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Piperine Alleviates Doxorubicin-Induced Cardiotoxicity via Activating PPAR-γ in Mice. 胡椒碱通过激活小鼠PPAR-γ减轻阿霉素诱导的心脏毒性。
IF 2.9 3区 医学 Q2 Medicine Pub Date : 2019-12-17 eCollection Date: 2019-01-01 DOI: 10.1155/2019/2601408
Jie Yan, Si-Chi Xu, Chun-Yan Kong, Xiao-Yang Zhou, Zhou-Yan Bian, Ling Yan, Qi-Zhu Tang

Background: Oxidative stress, inflammation and cardiac apoptosis were closely involved in doxorubicin (DOX)-induced cardiac injury. Piperine has been reported to suppress inflammatory response and pyroptosis in macrophages. However, whether piperine could protect the mice against DOX-related cardiac injury remain unclear. This study aimed to investigate whether piperine inhibited DOX-related cardiac injury in mice.

Methods: To induce DOX-related acute cardiac injury, mice in DOX group were intraperitoneally injected with a single dose of DOX (15 mg/kg). To investigate the protective effects of piperine, mice were orally treated for 3 weeks with piperine (50 mg/kg, 18:00 every day) beginning two weeks before DOX injection.

Results: Piperine treatment significantly alleviated DOX-induced cardiac injury, and improved cardiac function. Piperine also reduced myocardial oxidative stress, inflammation and apoptosis in mice with DOX injection. Piperine also improved cell viability, and reduced oxidative damage and inflammatory factors in cardiomyocytes. We also found that piperine activated peroxisome proliferator-activated receptor-γ (PPAR-γ), and the protective effects of piperine were abolished by the treatment of the PPAR-γ antagonist in vivo and in vitro.

Conclusions: Piperine could suppress DOX-related cardiac injury via activation of PPAR-γ in mice.

背景:氧化应激、炎症和心脏细胞凋亡与多柔比星(DOX)诱导的心脏损伤密切相关。据报道,胡椒碱可以抑制巨噬细胞的炎症反应和焦亡。然而,胡椒碱是否能保护小鼠免受dox相关的心脏损伤尚不清楚。本研究旨在探讨胡椒碱是否能抑制dox相关小鼠心脏损伤。方法:DOX组小鼠腹腔注射单剂量DOX (15 mg/kg),诱导DOX相关性急性心脏损伤。为了研究胡椒碱的保护作用,小鼠在注射DOX前2周开始口服胡椒碱(50 mg/kg,每天18:00)3周。结果:胡椒碱治疗可明显减轻dox致心脏损伤,改善心功能。胡椒碱还能降低DOX小鼠心肌氧化应激、炎症和细胞凋亡。胡椒碱还能提高细胞活力,减少心肌细胞的氧化损伤和炎症因子。我们还发现胡椒碱激活过氧化物酶体增殖激活受体-γ (PPAR-γ),并且胡椒碱的保护作用被PPAR-γ拮抗剂处理在体内和体外被取消。结论:胡椒碱可通过激活小鼠PPAR-γ抑制dox相关性心脏损伤。
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引用次数: 14
PPAR-γ Ligand Inhibits Nasopharyngeal Carcinoma Cell Proliferation and Metastasis by Regulating E2F2 PPAR-γ配体通过调节E2F2抑制鼻咽癌细胞增殖和转移
IF 2.9 3区 医学 Q2 Medicine Pub Date : 2019-08-01 DOI: 10.1155/2019/8679271
Ping Yang, Jiashui Wang, Xiaoxia Cheng, Jingchao Chen, Hui Zhu, Xiaolin Li, Li Cao, Wei-Wei Tang
Purpose Peroxisome proliferator-activated receptor-γ (PPAR-γ) is a nuclear hormone receptor with a key role in lipid metabolism. Previous studies have identified various roles of PPAR-γ in cell cycle progression, cellular proliferation, and tumor progression. However, no report has described a role for PPAR-γ in human nasopharyngeal carcinoma (NPC). Notably, some studies have reported a relationship between PPAR-γ and E2F transcription factor 2 (E2F2), which has been identified as a regulator of cell cycle, apoptosis, and the DNA damage response. Notably, E2F2 has also been reported to correlate with a poor prognosis in patients with various malignancies. Methods We used immunohistochemical (IHC) and western blot methods to evaluate PPAR-γ and E2F2 expression and function in nonkeratinizing NPC and nasopharyngitis (NPG) tissue samples, as well as western blotting and CCK8 analyses in the NPC cell lines, CNE1 and CNE2. Results We observed lower levels of PPAR-γ expression in nonkeratinizing NPC tissues compared with NPG tissues and determined an association between a low level of PPAR-γ expression with a more advanced tumor stage. Furthermore, strong E2F2 expression was detected in nonkeratinizing NPC tissues. We further demonstrated that rosiglitazone, a PPAR-γ agonist, reduced E2F2 expression and proliferation in NPC cell lines. Conclusions Our study results revealed a novel role for the PPAR-γ–E2F2 pathway in controlling NPC cell proliferation and metastasis.
目的过氧化物酶体增殖物激活受体-γ (PPAR-γ)是一种核激素受体,在脂质代谢中起关键作用。先前的研究已经确定了PPAR-γ在细胞周期进程、细胞增殖和肿瘤进展中的各种作用。然而,没有报道描述PPAR-γ在人鼻咽癌(NPC)中的作用。值得注意的是,一些研究报道了PPAR-γ与E2F转录因子2 (E2F2)之间的关系,E2F2已被确定为细胞周期、凋亡和DNA损伤反应的调节因子。值得注意的是,E2F2也被报道与各种恶性肿瘤患者的不良预后相关。方法采用免疫组化(IHC)和western blot方法检测非角化鼻咽癌和鼻咽炎(NPG)组织样品中PPAR-γ和E2F2的表达和功能,并对鼻咽癌细胞系、CNE1和CNE2进行western blot和CCK8检测。结果我们观察到,与NPG组织相比,非角化鼻咽癌组织中PPAR-γ的表达水平较低,并确定了PPAR-γ的低表达水平与更晚期的肿瘤阶段之间的关联。此外,在非角化的鼻咽癌组织中检测到强烈的E2F2表达。我们进一步证明了罗格列酮(PPAR-γ激动剂)可以降低鼻咽癌细胞系中E2F2的表达和增殖。结论PPAR -γ-E2F2通路在鼻咽癌细胞增殖转移调控中具有新的作用。
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引用次数: 14
15-Deoxy-∆-12,14-Prostaglandin J2 (15d-PGJ2), an Endogenous Ligand of PPAR-γ: Function and Mechanism 15-脱氧-∆-12,14-前列腺素J2(15d-PGJ2),PPAR-γ的内源性配体:功能和机制
IF 2.9 3区 医学 Q2 Medicine Pub Date : 2019-08-01 DOI: 10.1155/2019/7242030
Jingjing Li, Chuanyong Guo, Jianye Wu
15-Deoxy-∆-12,14-prostaglandin J2 (15d-PGJ2), a natural peroxisome proliferator-activated receptor-γ (PPAR-γ) agonist, has been explored in some detail over the last 20 years. By triggering the PPAR-γ signalling pathway, it plays many roles and exerts antitumour, anti-inflammatory, antioxidation, antifibrosis, and antiangiogenesis effects. Although many synthetic PPAR-γ receptor agonists have been developed, as an endogenous product of PPAR-γ receptors, 15d-PGJ2 has beneficial characteristics including rapid expression and the ability to contribute to a natural defence mechanism. In this review, we discuss the latest advances in our knowledge of the biological role of 15d-PGJ2 mediated through PPAR-γ. It is important to understand its structure, synthesis, and functional mechanisms to develop preventive agents and limit the progression of associated diseases.
15-Deoxy-∆-12,14-前列腺素J2 (15d-PGJ2)是一种天然过氧化物酶体增殖物激活受体-γ (PPAR-γ)激动剂,在过去的20年里,人们对其进行了详细的研究。它通过触发PPAR-γ信号通路发挥多种作用,具有抗肿瘤、抗炎、抗氧化、抗纤维化和抗血管生成等作用。虽然已经开发了许多合成的PPAR-γ受体激动剂,但作为PPAR-γ受体的内源性产物,15d-PGJ2具有快速表达和促进自然防御机制的有益特性。在这篇综述中,我们讨论了通过PPAR-γ介导的15d-PGJ2生物学作用的最新进展。了解其结构、合成和功能机制对开发预防药物和限制相关疾病的进展具有重要意义。
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引用次数: 59
Corrigendum to “PPARs in Human Neuroepithelial Tumors: PPAR Ligands as Anticancer Therapies for the Most Common Human Neuroepithelial Tumors” 《人类神经上皮肿瘤中的PPAR: PPAR配体作为最常见的人类神经上皮肿瘤的抗癌疗法》的勘误
IF 2.9 3区 医学 Q2 Medicine Pub Date : 2019-07-21 DOI: 10.1155/2019/4309068
E. Benedetti, R. Galzio, B. D'angelo, M. Ceru', A. Cimini
[This corrects the article DOI: 10.1155/2010/427401.].
[这更正了文章DOI:10.1155/2010/427401.]。
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引用次数: 0
Retracted: Possible Role of Interaction between PPARα and Cyclophilin D in Cardioprotection of AMPK against In Vivo Ischemia-Reperfusion in Rats 收缩:PPARα和亲环素D相互作用在AMPK对大鼠体内缺血再灌注心脏保护中的可能作用
IF 2.9 3区 医学 Q2 Medicine Pub Date : 2019-07-15 DOI: 10.1155/2019/9760941
PPAR Research
[This retracts the article DOI: 10.1155/2016/9282087.].
[本文撤回文章DOI: 10.1155/2016/9282087]。
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引用次数: 0
Activation and Expression of Peroxisome Proliferator-Activated Receptor Alpha Are Associated with Tumorigenesis in Colorectal Carcinoma 过氧化物酶体增殖因子激活受体α的激活和表达与大肠癌的发生有关
IF 2.9 3区 医学 Q2 Medicine Pub Date : 2019-07-03 DOI: 10.1155/2019/7486727
Tatsuya Morinishi, Yasunori Tokuhara, H. Ohsaki, Emi Ibuki, K. Kadota, E. Hirakawa
Peroxisome proliferator-activated receptor alpha (PPAR-α) belongs to the PPAR family and plays a critical role in inhibiting cell proliferation and tumorigenesis in various tumors. However, the role of PPAR-α in colorectal tumorigenesis is unclear. In the present study, we found that fenofibrate, a PPAR-α agonist, significantly inhibited cell proliferation and induced apoptosis in colorectal carcinoma cells. In addition, PPAR-α was expressed in the nucleus of colorectal carcinoma cells, and the expression of nuclear PPAR-α increased in colorectal carcinoma tissue compared with that of normal epithelium tissue (P<0.01). The correlation between the expression of nuclear PPAR-α and clinicopathological factors was evaluated in human colorectal carcinoma tissues, and the nuclear expression of PPAR-α was significantly higher in well-to-moderately differentiated adenocarcinoma than in mucinous adenocarcinoma (P<0.05). These findings indicate that activation of PPAR-α may be involved in anticancer effects in colorectal carcinomas, and nuclear expression of PPAR-α may be a therapeutic target for colorectal adenocarcinoma treatment.
过氧化物酶体增殖物激活受体α(PPAR-α)属于PPAR家族,在抑制各种肿瘤的细胞增殖和肿瘤发生方面发挥着关键作用。然而,PPAR-α在结直肠肿瘤发生中的作用尚不清楚。在本研究中,我们发现PPAR-α激动剂非诺贝特显著抑制结直肠癌细胞的增殖并诱导细胞凋亡。此外,PPAR-α在结直肠癌细胞核中表达,与正常上皮组织相比,结直肠癌细胞核PPAR-α的表达增加(P<0.01),PPAR-α在中分化腺癌中的核表达显著高于粘液腺癌(P<0.05)。这些发现表明PPAR-α的激活可能与结直肠癌的抗癌作用有关,PPAR-α核表达可能是结直肠癌治疗的治疗靶点。
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引用次数: 18
Peroxisome Proliferator-Activated Receptor-γ Antagonizes LOX-1-Mediated Endothelial Injury by Transcriptional Activation of miR-590-5p 过氧化物酶体增殖物激活受体-γ通过miR-590-5p的转录激活拮抗lox -1介导的内皮损伤
IF 2.9 3区 医学 Q2 Medicine Pub Date : 2019-07-01 DOI: 10.1155/2019/2715176
Lei Xu, Gang Zhao, Hong Zhu, Shijun Wang, A. Sun, Y. Zou, J. Ge
Lectin-like oxidized low-density lipoprotein receptor-1 (LOX-1) is one of the major receptors expressed on the endothelium of arterial wall with a key role in endothelial dysfunction and the development of atherosclerosis. Recent evidence suggested that LOX-1 is upregulated under the condition of insulin resistance and could be suppressed by the antidiabetic drugs. We previously also confirmed that Thiazolidinedione (TZD) has the inhibitory effect on LOX-1 in ox-LDL-induced endothelial cells. However, the underlying mechanism is unclear. Here we showed that Rosiglitazone treatment significantly attenuated the expressions of LOX-1, ICAM-1, VCAM-1, p47phox, and the atherosclerotic lesions in ApoE−/− mice with high-fat diet. In vitro, we revealed that Rosiglitazone inhibited LOX-1 by regulating miR-590-5p. Ox-LDL-mediated ICAM-1, VCAM-1, and p47phox were significantly reduced by Rosiglitazone, but all reversed after pretreating the cells with antagomiR-590-5p. Induction with Rosiglitazone activated PPAR-γ and promoted its nuclear translocation in cultured human umbilical vein endothelial cells (HUVECs). The nuclear PPAR-γ upregulated the miR-590-5p level through binding to its transcriptional promoter region. Retaining PPAR-γ in cytoplasm by transfecting with PPAR-γ⊿NLS plasmid in HUVECs failed to activate miR-590-5p. Mutation of the promoter region of PPAR-γ also reduced the miR-590-5p promoter luciferase activity. Collectively, these data indicated that PPAR-γ may have the therapeutic potential in atherosclerosis via the transcriptional regulation of miR-590-5p in endothelial cells.
凝集素样氧化低密度脂蛋白受体-1 (LOX-1)是在动脉壁内皮上表达的主要受体之一,在内皮功能障碍和动脉粥样硬化的发生中起关键作用。最近的证据表明,在胰岛素抵抗的情况下,LOX-1表达上调,并可能受到降糖药物的抑制。我们之前也证实了噻唑烷二酮(TZD)对ox- ldl诱导的内皮细胞中LOX-1有抑制作用。然而,潜在的机制尚不清楚。在高脂饮食的ApoE - / -小鼠中,我们发现罗格列酮治疗显著降低了LOX-1、ICAM-1、VCAM-1、p47phox的表达和动脉粥样硬化病变。在体外,我们发现罗格列酮通过调节miR-590-5p抑制LOX-1。罗格列酮显著降低ox - ldl介导的ICAM-1、VCAM-1和p47phox,但经安塔戈米-590-5p预处理后均逆转。罗格列酮诱导人脐静脉内皮细胞(HUVECs)活化PPAR-γ并促进其核易位。核PPAR-γ通过结合其转录启动子区域上调miR-590-5p水平。在HUVECs中转染PPAR-γ⊿NLS质粒,保留细胞质中的PPAR-γ,不能激活miR-590-5p。PPAR-γ启动子区域的突变也降低了miR-590-5p启动子荧光素酶的活性。总的来说,这些数据表明PPAR-γ可能通过内皮细胞中miR-590-5p的转录调控在动脉粥样硬化中具有治疗潜力。
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引用次数: 8
Short-Term Activation of Peroxisome Proliferator-Activated Receptors α and γ Induces Tissue-Specific Effects on Lipid Metabolism and Fatty Acid Composition in Male Wistar Rats. 短期激活过氧化物酶体增殖物激活受体α和γ对雄性Wistar大鼠脂质代谢和脂肪酸组成的组织特异性影响
IF 3.5 3区 医学 Q2 MEDICINE, RESEARCH & EXPERIMENTAL Pub Date : 2019-06-12 eCollection Date: 2019-01-01 DOI: 10.1155/2019/8047627
Elin Strand, Vegard Lysne, Mari Lausund Grinna, Pavol Bohov, Asbjørn Svardal, Ottar Nygård, Rolf K Berge, Bodil Bjørndal

Dietary fatty acids (FAs) affect certain metabolic routes, including pathways controlled by the peroxisome proliferator-activated receptors (PPARs), but tissue-specific effects are not well-defined. Thus, the aim was to compare the metabolic response in hepatic, adipose, and cardiac tissues after treatment with specific PPAR agonists. Male Wistar rats were randomized into three groups: a control group receiving placebo (n=8); a PPARα agonist group receiving WY-14,643 (n=6); and a PPARγ agonist group receiving rosiglitazone (n=6) for 12 days. All animals received a low-fat standard chow diet and were given a daily dose of placebo or agonist orally. Lipids and FA methyl esters were measured in plasma, liver, and heart and gene expression was measured in liver and adipose tissue, while enzyme activities were measured in liver. Treatment with the PPARα agonist was associated with higher liver mass relative to body weight (liver index), lower plasma, and hepatic total cholesterol, as well as lower plasma carnitine and acylcarnitines, compared with control. In heart, PPARα activation leads to overall lower levels of free FAs and specific changes in certain FAs, compared with control. Furthermore, β-oxidation in liver and the enzymatic activities of well-known PPARα targeted genes were higher following PPARα administration. Overall, rats treated with the PPARα agonist had higher hepatic saturated FAs (SFAs) and monounsaturated FAs (MUFAs) and lower n-6 and n-3 PUFAs, compared to control. Treatment with the PPARγ agonist was associated with a lower liver index, lower plasma triglycerides (TAG) and phospholipids, and higher hepatic phospholipids, compared with control. PPARγ target genes were increased specifically in adipose tissue. Moreover, lower total cardiac FAs and SFA and higher cardiac n-6 PUFA were also associated with PPARγ activation. Altogether, there were characteristic effects of PPARα activation in liver and heart, as well as in plasma. PPARγ effects were not only confined to adipose tissue, but specific effects were also seen in liver, heart, and plasma. In conclusion, short-term treatment with PPAR agonists induced tissue-specific effects on FA composition in liver and heart. Moreover, both PPARα and PPARγ activation lowered plasma TAG and phospholipids, most likely through effects on liver and adipose tissue, respectively. In future studies we aim to reveal whether similar patterns can be found through diet-induced activation of specific pathways.

膳食脂肪酸(FA)影响某些代谢途径,包括过氧化物酶体增殖物激活受体(PPARs)控制的途径,但组织特异性作用尚不明确。因此,目的是比较用特异性PPAR激动剂治疗后肝、脂肪和心脏组织的代谢反应。雄性Wistar大鼠被随机分为三组:对照组接受安慰剂(n=8);PPARα激动剂组接受WY-14643(n=6);γ激动剂组接受罗格列酮(n=6)治疗12天。所有动物均接受低脂标准饮食,并口服每日剂量的安慰剂或激动剂。在血浆、肝脏和心脏中测量脂质和FA甲酯,在肝脏和脂肪组织中测量基因表达,而在肝脏中测量酶活性。与对照组相比,PPARα激动剂治疗与肝脏质量相对于体重(肝脏指数)更高、血浆和肝脏总胆固醇更低以及血浆肉碱和酰基肉碱更低有关。在心脏中,与对照组相比,PPARα激活导致游离FAs水平总体较低,某些FAs发生特异性变化。此外,PPARα给药后,肝脏中的β-氧化和众所周知的PPARα靶向基因的酶活性更高。总体而言,与对照组相比,用PPARα激动剂治疗的大鼠具有更高的肝脏饱和脂肪酸(SFAs)和单不饱和脂肪酸,以及更低的n-6和n-3 PUFA。与对照组相比,PPARγ激动剂治疗与较低的肝脏指数、较低的血浆甘油三酯(TAG)和磷脂以及较高的肝脏磷脂有关。PPARγ靶基因在脂肪组织中特异性增加。此外,较低的心脏总FA和SFA以及较高的心脏n-6 PUFA也与PPARγ激活有关。总之,PPARα激活在肝脏、心脏以及血浆中都具有特征性作用。PPARγ效应不仅局限于脂肪组织,而且在肝脏、心脏和血浆中也有特异性作用。总之,PPAR激动剂的短期治疗诱导了对肝脏和心脏FA组成的组织特异性影响。此外,PPARα和PPARγ的激活都降低了血浆TAG和磷脂,很可能分别通过对肝脏和脂肪组织的影响。在未来的研究中,我们旨在揭示是否可以通过饮食诱导的特定途径激活来发现类似的模式。
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引用次数: 0
Expression of Concern on “Testosterone Replacement Modulates Cardiac Metabolic Remodeling after Myocardial Infarction by Upregulating PPARα” “睾酮替代通过上调PPARα调节心肌梗死后心脏代谢重塑”的关注表达
IF 2.9 3区 医学 Q2 Medicine Pub Date : 2019-06-11 DOI: 10.1155/2019/5137020
PPAR Research
PPAR Research would like to express concern with the article titled “Testosterone Replacement Modulates Cardiac Metabolic Remodeling a erMyocardial Infarction by Upregulating PPARα” [1] published in PPAR Research in June 2016 due to flaws found in the quality of the article. eEditorial Board believed that the experimental design is not solid enough as the control groups are missing. ey thought that it is confusing that most of the data sets are labeled with n=3 in the legends which is extremely low for animal experiments. In addition, the board found that the authors described each group number in the methods which is not n=3 but slightly higher. ere is no explanation why not all animals were included in all analyses and how a selection of data sets was performed. In some data sets, the authors use n=6 but some animal data sets are missing. e authors explained that, in theMaterials andMethods, additional normal rats that underwent the same procedure without LDA occlusion were used as the control group. Moreover, the number of animals which were alive a er the myocardial infarction was mentioned in the Materials and Methods and the number of animals in figure legendswas less than that in theMaterials andMethods as the remaining alive rats were divided into several parts for different experiments. ey added that, during echocardiographic measurement, two rats of Cas group died from anesthesia, so they took four rats from different groups to evaluate cardiac indexes. A er echocardiographic studies, the rats were immediately executed in addition to collecting blood and heart samples. e minimum number of different groups was 6 (8 S-Cas, 6 Cas, 7 Cas+T, and 6 Cas+T+F). Accordingly, they measured ATP content and sexual hormones of six rats. ree rats were performed by histological analysis, and the other three were performed by western blotting and real-time PCR. e Editorial Board was concerned about the death of several animals which should be clearly defined by the authors as they should state why the n was 3-6 when each treatment is mentioned with an n = 8. Moreover, the board found that the statistical analysis was not done properly and they recommended repeating the study to increase the sample size.
PPAR Research对2016年6月发表在PPAR Research上的题为“睾酮替代通过上调PPARα调节心脏代谢重塑和心肌梗死”的文章[1]表示关注,因为文章质量存在缺陷。编辑委员会认为,由于缺少对照组,实验设计不够可靠。我认为这很令人困惑大多数数据集在图例中被标记为n=3这对于动物实验来说是非常低的。此外,董事会发现作者在方法中描述的每组数都不是n=3,而是略高。没有解释为什么不是所有的动物都被包括在所有的分析中,以及如何选择数据集。在一些数据集中,作者使用n=6,但一些动物数据集缺失。作者解释说,在材料和方法中,使用额外的正常大鼠进行相同的手术,没有LDA闭塞作为对照组。此外,在材料和方法中提到了心肌梗死后存活的动物数量,图中图例中的动物数量比材料和方法中少,因为剩余的存活大鼠被分成几个部分进行不同的实验。ey补充说,在超声心动图测量过程中,Cas组有2只大鼠因麻醉死亡,所以他们从不同的组中取了4只大鼠来评估心脏指标。在超声心动图研究中,除了收集血液和心脏样本外,还立即将大鼠处死。不同组的最小数量为6例(8例S-Cas, 6例Cas, 7例Cas+T, 6例Cas+T+F)。据此,他们测量了6只大鼠的ATP含量和性激素。其余3只采用western blotting和real-time PCR方法。e编委会对几只动物的死亡表示关注,作者应该清楚地说明,为什么在提到每种治疗时,n = 8, n为3-6。此外,委员会发现统计分析没有做得很好,他们建议重复研究以增加样本量。
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引用次数: 0
PPARG2 Pro12Ala and TNFα -308G>A Polymorphisms Are Not Associated with Heart Failure Development in Patients with Ischemic Heart Disease after Coronary Artery Bypass Grafting. PPARG2 Pro12Ala和TNFα -308G>A多态性与缺血性心脏病患者冠状动脉搭桥术后心力衰竭的发生无关
IF 2.9 3区 医学 Q2 Medicine Pub Date : 2019-06-02 eCollection Date: 2019-01-01 DOI: 10.1155/2019/1932036
Izabela Wojtkowska, Tomasz A Bonda, Andrzej Tysarowski, Katarzyna Seliga, Janusz A Siedlecki, Maria M Winnicka, Janina Stępińska

TNFα and PPARγ are important modulators of metabolism, inflammation, and atherosclerosis. Coronary artery disease is the leading cause of heart failure (HF). The aim of the study was to assess whether polymorphisms of the TNFα (-308G>A) and PPARG2 (Pro12Ala) genes are associated with the risk of developing HF by patients with ischemic heart disease. Methods. 122 patients without HF (aged 63 ± 8.8 years, 85% males) with confirmed coronary artery disease qualified for coronary bypass grafting were enrolled in the study. After the procedure, they were screened for cardiac parameters. Those with elevated NT-proBNP or diminished left ventricular ejection fraction during follow-up were assigned to the HF group (n=78), and the remaining ones to the non-HF group (n=44). The TNFα -308G>A and PPARG2 Pro12Ala polymorphisms were detected using the TaqMan method. Results. The distributions of TNFα -308G>A and PPARG2 Pro12Ala did not differ between the HF and non-HF groups (-308G>A: 16% vs. 11.4% of alleles; Pro12Ala: 23.9% vs. 20.5% of alleles, respectively). IL-6 concentration in the plasma of TNFα A-allele carriers at months 1 and 12 after CABG was higher in the HF group compared to the non-HF group (1 month after CABG: 5.3 ± 3.4 vs. 3.1 ± 2.9, p<0.05; 12 months after CABG: 4.2 ± 3,9 vs. 1.4 ± 1.2, p<0.01, respectively). Both polymorphisms were not related to changes in the plasma TNFα concentration or other parameters related to HF. Conclusions. Our study did not reveal any correlation between the PPARG2 Pro12Ala and TNFα -308G>A polymorphisms and development of HF in patients with ischemic heart disease after coronary bypass grafting.

TNFα和PPARγ是代谢、炎症和动脉粥样硬化的重要调节剂。冠状动脉疾病是导致心力衰竭的主要原因。该研究的目的是评估TNFα (-308G>A)和PPARG2 (Pro12Ala)基因多态性是否与缺血性心脏病患者发生HF的风险相关。方法:122例无心衰患者(年龄63±8.8岁,男性85%)经证实有冠状动脉病变,符合冠状动脉搭桥术条件。手术后,他们接受了心脏参数的筛查。随访期间NT-proBNP升高或左室射血分数降低的患者被分配到HF组(n=78),其余患者被分配到非HF组(n=44)。TaqMan法检测TNFα -308G>A和PPARG2 Pro12Ala多态性。结果。TNFα -308G>A和PPARG2 Pro12Ala在HF组和非HF组之间的分布无差异(-308G>A: 16% vs. 11.4%;Pro12Ala: 23.9% vs. 20.5%)。在CABG术后1、12个月,HF组TNFα a等位基因携带者血浆IL-6浓度高于非HF组(CABG术后1个月:5.3±3.4 vs 3.1±2.9),pα浓度或其他与HF相关的参数。结论。我们的研究未发现PPARG2 Pro12Ala和TNFα -308G>A多态性与缺血性心脏病患者冠状动脉搭桥术后HF的发生之间存在相关性。
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引用次数: 1
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PPAR Research
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