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Total 16 results found since Jan 2013.

Peroxisome proliferator-activated receptor α (PPARα)-dependent regulation of fibroblast growth factor 23 (FGF23).
Abstract Bone cells secrete fibroblast growth factor 23 (FGF23), a hormone that inhibits the synthesis of active vitamin D (1,25(OH)2D3) and induces phosphate excretion in the kidney. In addition, it exerts paracrine effects on other cells including hepatocytes, cardiomyocytes, and immune cells. The production of FGF23 is controlled by different factors including parathyroid hormone, 1,25(OH)2D3, alimentary phosphate, insulin, inflammation, and AMP-dependent kinase (AMPK) regulation of store-operated Ca2+ entry (SOCE). Peroxisome proliferator-activated receptor α (PPARα) is a transcription factor with anti-infla...
Source: Pflugers Archiv : European Journal of Physiology - March 17, 2020 Category: Physiology Authors: Ewendt F, Hirche F, Feger M, Föller M Tags: Pflugers Arch Source Type: research

Shortening of telomere length by metabolic factors in diabetes: protective effects of fenofibrate.
Abstract People with diabetes mellitus have shorter telomeres compared with non-diabetic subjects. The aim of this study was to investigate an in-vitro model of telomere shortening under diabetes metabolic conditions. The mechanisms of the accelerated telomere length attrition and the potential telomere protective action of fenofibrate with related cellular mechanisms were also examined. Human dermal fibroblasts were passaged and cultured in normal (5.5 mM) or high (25 mM) D-glucose, across 7 days with hydrogen peroxide (H2O2), glucosamine (GA), or glycated albumin (AGEs-BSA). Relative telomere length (RTL) was...
Source: Journal of Cell Communication and Signaling - June 14, 2019 Category: Molecular Biology Authors: Sutanto SSI, McLennan SV, Keech AC, Twigg SM Tags: J Cell Commun Signal Source Type: research

β-hydroxybutyrate protects hepatocytes against endoplasmic reticulum stress in a sirtuin 1-independent manner.
Abstract β-hydroxybutyrate (BHB), a major ketone body in mammals, is produced from fatty acids through mitochondrial fatty acid oxidation in hepatocytes. To elucidate the role of BHB in the hepatic endoplasmic reticulum (ER), we examined the effects of BHB on hepatic ER stress induced by tunicamycin. In mouse hepatoma Hepa1c1c7 cells, BHB treatment suppressed the protein expression of ER stress responsive genes and increased cell viability, while reducing the protein expression of apoptosis inducible genes, without causing any alterations in the protein expression of sirtuin 1 (SIRT1) or the phosphorylation of AM...
Source: Archives of Biochemistry and Biophysics - January 18, 2019 Category: Biochemistry Authors: Tagawa R, Kawano Y, Minami A, Nishiumi S, Yano Y, Yoshida M, Kodama Y Tags: Arch Biochem Biophys Source Type: research

Effects of sera of rats fed with Huganqingzhi tablets on endoplasmic reticulum stress in a HepG2 cell model of nonalcoholic fatty liver disease.
CONCLUSIONS: HGT serum can effectively prevent FFAs-induced steatosis in HepG2 cells by alleviating ER stress, in which PKC-δ may act as an important target. PMID: 30514673 [PubMed - in process]
Source: Journal of Southern Medical University - November 30, 2018 Category: Universities & Medical Training Authors: Yang M, Chen Z, Xiao C, Tang W, Zhou B Tags: Nan Fang Yi Ke Da Xue Xue Bao Source Type: research

Delayed treatment with fenofibrate protects against high-fat diet-induced kidney injury in mice: the possible role of AMPK autophagy
Fenofibrate activates not only peroxisome proliferator-activated receptor-α (PPARα) but also adenosine monophosphate-activated protein kinase (AMPK). AMPK-mediated cellular responses protect kidney from high-fat diet (HFD)-induced injury, and autophagy resulting from AMPK activation has been regarded as a stress-response mechanism. Thus the present study examined the role of AMPK and autophagy in the renotherapeutic effects of fenofibrate. C57BL/6J mice were divided into three groups: normal diet (ND), HFD, and HFD + fenofibrate (HFD + FF). Fenofibrate was administered 4 wk after the initiation of the HFD when ...
Source: AJP: Renal Physiology - February 7, 2017 Category: Urology & Nephrology Authors: Sohn, M., Kim, K., Uddin, M. J., Lee, G., Hwang, I., Kang, H., Kim, H., Lee, J. H., Ha, H. Tags: RESEARCH ARTICLE Source Type: research

Endothelin-1-Induced Cell Hypertrophy in Cardiomyocytes is Improved by Fenofibrate: Possible Roles of Adiponectin.
CONCLUSIONS: Our study shows that fenofibrate may protect against ET-1-induced cardiomyocyte hypertrophy and enhanced adiponectin expression through modulation of PPARα expression in vitro and limitation of daunorubicin cardiotoxicity in vivo, suggesting a novel mechanistic insight into the role of PPARα and adiponectin in cardiac hypertrophy and heart failure. PMID: 27629528 [PubMed - as supplied by publisher]
Source: Journal of Atherosclerosis and Thrombosis - September 19, 2016 Category: Cardiology Tags: J Atheroscler Thromb Source Type: research

Delayed treatment with fenofibrate protects against high-fat diet-induced kidney injury in mice: the possible role of AMPK-autophagy.
Abstract Fenofibrate activates not only peroxisome proliferator-activated receptor α (PPARα) but also adenosine monophosphate-activated protein kinase (AMPK). AMPK-mediated cellular responses protect kidney from high-fat diet (HFD)-induced injury, and autophagy resulting from AMPK activation has been regarded as a stress-response mechanism. Thus, the present study examined the role of AMPK and autophagy in the renotherapeutic effects of fenofibrate. C57BL/6J mice were divided into 3 groups: normal diet (ND), HFD, and HFD+fenofibrate (HFD+FF). Fenofibrate was administered 4 weeks after the initiation of the HFD w...
Source: Am J Physiol Renal P... - July 26, 2016 Category: Urology & Nephrology Authors: Sohn M, Kim K, Uddin MJ, Lee G, Hwang I, Kang H, Kim H, Lee JH, Ha H Tags: Am J Physiol Renal Physiol Source Type: research

Effects of short‐chain acyl‐CoA dehydrogenase on cardiomyocyte apoptosis
In conclusion, for the first time our findings directly demonstrated that SCAD may be as a new target to prevent cardiomyocyte apoptosis through the AMPK/PPARα/SCAD signal pathways.
Source: Journal of Cellular and Molecular Medicine - March 17, 2016 Category: Molecular Biology Authors: Zhenhua Zeng, Qiuju Huang, Zhaohui Shu, Peiqing Liu, Shaorui Chen, Xuediao Pan, Linquan Zang, Sigui Zhou Tags: Original Article Source Type: research

Effects of short-chain acyl-CoA dehydrogenase on cardiomyocyte apoptosis.
In conclusion, for the first time our findings directly demonstrated that SCAD may be as a new target to prevent cardiomyocyte apoptosis through the AMPK/PPARα/SCAD signal pathways. PMID: 26989860 [PubMed - as supplied by publisher]
Source: J Cell Mol Med - March 17, 2016 Category: Molecular Biology Authors: Zeng Z, Huang Q, Shu Z, Liu P, Chen S, Pan X, Zang L, Zhou S Tags: J Cell Mol Med Source Type: research

Effects of short ‐chain acyl‐CoA dehydrogenase on cardiomyocyte apoptosis
In conclusion, for the first time our findings directly demonstrated that SCAD may be as a new target to prevent cardiomyocyte apoptosis through the AMPK/PPARα/SCAD signal pathways.
Source: Journal of Cellular and Molecular Medicine - March 16, 2016 Category: Molecular Biology Authors: Zhenhua Zeng, Qiuju Huang, Zhaohui Shu, Peiqing Liu, Shaorui Chen, Xuediao Pan, Linquan Zang, Sigui Zhou Tags: Original Article Source Type: research

Fenofibrate inhibited pancreatic cancer cells proliferation via activation of p53 mediated by upregulation of LncRNA MEG3.
Abstract There is still no suitable drug for pancreatic cancer treatment, which is one of the most aggressive human tumors. Maternally expressed gene 3 (MEG3), a LncRNA, has been suggested as a tumor suppressor in a range of human tumors. Studies found fenofibrate exerted anti-tumor roles in various human cancer cell lines. However, its role in pancreatic cancer remains unknown. The present study aimed to explore the impacts of fenofibrate on pancreatic cancer cell lines, and to investigate MEG3 role in its anti-tumor mechanisms. We used MTT assay to determine cells proliferation, genome-wide LncRNA microarray ana...
Source: Biochemical and Biophysical Research communications - February 2, 2016 Category: Biochemistry Authors: Hu D, Su C, Jiang M, Shen Y, Shi A, Zhao F, Chen R, Shen Z, Bao J, Tang W Tags: Biochem Biophys Res Commun Source Type: research

Activation of PPAR alpha by fenofibrate inhibits apoptosis in vascular adventitial fibroblasts partly through SIRT1-mediated deacetylation of FoxO1.
In this study, we aimed to determine the effect of PPARα agonist fenofibrate on cell apoptosis and SIRT1 expression and related mechanisms in ApoE(-/-) mice and VAFs in vitro. We found that fenofibrate inhibited cell apoptosis in vascular adventitia and up-regulated SIRT1 expression in aorta of ApoE(-/-) mice. Moreover, SIRT1 activator resveratrol (RSV) further enhanced these effects of fenofibrate. In vitro study showed that activation of PPARα by fenofibrate inhibited TNF-α-induced cell apoptosis and cell cycle arrest in VAFs. Meanwhile, fenofibrate up-regulated SIRT1 expression and inhibited SIRT1 translocation from ...
Source: Experimental Cell Research - July 27, 2015 Category: Cytology Authors: Wang WR, Liu EQ, Zhang JY, Li YX, Yang XF, He YH, Zhang W, Lin R Tags: Exp Cell Res Source Type: research

Fenofibrate suppressed proliferation and migration of human neuroblastoma cells via oxidative stress dependent of TXNIP upregulation.
Abstract There are no appropriate drugs for metastatic neuroblastoma (NB), which is the most common extra-cranial solid tumor for childhood. Thioredoxin binding protein (TXNIP), the endogenous inhibitor of ROS elimination, has been identified as a tumor suppressor in various solid tumors. It reported that fenofibrate exerts anti-tumor effects in several human cancer cell lines. However, its detail mechanisms remain unclear. The present study assessed the effects of fenofibrate on NB cells and investigated TXNIP role in its anti-tumor mechanisms. We used MTT assay to detect cells proliferation, starch wound test to...
Source: Biochemical and Biophysical Research communications - March 31, 2015 Category: Biochemistry Authors: Su C, Shi A, Cao G, Tao T, Chen R, Hu Z, Shen Z, Tao H, Cao B, Hu D, Bao J Tags: Biochem Biophys Res Commun Source Type: research

Changes in short-chain acyl-coA dehydrogenase during rat cardiac development and stress.
This study was designed to investigate the expression of short-chain acyl-CoA dehydrogenase (SCAD), a key enzyme of fatty acid β-oxidation, during rat heart development and the difference of SCAD between pathological and physiological cardiac hypertrophy. The expression of SCAD was lowest in the foetal and neonatal heart, which had time-dependent increase during normal heart development. In contrast, a significant decrease in SCAD expression was observed in different ages of spontaneously hypertensive rats (SHR). On the other hand, swim-trained rats developed physiological cardiac hypertrophy, whereas SHR developed pathol...
Source: J Cell Mol Med - March 8, 2015 Category: Molecular Biology Authors: Huang J, Xu L, Huang Q, Luo J, Liu P, Chen S, Yuan X, Lu Y, Wang P, Zhou S Tags: J Cell Mol Med Source Type: research

Changes in short‐chain acyl‐coA dehydrogenase during rat cardiac development and stress
This study was designed to investigate the expression of short‐chain acyl‐CoA dehydrogenase (SCAD), a key enzyme of fatty acid β‐oxidation, during rat heart development and the difference of SCAD between pathological and physiological cardiac hypertrophy. The expression of SCAD was lowest in the foetal and neonatal heart, which had time‐dependent increase during normal heart development. In contrast, a significant decrease in SCAD expression was observed in different ages of spontaneously hypertensive rats (SHR). On the other hand, swim‐trained rats developed physiological cardiac hypertrophy, whereas SHR develo...
Source: Journal of Cellular and Molecular Medicine - March 8, 2015 Category: Molecular Biology Authors: Jinxian Huang, Lipeng Xu, Qiuju Huang, Jiani Luo, Peiqing Liu, Shaorui Chen, Xi Yuan, Yao Lu, Ping Wang, Sigui Zhou Tags: Original Article Source Type: research