噻唑烷二酮类药物在动脉粥样硬化中的抗炎作用

噻唑烷二酮类药物是一类新的治疗2型糖尿病和胰岛素抵抗的药物。越来越多的证据表明噻唑烷二酮类药物在防治动脉粥样硬化方面有良好的疗效。噻唑烷二酮类药物通过对动脉粥样硬化炎症反应细胞、炎症因子、心血管事件的影响,在动脉粥样硬化中发挥其积极的抗炎作用。     

噻唑烷二酮类药物肾脏保护作用研究进展

噻唑烷二酮类(TZDs)药物为过氧化物酶体增殖物活化受体(PPAR)γ激动剂,是一类通过胰岛素增敏作用来治疗2型糖尿病的药物.研究表明,肾脏系膜细胞、肾小管细胞及足细胞上均存在PPART.越来越多的动物及临床证据支持TZDs药物可以通过改善肾脏血流动力学和内皮功能、抗糖基化、抑制炎性反应、氧化应激等多种机制来延缓肾脏衰竭.发挥直接的肾脏保护作用.且不依赖于改善糖、脂代谢,降低高胰岛素血症的全身作用.因此,为糖尿病肾病及其他慢性肾病的药物治疗提供了新的思路和方法.     

噻唑烷二酮类药物肾脏保护作用研究进展

Thiazolidinediones (TZDs) --peroxisome proliferators activated receptor (PPAR)γ activa-tor,are a class of antidiabetic drugs for type 2 diabetes mellitus through their insulin sensitizing action. Stud-ies have shown that PPARγ lies in intercapillary cell, tubular cell and podocyte, etc. More and more animal and clinic evidences support the concept that TZDs can delay renal failure and have a directly protective effect against kidney by several mechanisms ,such as improving kidney hacmodynamics and endothelium func-tion, inhibiting glycosylation,anti-inflammatiou, reduction of oxidative stress, etc. In addition, these effects are independent of lowing hyperglycacmia, hypedipemia and hypetinsulinism. TZDs provide new concept and method in treating diabetic nephropathy and other chronic kidney diseases.     

噻唑烷二酮类药物肾脏保护作用研究进展

Thiazolidinediones (TZDs) --peroxisome proliferators activated receptor (PPAR)γ activa-tor,are a class of antidiabetic drugs for type 2 diabetes mellitus through their insulin sensitizing action. Stud-ies have shown that PPARγ lies in intercapillary cell, tubular cell and podocyte, etc. More and more animal and clinic evidences support the concept that TZDs can delay renal failure and have a directly protective effect against kidney by several mechanisms ,such as improving kidney hacmodynamics and endothelium func-tion, inhibiting glycosylation,anti-inflammatiou, reduction of oxidative stress, etc. In addition, these effects are independent of lowing hyperglycacmia, hypedipemia and hypetinsulinism. TZDs provide new concept and method in treating diabetic nephropathy and other chronic kidney diseases.     

噻唑烷二酮类药物的心血管保护作用

噻唑烷二酮类药物(TZDs)是近年来应用于临床的一类新型胰岛素增敏剂,是过氧化物酶体增殖物激活受体γ的人工合成激动剂,用于改善胰岛素抵抗,降低糖尿病患者的血糖,近年研究发现,TZDs还具有改善胰岛素抵抗和降低血糖以外的作用,如对炎性反应,动脉粥样硬化的影响以及对肾脏的保护作用和对缺血心肌的保护作用等。     

噻唑烷二酮类药物对糖尿病肾脏的保护作用

噻唑烷二酮类药物(TZDs)是一类新型的糖尿病治疗药物。大量的研究表明，TZDs通过抑制二脂酰甘油(DAG)—蛋白激酶C(PKC)—细胞外信号调节激酶(ERK)信号转导途径，改善肾小球高滤过状态；调节系膜细胞及肾小管上皮细胞增殖、分化，减轻肾脏损害；减少炎性细胞因子产生，改善胰岛素抵抗；纠正脂代谢紊乱，减轻对肾脏的脂毒性，从而发挥对糖尿病肾脏的保护作用。     

噻唑烷二酮类药物的血管保护作用研究进展

噻唑烷二酮类药物(Thiazolidinediones,TZDs)是人工合成的高亲合性的过氧化物酶体增殖物激活受体γ(Peroxisome proliferator-activated receptors,PPARs)配体。TZDs除通过改善胰岛素抵抗、降糖作用外,尚可通过改善内皮功能、抗炎、抑制平滑肌增生和新生内膜形成、预防动脉再狭窄等方面发挥血管保护作用。     

噻唑烷二酮类药物与糖尿病肾病关系的研究进展

噻唑烷二酮(TZDs)是一类通过改善胰岛素敏感性降低血糖的经典药物。动物实验和临床研究证实TZDs除了通过降低血胰岛素和血糖水平之外,尚可通过抗炎、调节脂质紊乱、改善内皮等多种途径防治糖尿病肾病。     

噻唑烷二酮类药物抗动脉粥样硬化的作用机制

噻唑烷二酮类药物是临床治疗2型糖尿病的口服降糖药之一,通过结合与过氧化酶增殖体活化受体γ发挥作用,除了对胰岛素敏感组织产生作用而改善胰岛素抵抗外,还通过改善脂质代谢紊乱、改善血管内皮功能、抑制炎症介质的释放和基质金属蛋白酶的合成、影响血管紧张素Ⅱ受体的表达和泡沫细胞的形成、增加脂联素的表达、抑制核因子κB的激活等机制发挥抗动脉粥样硬化的作用。     

噻唑烷二酮类药物对骨骼的影响及其机制

噻唑烷二酮类(TZDs)药物是一种过氧化物酶体增殖物活化受体(PPAR)-γ激动剂,可减轻胰岛素抵抗,降低血糖,在2型糖尿病的治疗中发挥重要作用.动物实验显示其可抑制成骨细胞分化,降低骨形成,从而减少骨量.临床研究也显示其可降低患者骨密度,增加骨折发生率.其降低骨量的机制目前尚不明确,考虑与如下因素有关:降低Runt相关转录因子(Runx)2和osrerix的表达,抑制成骨细胞分化;下调其他与骨形成相关的细胞因子及信号分子的表达;抑制骨钙素基因的表达;加速成骨细胞凋亡.     

噻唑烷二酮类药物不良反应的再认识

噻唑烷二酬类药物(TZDs)通过激活过氧化物酶体增殖物活化受体-γ,增加外周组织对胰岛素的敏感性而改善胰岛素抵抗,以其独特的作用机制在口服抗糖尿病药物中独树一帜.然而,近年来有关TZDs不良反应的报道日渐增多.在肝毒性、体重增加、水肿、心力衰竭等不良反应得到确认的同时,关于其心血管与骨代谢方面的不良反应更是备受关注.科学面合理地分析与认识这些不良反应,对指导临床实践具有重要意义.     

舒林酸对结肠腺癌HT-29细胞增殖调控的实验研究

目的 观察舒林酸对结肠腺癌ＨＴ－２９细胞增殖的影响,探讨其作用机制。方法 采用ＭＴＴ比色法观察舒林酸对ＨＴ－２９细胞增殖的影响;采用流式细胞仪检测舒林酸对ＨＴ－２９细胞周期的影响,同时结合ＤＮＡ电泳和透射电镜观察舒林酸对ＨＴ－２９细胞有无促凋亡作用。结果 舒林酸可抑制ＨＴ－２９细胞增殖,使Ｇ０／Ｇ１期细胞比例增高,Ｓ期比例降低,７２ｈ后,ＨＴ－２９细胞凋亡分别上升至１２．５＾、１５．４＾和２４．２     

2型糖尿病患者噻唑烷二酮类药物疗效差异性的分析

临床研究表明,2型糖尿病患者噻唑烷二酮类药物疗效具有差异性,其差异性的原因可能与过氧化物酶体增殖物活化受体γ(PPARγ)、PPARγ协同刺激因子、脂联素、解耦联蛋白2、β3肾上腺素能受体基因、视黄醇结合蛋白4、细胞色素酶、脂素基因1等基因多态性相关,但是目前尚无一致性结论.目前国内、外关于PPARγ、PPARγ共激活因子、脂联素基因多态性与2型糖尿病患者噻唑烷二酮类药物疗效差异性的研究较多.     

The potential role of thiazolidinediones in atrial fibrillation

Thiazolidinediones (TZDs) represent insulin sensitizing drugs that are being increasingly used for the treatment of type 2 diabetes. These agents have also pleiotropic properties that possibly contribute to their favorable cardiovascular effects. In particular, TZDs have anti-inflammatory and anti-oxidant potential while they modulate cardiovascular remodeling. On the other hand, atrial electrical and structural remodeling constitutes the substrate for atrial fibrillation (AF) development and perpetuation. Of note, inflammation and oxidative stress have been recently implicated in the pathogenesis of AF while non-channel blocking drugs with pleiotropic properties, including anti-inflammatory and anti-oxidant, seem to favorably affect atrial remodeling. It is therefore reasonable to assume that TZDs may have a role in the management of AF. Despite some limited observations, no study to date has examined the effect of TZDs therapy on AF development. In addition, the role of these agents in atrial remodeling has not been clarified yet.     

Role of thiazolidinediones,insulin sensitizers,in non‐alcoholic fatty liver disease

The prevalence of metabolic syndrome, obesity and insulin resistance has become an epidemic in the world. A strong association exists between metabolic syndrome and non‐alcoholic fatty liver disease (NAFLD), though the etiology of NAFLD is still unclear. This close association leads to numerous clinical studies to investigate the effects of insulin sensitizers, thiazolidinediones (TZDs), on hepatic fat accumulation. Thiazolidinediones affect glucose and lipid metabolism in insulin‐sensitive tissues, which in turn reduces the lipid content in the liver by modulating several mediators. In the present review, we discuss key modulators – adiponectin and sirtulin‐adenosine monophosphate activated protein kinase signaling – as the mechanisms responsible for NAFLD related to metabolic syndrome.     

Nonhypoglycemic effects of thiazolidinediones

The thiazolidinediones are a new class of compounds for treatment of type 2 diabetes. Troglitazone became available in the United States in 1997 but was withdrawn from the market in March 2000 because it caused severe idiosyncratic liver injury. Rosiglitazone and pioglitazone have been available since 1999. Because these drugs directly improve insulin resistance and decrease plasma insulin levels (a risk factor for coronary artery disease), they may decrease risk for cardiovascular disease in patients with type 2 diabetes. Research on the non-glucose lowering effects of troglitazone and, to a lesser extent, of rosiglitazone and pioglitazone have demonstrated changes in several cardiovascular risk factors associated with the insulin resistance syndrome. These beneficial effects include a decrease in blood pressure, correction of diabetic dyslipidemia, improvement of fibrinolysis, and decrease in carotid artery intima-media thickness. Other in vitro effects related to the ability of these agents to bind a newly described class of receptors (peroxisome proliferator-activated receptors) may also have implications for atherosclerosis. However, these drugs increase low-density lipoprotein (LDL) cholesterol levels and may favorably change LDL particle size and susceptibility to oxidation (although the implications of the latter changes are not dear). Furthermore, these drugs tend to cause weight gain. The authors' enthusiasm for these drugs has diminished somewhat because of reported adverse events, including rare liver failure. Nevertheless, because of the mechanism of action of the thiazolidinediones, clinical trials designed to determine whether they (or similar "insulin sensitizers") decrease cardiovascular events in people with type 2 diabetes will be of interest.