PPAR Research最新文献

{"title":"Rosiglitazone Alleviates Mechanical Allodynia of Rats with Bone Cancer Pain through the Activation of PPAR-<i>γ</i> to Inhibit the NF-<i>κ</i>B/NLRP3 Inflammatory Axis in Spinal Cord Neurons.","authors":"Jie Fu,&nbsp;Baoxia Zhao,&nbsp;Chaobo Ni,&nbsp;Huadong Ni,&nbsp;Longsheng Xu,&nbsp;Qiuli He,&nbsp;Miao Xu,&nbsp;Chengfei Xu,&nbsp;Ge Luo,&nbsp;Jianjun Zhu,&nbsp;Jiachun Tao,&nbsp;Ming Yao","doi":"10.1155/2021/6086265","DOIUrl":"https://doi.org/10.1155/2021/6086265","url":null,"abstract":"<p><p>Bone cancer pain (BCP) is a serious clinical problem that affects the quality of life of cancer patients. However, the current treatment methods for this condition are still unsatisfactory. This study investigated whether intrathecal injection of rosiglitazone modulates the noxious behaviors associated with BCP, and the possible mechanisms related to this effect were explored. We found that rosiglitazone treatment relieved bone cancer-induced mechanical hyperalgesia in a dose-dependent manner, promoted the expression of peroxisome proliferator-activated receptor-<i>γ</i> (PPAR-<i>γ</i>) in spinal cord neurons, and inhibited the activation of the nuclear factor-kappa B (NF-<i>κ</i>B)/nod-like receptor protein 3 (NLRP3) inflammatory axis induced by BCP. However, concurrent administration of the PPAR-<i>γ</i> antagonist GW9662 reversed these effects. The results show that rosiglitazone inhibits the NF-<i>κ</i>B/NLRP3 inflammation axis by activating PPAR-<i>γ</i> in spinal neurons, thereby alleviating BCP. Therefore, the PPAR-<i>γ</i>/NF-<i>κ</i>B/NLRP3 signaling pathway may be a potential target for the treatment of BCP in the future.</p>","PeriodicalId":20439,"journal":{"name":"PPAR Research","volume":" ","pages":"6086265"},"PeriodicalIF":2.9,"publicationDate":"2021-08-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8413064/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39385923","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<i>α</i> Gene Is Involved in Body Composition Variation in Response to an Aerobic Training Program in Overweight/Obese.","authors":"Glêbia A Cardoso,&nbsp;Mateus D Ribeiro,&nbsp;Bruno R V Sousa,&nbsp;Yohanna de Oliveira,&nbsp;Klécia F Sena,&nbsp;Joane R E Batista,&nbsp;Antônio E M Almeida,&nbsp;João M Filho,&nbsp;Raquel S B Silva,&nbsp;Darlene C Persuhn,&nbsp;Alexandre S Silva","doi":"10.1155/2021/8880042","DOIUrl":"https://doi.org/10.1155/2021/8880042","url":null,"abstract":"<p><p>The objective of this study was to investigate the relationship of the polymorphism in Intron 7 G/C (rs 4253778) of the peroxisome proliferator-activated receptor alpha (PPAR<i>α</i>) gene with the magnitude of changes in the body composition of an overweight and obese population that underwent an aerobic training program. Fifty-eight previously inactive men and women, body mass index (BMI) 31.5 ± 2.8 kg/m², 46.5% (<i>n</i> = 27) genotyped as CC genotype and 53.5% (<i>n</i> = 31) as CA+AA, underwent a 12-week aerobic training (walking/running). Aerobic capacity (ergospirometry), body composition (DXA), and nutritional assessment were made before and 48 h after the experimental protocol. Two-way ANOVA, chi-square test, and logistic regression were used (<i>p</i> < 0.05). Twenty-seven volunteers (46.5%) were identified as CC genotype and 31 (53.5%) as CA+AA genotype. Time-group interaction showed that there was no difference in these between two allele groups. However, differences in distribution of respondents or nonresponders according to allele A were identified for fat mass (<i>p</i> ≤ 0.003), percentage fat mass (<i>p</i> ≤ 0.002), the waist (<i>p</i> ≤ 0.009), abdomen (<i>p</i> ≤ 0.000), and hip (<i>p</i> ≤ 0.001), this difference being independent for the fat mass. Meanwhile, sex, age, and nutritional management have also been found to be influential factors. It is concluded that the PPAR<i>α</i> gene is involved in varying body composition in response to an aerobic training program.</p>","PeriodicalId":20439,"journal":{"name":"PPAR Research","volume":" ","pages":"8880042"},"PeriodicalIF":2.9,"publicationDate":"2021-08-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8371623/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39347990","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":"Nobiletin Attenuates Pathological Cardiac Remodeling after Myocardial Infarction via Activating PPAR<i>γ</i> and PGC1<i>α</i>.","authors":"Yufei Zhou,&nbsp;Ting Yin,&nbsp;Mengsha Shi,&nbsp;Mengli Chen,&nbsp;Xiaodong Wu,&nbsp;Kai Wang,&nbsp;Iokfai Cheang,&nbsp;Yanxiu Li,&nbsp;Hongcai Shang,&nbsp;Haifeng Zhang,&nbsp;Xinli Li","doi":"10.1155/2021/9947656","DOIUrl":"https://doi.org/10.1155/2021/9947656","url":null,"abstract":"<p><strong>Materials and methods: </strong>C57BL/6 mice were treated with coronary artery ligation to generate an MI model, followed by treatment for 3 weeks with NOB (50 mg/kg/d) or vehicle (50 mg/kg/d), with or without the peroxisome proliferator-activated receptor gamma (PPAR<i>γ</i>) inhibitor T0070907 (1 mg/kg/d). Cardiac function (echocardiography, survival rate, Evans blue, and triphenyl tetrazolium chloride staining), fibrosis (Masson's trichrome staining, quantitative real-time polymerase chain reaction (qRT-PCR), and western blot (WB)), hypertrophy (haematoxylin-eosin staining, wheat germ agglutinin staining, and qRT-PCR), and apoptosis (WB and terminal deoxynucleotidyl transferase dUTP nick-end labelling (TUNEL) staining) were evaluated. Hypoxia-induced apoptosis (TUNEL, WB) and phenylephrine- (PE-) induced pathological hypertrophy (immunofluorescence staining, qRT-PCR) models were established in primary neonatal rat ventricular myocytes (NRVMs). The effects of NOB with or without T0070907 were examined for the expression of PPAR<i>γ</i> and PPAR<i>γ</i> coactivator 1<i>α</i> (PGC1<i>α</i>) by WB in mice and NRVMs. The potential downstream effectors of PPAR<i>γ</i> were further analyzed by WB in mice.</p><p><strong>Results: </strong>Following MI in mice, NOB intervention enhanced cardiac function across three predominant dimensions of pathological cardiac remodeling, which reflected in decreasing cardiac fibrosis, apoptosis, and hypertrophy decompensation. NOB intervention also alleviated apoptosis and hypertrophy in NRVMs. NOB intervention upregulated PPAR<i>γ</i> and PGC1<i>α in vivo</i> and <i>in vitro</i>. Furthermore, the PPAR<i>γ</i> inhibitor abolished the protective effects of NOB against pathological cardiac remodeling during the progression from MI to CHF. The potential downstream effectors of PPAR<i>γ</i> were nuclear factor erythroid 2-related factor 2 (Nrf-2) and heme oxygenase 1 (HO-1).</p><p><strong>Conclusions: </strong>Our findings suggested that NOB alleviates pathological cardiac remodeling after MI via PPAR<i>γ</i> and PGC1<i>α</i> upregulation.</p>","PeriodicalId":20439,"journal":{"name":"PPAR Research","volume":" ","pages":"9947656"},"PeriodicalIF":2.9,"publicationDate":"2021-08-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8373512/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39347991","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":"Computational Analysis of Gly482Ser Single-Nucleotide Polymorphism in PPARGC1A Gene Associated with CAD, NAFLD, T2DM, Obesity, Hypertension, and Metabolic Diseases.","authors":"Somayye Taghvaei,&nbsp;Leila Saremi,&nbsp;Sepideh Babaniamansour","doi":"10.1155/2021/5544233","DOIUrl":"https://doi.org/10.1155/2021/5544233","url":null,"abstract":"<p><p>Peroxisome proliferator-activated receptor-gamma coactivator 1-alpha (PPARGC1A) regulates the expression of energy metabolism's genes and mitochondrial biogenesis. The essential roles of PPARGC1A encouraged the researchers to assess the relation between metabolism-related diseases and its variants. To study Gly482Ser (+1564G/A) single-nucleotide polymorphism (SNP) after PPARGC1A modeling, we substitute Gly482 for Ser482. Stability prediction tools showed that this substitution decreases the stability of PPARGC1A or has a destabilizing effect on this protein. We then utilized molecular dynamics simulation of both the Gly482Ser variant and wild type of the PPARGC1A protein to analyze the structural changes and to reveal the conformational flexibility of the PPARGC1A protein. We observed loss flexibility in the RMSD plot of the Gly482Ser variant, which was further supported by a decrease in the SASA value in the Gly482Ser variant structure of PPARGC1A and an increase of H-bond with the increase of <i>β</i>-sheet and coil and decrease of turn in the DSSP plot of the Gly482Ser variant. Such alterations may significantly impact the structural conformation of the PPARGC1A protein, and it might also affect its function. It showed that the Gly482Ser variant affects the PPARGC1A structure and makes the backbone less flexible to move. In general, molecular dynamics simulation (MDS) showed more flexibility in the native PPARGC1A structure. Essential dynamics (ED) also revealed that the range of eigenvectors in the conformational space has lower extension of motion in the Gly482Ser variant compared with WT. The Gly482Ser variant also disrupts PPARGC1A interaction. Due to this single-nucleotide polymorphism in PPARGC1A, it became more rigid and might disarray the structural conformation and catalytic function of the protein and might also induce type 2 diabetes mellitus (T2DM), coronary artery disease (CAD), and nonalcoholic fatty liver disease (NAFLD). The results obtained from this study will assist wet lab research in expanding potent treatment on T2DM.</p>","PeriodicalId":20439,"journal":{"name":"PPAR Research","volume":" ","pages":"5544233"},"PeriodicalIF":2.9,"publicationDate":"2021-08-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8360745/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39314666","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":"Activation of the Peroxisome Proliferator-Activated Receptors (PPAR-<i>α</i>/<i>γ</i>) and the Fatty Acid Metabolizing Enzyme Protein CPT1A by Camel Milk Treatment Counteracts the High-Fat Diet-Induced Nonalcoholic Fatty Liver Disease.","authors":"Haifa M AlNafea,&nbsp;Aida A Korish","doi":"10.1155/2021/5558731","DOIUrl":"https://doi.org/10.1155/2021/5558731","url":null,"abstract":"<p><p>Camel milk (CM) has a unique composition rich in antioxidants, trace elements, immunoglobulins, insulin, and insulin-like proteins. Treatment by CM demonstrated protective effects against nonalcoholic fatty liver disease (NAFLD) induced by a high-fat cholesterol-rich diet (HFD-C) in rats. CM dampened the steatosis, inflammation, and ballooning degeneration of the hepatocytes. It also counteracted hyperlipidemia, insulin resistance (IR), glucose intolerance, and oxidative stress. The commencement of NAFLD triggered the peroxisome proliferator-activated receptor-<i>α</i> (PPAR-<i>α</i>), carnitine palmitoyl-transferase-1 (CPT1A), and fatty acid-binding protein-1 (FABP1) and decreased the PPAR-<i>γ</i> expression in the tissues of the animals on HFD-C. This was associated with increased levels of the inflammatory cytokines IL-6 and TNF-<i>α</i> and leptin and declined levels of the anti-inflammatory adiponectin. Camel milk treatment to the NAFLD animals remarkably upregulated PPARs (<i>α</i>, <i>γ</i>) and the downstream enzyme CPT1A in the metabolically active tissues involved in cellular uptake and beta-oxidation of fatty acids. The enhanced lipid metabolism in the CM-treated animals was linked with decreased expression of FABP1 and suppression of IL-6, TNF-<i>α</i>, and leptin release with augmented adiponectin production. The protective effects of CM against the histological and biochemical features of NAFLD are at least in part related to the activation of the hepatic and extrahepatic PPARs (<i>α</i>, <i>γ</i>) with consequent activation of the downstream enzymes involved in fat metabolism. Camel milk treatment carries a promising therapeutic potential to NAFLD through stimulating PPARs actions on fat metabolism and glucose homeostasis. This can protect against hepatic steatosis, IR, and diabetes mellitus in high-risk obese patients.</p>","PeriodicalId":20439,"journal":{"name":"PPAR Research","volume":" ","pages":"5558731"},"PeriodicalIF":2.9,"publicationDate":"2021-07-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8285205/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39221282","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<i>γ</i> Plays an Important Role in Acute Hepatic Ischemia-Reperfusion Injury via AMPK/mTOR Pathway.","authors":"Liwei Wu,&nbsp;Qiang Yu,&nbsp;Ping Cheng,&nbsp;Chuanyong Guo","doi":"10.1155/2021/6626295","DOIUrl":"https://doi.org/10.1155/2021/6626295","url":null,"abstract":"<p><strong>Background: </strong>Hepatic ischemia-reperfusion (IR) injury is one of the severe complications associated with liver surgery and leads to liver dysfunction. PPAR<i>γ</i> is always linked with various physiologic pathways, and it can alleviate liver damage in IR injury.</p><p><strong>Aim: </strong>In this study, we explored the potential mechanism of PPAR<i>γ</i> in the pathogenesis of hepatic IR injury by mice model.</p><p><strong>Methods: </strong>After treated with si-PPAR<i>γ</i> or rosiglitazone, mice were subjected to hepatic ischemia-reperfusion. Liver tissue and blood samples were collected to evaluate liver injury and detected relative mRNA and protein expressions.</p><p><strong>Results: </strong>The expression of PPAR<i>γ</i> was increased after reperfusion. And the alleviation of PPAR<i>γ</i> aggravated the liver damage in IR; at the same time, upregulation of the expression of PPAR<i>γ</i> released the liver damage. And these effects of PPAR<i>γ</i> in IR were related to the AMPK/mTOR/autophagy signaling pathway.</p><p><strong>Conclusion: </strong>PPAR<i>γ</i> plays an important role in hepatic IR injury at least partly via the AMPK/mTOR/autophagy pathway.</p>","PeriodicalId":20439,"journal":{"name":"PPAR Research","volume":" ","pages":"6626295"},"PeriodicalIF":2.9,"publicationDate":"2021-07-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8275421/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39203189","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":"Variation of PPARG Expression in Chemotherapy-Sensitive Patients of Hypopharyngeal Squamous Cell Carcinoma.","authors":"Meng Lian,&nbsp;Yong Tao,&nbsp;Jiaming Chen,&nbsp;Xixi Shen,&nbsp;Lizhen Hou,&nbsp;Shaolong Cao,&nbsp;Jugao Fang","doi":"10.1155/2021/5525091","DOIUrl":"https://doi.org/10.1155/2021/5525091","url":null,"abstract":"<p><p>Our previous study showed that the upregulation of peroxisome proliferator-activated receptor gamma (PPARG) could promote chemosensitivity of hypopharyngeal squamous cell carcinoma (HSCC) in chemotherapeutic treatments. Here, we acquired two more independent expression data of PPARG to validate the expression levels of PPARG in chemotherapy-sensitive patients (CSP) and its individualized variations compared to chemotherapy-non-sensitive patients (CNSP). Our results showed that overall PPARG expression was mildly downregulated (log fold change = -0.55; <i>p</i> value = 0.42; overexpression in three CSPs and reduced expression in four CSPs), which was not consistent with previous results (log fold change = 0.50; <i>p</i> = 0.22; overexpression in nine CSPs and reduced expression in three CSPs). Both studies indicated that PPARG expression variation was significantly associated with the Tumor-Node-Metastasis (TNM) stage (<i>p</i> = 7.45<i>e</i> - 7 and 6.50<i>e</i> - 4, for the first and second studies, respectively), which was used as one of the predictors of chemosensitivity. The new dataset analysis revealed 51 genes with significant gene expression changes in CSPs (LFC > 1 or <-1; <i>p</i> value < 0.01), and two of them (TMEM45A and RBP1) demonstrated strong coexpression with PPARG (Pearson correlation coefficient > 0.6 or <-0.6). There were 21 significant genes in the data from the first study, with no significant association with PPARG and no overlap with the 51 genes revealed in this study. Our results support the connection between PPARG and chemosensitivity in HSCC tumor cells. However, significant PPARG variation exists in CSPs, which may be influenced by multiple factors, including the TNM stage.</p>","PeriodicalId":20439,"journal":{"name":"PPAR Research","volume":" ","pages":"5525091"},"PeriodicalIF":2.9,"publicationDate":"2021-05-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8149230/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38953293","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":"PPARD May Play a Protective Role for Major Depressive Disorder.","authors":"Tao Yang,&nbsp;Juhua Li,&nbsp;Liyuan Li,&nbsp;Xuehua Huang,&nbsp;Jiajun Xu,&nbsp;Xia Huang,&nbsp;Lijuan Huang,&nbsp;Kamil Can Kural","doi":"10.1155/2021/5518138","DOIUrl":"https://doi.org/10.1155/2021/5518138","url":null,"abstract":"<p><p>Activation of PPARD has been shown to inhibit depressive behaviors and enhances neurogenesis. However, whether PPARD is involved in the pathological development of major depressive disorder (MDD) is largely unknown. To explore the potential connection between PPARD and MDD, we first conducted a literature-based data mining to construct a PPARD-driven MDD regulating network. Then, we tested the PPARD expression changes in MDD patients from 18 independent MDD RNA expression datasets, followed by coexpression analysis, multiple linear regression analysis, and a heterogeneity analysis to study the influential factors for PPARD expression levels. Our results showed that overexpression of PPARD could inhibit inflammatory cytokine signaling pathways and the ROS and glutamate pathways that have been shown to play important roles in the pathological development of MDD. However, PPARD could also activate nitric oxide formation and ceramide synthesis, which was implicated as promoters in the pathogenesis of MDD, indicating the complexity of the relationship between PPARD and MDD. PPARG presented significant within- and between-study variations in the 18 MDD datasets (<i>p</i> value = 0.97), which were significantly associated with the population region (country) and sample source (<i>p</i> < 2.67<i>e</i> - 5). Our results suggested that PPARD could be a potential regulator rather than a biomarker in the pathological development of MDD. This study may add new insights into the understanding of the PPARD-MDD relationship.</p>","PeriodicalId":20439,"journal":{"name":"PPAR Research","volume":" ","pages":"5518138"},"PeriodicalIF":2.9,"publicationDate":"2021-04-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8081621/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38963728","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":"Inhibition of miR-128-3p Attenuated Doxorubicin-Triggered Acute Cardiac Injury in Mice by the Regulation of PPAR-<i>γ</i>.","authors":"Wen-Bin Zhang,&nbsp;Yong-Fa Zheng,&nbsp;Yao-Gui Wu","doi":"10.1155/2021/7595374","DOIUrl":"https://doi.org/10.1155/2021/7595374","url":null,"abstract":"<p><strong>Background: </strong>The clinical usefulness of doxorubicin (DOX), an anthracycline with antitumor activity, is limited by its cardiotoxicity. Oxidative stress and myocardial apoptosis were closely associated with DOX-induced cardiac dysfunction. It has been reported that microRNA-128-3p (miR-128-3p) was involved into the regulation of redox balance. However, the role of miR-128-3p in DOX-related cardiac injury remains not yet understood. The aim of this study was to investigate the biological effect of miR-128-3p in DOX-induced cardiotoxicity.</p><p><strong>Methods: </strong>To induce DOX-related acute cardiac injury, mice were subjected to a single injection of DOX. Inhibition of myocardial miR-128-3p was achieved by an adeno-associated virus (AAV9) system carrying a miR-128-3p sponge.</p><p><strong>Results: </strong>The data in our study indicated that miR-128-3p was upregulated in DOX-treated hearts and cardiomyocytes. Inhibition of miR-128-3p attenuated DOX-related cardiac injury and improved cardiac function in mice. Moreover, miR-128-3p inhibition could suppress myocardial inflammatory response, oxidative damage, and cell apoptotic death in DOX-treated mice. Further analysis showed that miR-128-3p could directly target peroxisome proliferator-activated receptor <i>γ</i> (PPAR-<i>γ</i>) and decrease PPAR-<i>γ</i> expression. Moreover, the protective effects provided by miR-128-3p inhibition were abolished by a PPAR-<i>γ</i> antagonist in vivo and in vitro.</p><p><strong>Conclusions: </strong>miR-128-3p inhibition attenuated DOX-related acute cardiac injury via the regulation of PPAR-<i>γ</i> in mice.</p>","PeriodicalId":20439,"journal":{"name":"PPAR Research","volume":" ","pages":"7595374"},"PeriodicalIF":2.9,"publicationDate":"2021-04-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8079209/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38980397","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-Alpha Agonist Fenofibrate Combined with Octreotide Acetate in the Treatment of Acute Hyperlipidemia Pancreatitis.","authors":"Wen Bao,&nbsp;Rui Kong,&nbsp;Nan Wang,&nbsp;Wei Han,&nbsp;Jie Lu","doi":"10.1155/2021/6629455","DOIUrl":"https://doi.org/10.1155/2021/6629455","url":null,"abstract":"<p><p>At present, there are more and more patients with acute hypertriglyceridemia pancreatitis in clinical practice. Common treatment measures include fasting and water withdrawal, fluid resuscitation, and somatostatin. In recent years, studies have pointed out that the PPARa agonist fenofibrate may help improve the condition of such patients. Therefore, through clinical research and analysis, we reported for the first time that fenofibrate combined with octreotide acetate has a more excellent effect in the treatment of patients with acute hypertriglyceridemia pancreatitis, and from the perspective of signal pathways, we revealed that the combination of the two drugs has an effect on NF-<i>κ</i>B P65. The synergistic inhibitory effect proves that the combined treatment is beneficial to control inflammation, protect liver function, and improve the prognosis of patients. It is worthy of clinical promotion.</p>","PeriodicalId":20439,"journal":{"name":"PPAR Research","volume":" ","pages":"6629455"},"PeriodicalIF":2.9,"publicationDate":"2021-04-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8081610/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38963729","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}