高脂饲料连续喂养8周构建NAFLD小鼠模型后,随机分为安慰剂组、MK-4074组、非诺贝特组以及MK-4074联合非诺贝特治疗组,每组各5只,继续高脂喂养并分别给予安慰剂(Placebo)、MK-4074(10 mg/kg/天)、非诺贝特(30 mg/kg/天)、以及MK-4074(10 mg/kg/天)+ 非诺贝特(30 mg/kg/天)治疗持续8周。治疗结束后对小鼠体重、肝指数、肝脏脂质含量、肝功能以及肝脏病理和肝脏中性粒细胞和巨噬细胞浸润情况进行分析。结果:与安慰剂组相比,单用MK-4074治疗可显著降低肝指数、肝脏甘油三酯(TG)、胆固醇(TC)、非酯化脂肪酸(NEFA)的含量以及血清ALT和AST水平,而对小鼠体重和血清TC没有显著影响;单用非诺贝特可显著降低小鼠体重,肝脏TG、TC、NEFA以及血清TG、 ALT和AST水平,对小鼠的肝指数、血清TC没有显著影响;而MK-4074与非诺贝特联合治疗可显著降低小鼠体重、肝脏TG、TC、NEFA,以及血清TG、ALT和AST水平,降低肝脏脂质积累以及中性粒细胞与巨噬细胞浸润,效果优于MK-4074或非诺贝特单药治疗。结论:MK-4074联合非诺贝特可显著减少NAFLD小鼠肝脏的脂质含量,改善肝功能。  相似文献   
4.
Elevated levels of plasma homocysteine (Hcy) are associated with increased risk of cardiovascular disease though it is uncertain whether increases in Hcy represent a cause or a consequence of the disease process. Plasma Hcy exists in reduced, free oxidized, and protein-bound forms, that together comprise total Hcy (tHcy). Free reduced Hcy is thought to be the atherogenic, though minor, sub-fraction of tHcy. Recent reports have indicated that fenofibrate and other fibrates are capable of moderately increasing plasma tHcy. As many of the effects of fibrates are known to be mediated by the nuclear receptor PPARalpha, we determined the effect of fenofibrate on tHcy in PPARalpha-deficient mice. We further examined the effect of fenofibrate and fenofibrate plus folate supplementation on total as well as protein-bound Hcy in rats. Fenofibrate significantly increased serum tHcy in wild-type mice but not in PPARalpha deficient mice. In rats, fenofibrate increased serum tHcy by 69%, while the co-administration of folate with fenofibrate increased tHcy by only 7%. In spite of the above increase in tHcy in rats, only the protein-bound fraction of Hcy was increased. In a further study, fenofibrate also induced a significant increase in tHcy, while in spite of this, ex vivo peroxidation of VLDL+LDL was beneficially lowered and the lag time prolonged. In summary, fenofibrate increases serum tHcy in rodents in a PPARalpha-dependent manner. The increase in rats is solely due to protein-bound Hcy as atherogenic, reduced Hcy was unchanged. While awaiting corroboration in human, our results suggest that the extent and mechanism of the increase in total Hcy in patients treated with fenofibrate should not a priori be associated with relevant risk.  相似文献   
5.
We investigated whether fenofibrate improves lipid metabolism and obesity in female ovariectomized (OVX) or sham-operated (SO) low density lipoprotein receptor-null (LDLR-null) mice. All mice fed a high-fat diet exhibited increases in serum triglycerides and cholesterol as well as in body weight and white adipose tissue (WAT) mass compared to mice fed a low fat control diet. However, fenofibrate prevented high-fat diet-induced increases in body weight and WAT mass in female OVX LDLR-null mice, but not in SO mice. In addition, administration of fenofibrate reduced serum lipids and hepatic apolipoprotein C-III mRNA while increasing the mRNA of acyl-CoA oxidase in both groups of mice, however, these effects were more pronounced in OVX LDLR-null mice. The results of this study provide first evidence that fenofibrate improves both lipid metabolism and obesity, in part through PPARalpha activation, in female OVX LDLR-null mice.  相似文献   
6.
Zungu M  Felix R  Essop MF 《Mitochondrion》2006,6(6):315-322
We investigated the direct effects of two selective PPARalpha ligands, fenofibrate and Wy-14,643, on mitochondrial respiratory function using isolated rat cardiac mitochondria. Isolated left ventricular mitochondria were incubated with increasing concentrations of fenofibrate or Wy-14,643 (10, 100, and 500 microM) and mitochondrial respiration determined using: malate/glutamate (complex I), succinate (complex II) and palmitoyl-l-carnitine as oxidative substrates. Our data show that acute exposure to Wy-14,643 and fenofibrate differentially perturb cardiac mitochondrial respiration i.e., fenofibrate more potently inhibited mitochondrial respiration and bioenergetic capacity compared to Wy-14,643. Moreover, we found that both agents increased uncoupling of mitochondrial oxidative phosphorylation.  相似文献   
7.
目的:观察辛伐他汀和非诺贝特及两者联合对HepG2细胞载脂蛋白M表达的影响。方法:分别以不同浓度的辛伐他汀(0、1、5、10、25μmol/L)和非诺贝特(0、50、100mmol/L)及辛伐他汀(5.0μmol/L)+非诺贝特(50mmol/L)干预HepG2细胞24h。提取各组细胞总RNA和蛋白质,分别采用实时RT-PCR和WesternBlot检测apoM的mRNA和蛋白的表达。结果:辛伐他汀和非诺贝特均呈剂量依赖性上调载脂蛋白M基因和蛋白的表达(P<0.05)。联合用药比单药更能显著上调载脂蛋白M的表达(P<0.05)。结论:他汀类和贝特类药物均可上调载脂蛋白M表达,两药联合的作用更为显著。  相似文献   
8.
Drugs used in the treatment of type 2 diabetes and cardiovascular disease, specifically peroxisome proliferator‐activated receptor (PPAR) agonists, have been reported to affect bone cell function and fracture risk. In this study, we assessed the direct effects of PPAR‐γ agonists (rosiglitazone and troglitazone), used in the treatment of diabetes, and a PPAR‐α agonist (fenofibrate), used to treat hyperlipidaemia, on the function of primary osteoblasts and osteoclasts. Formation of ‘trabecular’ bone structures by rat calvarial osteoblasts was reduced by up to 85% in cultures treated with rosiglitazone and by 45% in troglitazone‐treated or fenofibrate‐treated cultures; at the same time, lipid droplet formation was increased by 40–70%. The expression of key osteogenic markers was similarly downregulated in cultures treated with PPAR agonists, whereas adipogenesis markers were upregulated. Formation of osteoclasts in cultures derived from mouse marrow diminished with fenofibrate treatment, whereas both glitazones reduced resorptive activity without affecting osteoclast number. Metformin, although not a PPAR agonist, is also commonly used in the treatment of type 2 diabetes. Here, metformin was found to have no effect on bone cell function. Taken together, these data suggest that PPAR‐γ agonists may enhance bone loss via increased adipogenesis at the expense of osteoblast formation. In contrast, PPAR‐α agonists may prevent bone loss. Given that the prevalence of diabetes and cardiovascular disease is expected to rise significantly, greater attention may need to be paid to the effects of PPAR agonists on bone homeostasis. Copyright © 2014 John Wiley & Sons, Ltd.  相似文献   
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