PPAR Research最新文献

{"title":"Piperine Alleviates Doxorubicin-Induced Cardiotoxicity via Activating PPAR-<i>γ</i> in Mice.","authors":"Jie Yan,&nbsp;Si-Chi Xu,&nbsp;Chun-Yan Kong,&nbsp;Xiao-Yang Zhou,&nbsp;Zhou-Yan Bian,&nbsp;Ling Yan,&nbsp;Qi-Zhu Tang","doi":"10.1155/2019/2601408","DOIUrl":"https://doi.org/10.1155/2019/2601408","url":null,"abstract":"<p><strong>Background: </strong>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.</p><p><strong>Methods: </strong>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.</p><p><strong>Results: </strong>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-<i>γ</i> (PPAR-<i>γ</i>), and the protective effects of piperine were abolished by the treatment of the PPAR-<i>γ</i> antagonist in vivo and in vitro.</p><p><strong>Conclusions: </strong>Piperine could suppress DOX-related cardiac injury via activation of PPAR-<i>γ</i> in mice.</p>","PeriodicalId":20439,"journal":{"name":"PPAR Research","volume":null,"pages":null},"PeriodicalIF":2.9,"publicationDate":"2019-12-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1155/2019/2601408","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"37539008","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"PPAR-γ Ligand Inhibits Nasopharyngeal Carcinoma Cell Proliferation and Metastasis by Regulating E2F2","authors":"Ping Yang, Jiashui Wang, Xiaoxia Cheng, Jingchao Chen, Hui Zhu, Xiaolin Li, Li Cao, Wei-Wei Tang","doi":"10.1155/2019/8679271","DOIUrl":"https://doi.org/10.1155/2019/8679271","url":null,"abstract":"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.","PeriodicalId":20439,"journal":{"name":"PPAR Research","volume":null,"pages":null},"PeriodicalIF":2.9,"publicationDate":"2019-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1155/2019/8679271","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"43105056","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"15-Deoxy-∆-12,14-Prostaglandin J2 (15d-PGJ2), an Endogenous Ligand of PPAR-γ: Function and Mechanism","authors":"Jingjing Li, Chuanyong Guo, Jianye Wu","doi":"10.1155/2019/7242030","DOIUrl":"https://doi.org/10.1155/2019/7242030","url":null,"abstract":"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.","PeriodicalId":20439,"journal":{"name":"PPAR Research","volume":null,"pages":null},"PeriodicalIF":2.9,"publicationDate":"2019-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1155/2019/7242030","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"46585936","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Corrigendum to “PPARs in Human Neuroepithelial Tumors: PPAR Ligands as Anticancer Therapies for the Most Common Human Neuroepithelial Tumors”","authors":"E. Benedetti, R. Galzio, B. D'angelo, M. Ceru', A. Cimini","doi":"10.1155/2019/4309068","DOIUrl":"https://doi.org/10.1155/2019/4309068","url":null,"abstract":"[This corrects the article DOI: 10.1155/2010/427401.].","PeriodicalId":20439,"journal":{"name":"PPAR Research","volume":null,"pages":null},"PeriodicalIF":2.9,"publicationDate":"2019-07-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1155/2019/4309068","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"49033670","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Retracted: Possible Role of Interaction between PPARα and Cyclophilin D in Cardioprotection of AMPK against In Vivo Ischemia-Reperfusion in Rats","authors":"PPAR Research","doi":"10.1155/2019/9760941","DOIUrl":"https://doi.org/10.1155/2019/9760941","url":null,"abstract":"[This retracts the article DOI: 10.1155/2016/9282087.].","PeriodicalId":20439,"journal":{"name":"PPAR Research","volume":null,"pages":null},"PeriodicalIF":2.9,"publicationDate":"2019-07-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1155/2019/9760941","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"42403823","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Activation and Expression of Peroxisome Proliferator-Activated Receptor Alpha Are Associated with Tumorigenesis in Colorectal Carcinoma","authors":"Tatsuya Morinishi, Yasunori Tokuhara, H. Ohsaki, Emi Ibuki, K. Kadota, E. Hirakawa","doi":"10.1155/2019/7486727","DOIUrl":"https://doi.org/10.1155/2019/7486727","url":null,"abstract":"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.","PeriodicalId":20439,"journal":{"name":"PPAR Research","volume":null,"pages":null},"PeriodicalIF":2.9,"publicationDate":"2019-07-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1155/2019/7486727","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"44527608","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Peroxisome Proliferator-Activated Receptor-γ Antagonizes LOX-1-Mediated Endothelial Injury by Transcriptional Activation of miR-590-5p","authors":"Lei Xu, Gang Zhao, Hong Zhu, Shijun Wang, A. Sun, Y. Zou, J. Ge","doi":"10.1155/2019/2715176","DOIUrl":"https://doi.org/10.1155/2019/2715176","url":null,"abstract":"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.","PeriodicalId":20439,"journal":{"name":"PPAR Research","volume":null,"pages":null},"PeriodicalIF":2.9,"publicationDate":"2019-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1155/2019/2715176","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"44875453","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Short-Term Activation of Peroxisome Proliferator-Activated Receptors <i>α</i> and <i>γ</i> Induces Tissue-Specific Effects on Lipid Metabolism and Fatty Acid Composition in Male Wistar Rats.","authors":"Elin Strand, Vegard Lysne, Mari Lausund Grinna, Pavol Bohov, Asbjørn Svardal, Ottar Nygård, Rolf K Berge, Bodil Bjørndal","doi":"10.1155/2019/8047627","DOIUrl":"10.1155/2019/8047627","url":null,"abstract":"<p><p>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 PPAR<i>α</i> agonist group receiving WY-14,643 (n=6); and a PPAR<i>γ</i> 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 PPAR<i>α</i> 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, PPAR<i>α</i> activation leads to overall lower levels of free FAs and specific changes in certain FAs, compared with control. Furthermore, <i>β</i>-oxidation in liver and the enzymatic activities of well-known PPAR<i>α</i> targeted genes were higher following PPAR<i>α</i> administration. Overall, rats treated with the PPAR<i>α</i> 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 PPAR<i>γ</i> agonist was associated with a lower liver index, lower plasma triglycerides (TAG) and phospholipids, and higher hepatic phospholipids, compared with control. PPAR<i>γ</i> 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 PPAR<i>γ</i> activation. Altogether, there were characteristic effects of PPAR<i>α</i> activation in liver and heart, as well as in plasma. PPAR<i>γ</i> 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 PPAR<i>α</i> and PPAR<i>γ</i> 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.</p>","PeriodicalId":20439,"journal":{"name":"PPAR Research","volume":null,"pages":null},"PeriodicalIF":3.5,"publicationDate":"2019-06-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6594300/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"47927168","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Expression of Concern on “Testosterone Replacement Modulates Cardiac Metabolic Remodeling after Myocardial Infarction by Upregulating PPARα”","authors":"PPAR Research","doi":"10.1155/2019/5137020","DOIUrl":"https://doi.org/10.1155/2019/5137020","url":null,"abstract":"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.","PeriodicalId":20439,"journal":{"name":"PPAR Research","volume":null,"pages":null},"PeriodicalIF":2.9,"publicationDate":"2019-06-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1155/2019/5137020","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41856444","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"PPARG2 Pro12Ala and TNF<i>α</i> -308G>A Polymorphisms Are Not Associated with Heart Failure Development in Patients with Ischemic Heart Disease after Coronary Artery Bypass Grafting.","authors":"Izabela Wojtkowska,&nbsp;Tomasz A Bonda,&nbsp;Andrzej Tysarowski,&nbsp;Katarzyna Seliga,&nbsp;Janusz A Siedlecki,&nbsp;Maria M Winnicka,&nbsp;Janina Stępińska","doi":"10.1155/2019/1932036","DOIUrl":"https://doi.org/10.1155/2019/1932036","url":null,"abstract":"<p><p>TNF<i>α</i> and PPAR<i>γ</i> 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 <i>TNFα</i> (-308G>A) and <i>PPARG2</i> (Pro12Ala) genes are associated with the risk of developing HF by patients with ischemic heart disease. <i>Methods</i>. 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 <i>TNFα</i> -308G>A and <i>PPARG</i>2 Pro12Ala polymorphisms were detected using the TaqMan method. <i>Results</i>. The distributions of <i>TNFα</i> -308G>A and <i>PPARG</i>2 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 <i>TNFα</i> 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 TNF<i>α</i> concentration or other parameters related to HF. <i>Conclusions</i>. Our study did not reveal any correlation between the <i>PPARG2</i> Pro12Ala and <i>TNFα</i> -308G>A polymorphisms and development of HF in patients with ischemic heart disease after coronary bypass grafting.</p>","PeriodicalId":20439,"journal":{"name":"PPAR Research","volume":null,"pages":null},"PeriodicalIF":2.9,"publicationDate":"2019-06-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1155/2019/1932036","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"37392487","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}