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uncoupling</title> <meta name="description" content="Search results for: uncoupling"> <meta name="keywords" content="uncoupling"> <meta name="viewport" content="width=device-width, initial-scale=1, minimum-scale=1, maximum-scale=1, user-scalable=no"> <meta charset="utf-8"> <link href="https://cdn.waset.org/favicon.ico" type="image/x-icon" rel="shortcut icon"> <link href="https://cdn.waset.org/static/plugins/bootstrap-4.2.1/css/bootstrap.min.css" rel="stylesheet"> <link href="https://cdn.waset.org/static/plugins/fontawesome/css/all.min.css" rel="stylesheet"> <link href="https://cdn.waset.org/static/css/site.css?v=150220211555" rel="stylesheet"> </head> <body> <header> <div class="container"> <nav class="navbar navbar-expand-lg navbar-light"> <a class="navbar-brand" href="https://waset.org"> <img src="https://cdn.waset.org/static/images/wasetc.png" alt="Open Science Research Excellence" title="Open Science Research Excellence" /> </a> <button class="d-block d-lg-none navbar-toggler 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style="font-size:.9rem"><span class="badge badge-info">7</span> ANXA1 Plays A Nephroprotective Role By Maintaining Mitochondrial Homeostasis Via Upregulating Uncoupling Protein 1 In Diabetic Nephropathy</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Zi-Han%20Li">Zi-Han Li</a>, <a href="https://publications.waset.org/abstracts/search?q=Lu%20Fang"> Lu Fang</a>, <a href="https://publications.waset.org/abstracts/search?q=Liang%20Wu"> Liang Wu</a>, <a href="https://publications.waset.org/abstracts/search?q=Dong-Yuan%20Chang"> Dong-Yuan Chang</a>, <a href="https://publications.waset.org/abstracts/search?q=Manyuan%20Dong"> Manyuan Dong</a>, <a href="https://publications.waset.org/abstracts/search?q=Liang%20Ji"> Liang Ji</a>, <a href="https://publications.waset.org/abstracts/search?q=Qi%20Zhang"> Qi Zhang</a>, <a href="https://publications.waset.org/abstracts/search?q=Ming-Hui%20Zhao"> Ming-Hui Zhao</a>, <a href="https://publications.waset.org/abstracts/search?q=Sydney%20C.W.%20Tang"> Sydney C.W. Tang</a>, <a href="https://publications.waset.org/abstracts/search?q=Lemin%20Zheng"> Lemin Zheng</a>, <a href="https://publications.waset.org/abstracts/search?q=Min%20Chen"> Min Chen</a> </p> <p class="card-text"><strong>Abstract:</strong></p> Uncoupling of mitochondrial respiration by chemical uncouplers has proven effective in ameliorating obesity, insulin resistance, and hyperglycemia, which were risk factors for diabetic nephropathy (DN). Recently, it was found that annexin A1(ANXA1) could improve mitochondrial function to mitigate DN progression. However, the underlying mechanism is not fully clear yet. Here, it was identified that uncoupling protein 1 (UCP1), an inner membrane protein of mitochondria, as a key to mitochondrial homeostasis improved by ANXA1. Specifically, ANXA1 attenuated mitochondrial dysfunction via appropriately upregulating UCP1 by stabilizing its transcription factor GATA binding protein 3 (GATA3) through combining with thioredoxin. Moreover, specific overexpression of UCP1 in renal cortex rescued renal injuries in diabetic Anxa1-KO mice. UCP1 deletion aggravated renal injuries in HFD/STZ-induced diabetic mice. Mechanistically, UCP1 reduced mitochondrial fission through the aristaless-related homeobox (ARX)/cardiolipin synthase 1 (CRLS1) pathway. Therapeutically, CL316243, a UCP1 agonist, could attenuate established DN in db/db mice. This work established a novel principle to harness the power of uncouplers for the treatment of DN. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=diabetic%20nephropathy" title="diabetic nephropathy">diabetic nephropathy</a>, <a href="https://publications.waset.org/abstracts/search?q=uncoupling%20protein%201" title=" uncoupling protein 1"> uncoupling protein 1</a>, <a href="https://publications.waset.org/abstracts/search?q=mitochondrial%20homeostasis" title=" mitochondrial homeostasis"> mitochondrial homeostasis</a>, <a href="https://publications.waset.org/abstracts/search?q=cardiolipin%20metabolism" title=" cardiolipin metabolism"> cardiolipin metabolism</a> </p> <a href="https://publications.waset.org/abstracts/178984/anxa1-plays-a-nephroprotective-role-by-maintaining-mitochondrial-homeostasis-via-upregulating-uncoupling-protein-1-in-diabetic-nephropathy" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/178984.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">83</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">6</span> UCP1 Regulates Cardiolipin Metabolism and Mediates Mitochondrial Homeostasis Maintenance of ANXA1 in Diabetic Nephropathy</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Zi-Han%20Li">Zi-Han Li</a>, <a href="https://publications.waset.org/abstracts/search?q=Lu%20Fang"> Lu Fang</a>, <a href="https://publications.waset.org/abstracts/search?q=Liang%20Wu"> Liang Wu</a>, <a href="https://publications.waset.org/abstracts/search?q=Dong-Yuan%20Chang"> Dong-Yuan Chang</a>, <a href="https://publications.waset.org/abstracts/search?q=Manyuan%20Dong"> Manyuan Dong</a>, <a href="https://publications.waset.org/abstracts/search?q=Liang%20Ji"> Liang Ji</a>, <a href="https://publications.waset.org/abstracts/search?q=Qi%20Zhang"> Qi Zhang</a>, <a href="https://publications.waset.org/abstracts/search?q=Ming-Hui%20Zhao"> Ming-Hui Zhao</a>, <a href="https://publications.waset.org/abstracts/search?q=Sydney%20C.%20W.%20Tang"> Sydney C. W. Tang</a>, <a href="https://publications.waset.org/abstracts/search?q=Lemin%20Zheng"> Lemin Zheng</a>, <a href="https://publications.waset.org/abstracts/search?q=Min%20Chen"> Min Chen</a> </p> <p class="card-text"><strong>Abstract:</strong></p> Uncoupling of mitochondrial respiration by chemical uncouplers has proven effective in ameliorating obesity, insulin resistance, and hyperglycemia, which were risk factors for diabetic nephropathy (DN). Recently, we found that ANXA1 could improve mitochondrial function to mitigate DN progression. However, the underlying mechanism is not fully clear yet. Here, we identified uncoupling protein 1 (UCP1), an inner membrane protein of mitochondria, as a key to mitochondrial homeostasis improved by ANXA1. Specifically, ANXA1 attenuated mitochondrial dysfunction via appropriately upregulating UCP1 by stabilizing its transcription factor GATA binding protein 3 (GATA3) by combining it with thioredoxin. Moreover, specific overexpression of UCP1 in the renal cortex rescued renal injuries in diabetic Anxa1-KO mice. UCP1 deletion aggravated renal injuries in HFD/STZ-induced diabetic mice. Mechanistically, UCP1 reduced mitochondrial fission through the aristaless-related homeobox (ARX)/cardiolipin synthase 1 (CRLS1) pathway. Therapeutically, CL316243, a UCP1 agonist, could attenuate established DN in db/db mice. This work established an alternative principle to harness the power of uncouplers for the treatment of DN. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=diabetic%20nephropathy" title="diabetic nephropathy">diabetic nephropathy</a>, <a href="https://publications.waset.org/abstracts/search?q=uncoupling%20protein%201" title=" uncoupling protein 1"> uncoupling protein 1</a>, <a href="https://publications.waset.org/abstracts/search?q=mitochondrial%20homeostasis" title=" mitochondrial homeostasis"> mitochondrial homeostasis</a>, <a href="https://publications.waset.org/abstracts/search?q=cardiolipin%20metabolism" title=" cardiolipin metabolism"> cardiolipin metabolism</a> </p> <a href="https://publications.waset.org/abstracts/178981/ucp1-regulates-cardiolipin-metabolism-and-mediates-mitochondrial-homeostasis-maintenance-of-anxa1-in-diabetic-nephropathy" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/178981.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">74</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">5</span> Pyrroloquinoline Quinone Enhances the Mitochondrial Function by Increasing Beta-Oxidation and a Balanced Mitochondrial Recycling in Mice Granulosa Cells</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Moustafa%20Elhamouly">Moustafa Elhamouly</a>, <a href="https://publications.waset.org/abstracts/search?q=Masayuki%20Shimada"> Masayuki Shimada</a> </p> <p class="card-text"><strong>Abstract:</strong></p> The production of competent oocytes is essential for reproductivity in mammals. Maintenance of mitochondrial efficiency is required to supply the ATP necessary for granulosa cell proliferation during the follicular development process. Treatment with Pyrroloquinoline quinone (PQQ) has been reported to increase the number of ovulated oocytes and pups per delivery in mice by maintaining healthy mitochondrial function. This study aimed to elucidate how PQQ maintains mitochondrial function during ovarian follicle growth. To do this, both in vitro and in vivo experiments were performed with granulosa cells from superovulated immature (3-week-old) mice that were pretreated with or without PQQ. The effects of PQQ on beta-oxidation, mitochondrial function, mitophagy, and mitochondrial biogenesis were examined. PQQ increased beta-oxidation-related genes and CPT1 protein content in granulosa cells and this was associated with a decreased phosphorylation of P38 signaling protein. Using the fatty acid oxidation assay on the flux analyzer, PQQ increased the reliance of beta-oxidation on the endogenous fatty acids and was associated with a mild UCP-dependant mitochondrial uncoupling, ATP production, mitophagy, and mitochondrial biogenesis. PQQ also increased the expression of endogenous antioxidant enzymes. Thus, PQQ induced beta-oxidation in growing granulosa cells relying on endogenous fatty acids. And reduced the Reactive oxygen species (ROS) production by inducing a mild mitochondrial uncoupling with keeping high mitochondrial function. Damaged mitochondria were recycled by the induced mitophagy and replaced by the increased mitochondrial biogenesis. Collectively, PQQ may enhance reproductivity by maintaining the efficiency of mitochondria to produce enough ATP required for normal folliculogenesis. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=granulosa%20cells" title="granulosa cells">granulosa cells</a>, <a href="https://publications.waset.org/abstracts/search?q=mitochondrial%20uncoupling" title=" mitochondrial uncoupling"> mitochondrial uncoupling</a>, <a href="https://publications.waset.org/abstracts/search?q=mitophagy" title=" mitophagy"> mitophagy</a>, <a href="https://publications.waset.org/abstracts/search?q=pyrroloquinoline%20quinone%20%28PQQ%29" title=" pyrroloquinoline quinone (PQQ)"> pyrroloquinoline quinone (PQQ)</a>, <a href="https://publications.waset.org/abstracts/search?q=reactive%20oxygen%20species%20%28ROS%29." title=" reactive oxygen species (ROS)."> reactive oxygen species (ROS).</a> </p> <a href="https://publications.waset.org/abstracts/156680/pyrroloquinoline-quinone-enhances-the-mitochondrial-function-by-increasing-beta-oxidation-and-a-balanced-mitochondrial-recycling-in-mice-granulosa-cells" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/156680.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">82</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">4</span> Application of Axiomatic Design in Industrial Control and Automation Software</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Aydin%20Homay">Aydin Homay</a>, <a href="https://publications.waset.org/abstracts/search?q=Mario%20de%20Sousa"> Mario de Sousa</a>, <a href="https://publications.waset.org/abstracts/search?q=Martin%20Wollschlaeger"> Martin Wollschlaeger</a> </p> <p class="card-text"><strong>Abstract:</strong></p> Axiomatic design is a system design methodology that systematically analyses the transformation of customer needs into functional requirements, design parameters, and process variables. This approach aims to create high-quality product or system designs by adhering to specific design principles or axioms, namely, the independence and information axiom. The application of axiomatic design in the design of industrial control and automation software systems could be challenging due to the high flexibility exposed by the software system and the coupling enforced by the hardware part. This paper aims to present how to use axiomatic design for designing industrial control and automation software systems and how to satisfy the independence axiom within these tightly coupled systems. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=axiomatic%20design" title="axiomatic design">axiomatic design</a>, <a href="https://publications.waset.org/abstracts/search?q=decoupling" title=" decoupling"> decoupling</a>, <a href="https://publications.waset.org/abstracts/search?q=uncoupling" title=" uncoupling"> uncoupling</a>, <a href="https://publications.waset.org/abstracts/search?q=automation" title=" automation"> automation</a> </p> <a href="https://publications.waset.org/abstracts/186917/application-of-axiomatic-design-in-industrial-control-and-automation-software" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/186917.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">49</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">3</span> Effects of Pterostilbene in Brown Adipose Tissue from Obese Rats</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Leixuri%20Aguirre">Leixuri Aguirre</a>, <a href="https://publications.waset.org/abstracts/search?q=I%C3%B1aki%20Milton-Laskibar"> I帽aki Milton-Laskibar</a>, <a href="https://publications.waset.org/abstracts/search?q=Elizabeth%20Hijona"> Elizabeth Hijona</a>, <a href="https://publications.waset.org/abstracts/search?q=Luis%20Bujanda"> Luis Bujanda</a>, <a href="https://publications.waset.org/abstracts/search?q=Agnes%20M.%20Rimando"> Agnes M. Rimando</a>, <a href="https://publications.waset.org/abstracts/search?q=Maria%20P.%20Portillo"> Maria P. Portillo</a> </p> <p class="card-text"><strong>Abstract:</strong></p> Introduction: In recent years great attention has been paid by scientific community to phenolic compounds as active biomolecules naturally present in foodstuffs due to their beneficial effects on health. Pterostilbene is a resveratrol dimethylether derivative which shows higher biodisponibility. Objective. To analyze the effects of two doses of pterostilbene on several markers of thermogenic capacity in a model of genetic obesity, which shows reduced thermogenesis. Methods: The experiment was conducted with thirty Zucker (fa/fa) rats that were distributed in 3 experimental groups, the control group and two groups orally administered with pterostilbene at 15 and 30 mg/kg body weight/day for 6 weeks. Gene expression of Ucp1, Pgc-1伪, Cpt1b, Ppar伪, Nfr1, Tfam and Cox-2 were assessed by RT-PCR, protein expression of UCP1 and GLUT4 by western blot and enzyme activity of carnitine palmitoyl transferase 1b and citrate synthase by spectrophotometry in interscapular brown adipose tissue (iBAT). Statistical analysis was performed by using one way ANOVA and Newman-Keuls as post-hoc test. Results: Pterostilbene did not change gene expression of Pgc-1伪. However, significant increases were found in the expression of Ucp1, Ppar伪, Nfr-1 and Cox-2. Protein expression of UCP1 and GLUT4 was increased in animals treated with pterostilbene, as well as the activities of CPT-1b and CS. These effects were observed with both doses of pterostilbene, without differences between them. Conclusions: These results show that pterostilbene increases thermogenic and oxidative capacity of brown adipose tissue in obese rats. Whether these effects effectively contribute to the anti-obesity properties of these compound needs further research. Acknowledgments: MINECO-FEDER (AGL2015-65719-R), Basque Government (IT-572-13), University of the Basque Country (ELDUNANOTEK UFI11/32), Institut of Health Carlos III (CIBERobn). I帽aki Milton is a fellowship from the Basque Government. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=brown%20adipose%20tissue" title="brown adipose tissue">brown adipose tissue</a>, <a href="https://publications.waset.org/abstracts/search?q=pterostilbene" title=" pterostilbene"> pterostilbene</a>, <a href="https://publications.waset.org/abstracts/search?q=thermogenesis" title=" thermogenesis"> thermogenesis</a>, <a href="https://publications.waset.org/abstracts/search?q=uncoupling%20protein%201" title=" uncoupling protein 1"> uncoupling protein 1</a> </p> <a href="https://publications.waset.org/abstracts/61153/effects-of-pterostilbene-in-brown-adipose-tissue-from-obese-rats" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/61153.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">296</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">2</span> Relative Importance of Different Mitochondrial Components in Maintaining the Barrier Integrity of Retinal Endothelial Cells: Implications for Vascular-associated Retinal Diseases</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Shaimaa%20Eltanani">Shaimaa Eltanani</a>, <a href="https://publications.waset.org/abstracts/search?q=Thangal%20Yumnamcha"> Thangal Yumnamcha</a>, <a href="https://publications.waset.org/abstracts/search?q=Ahmed%20S.%20Ibrahim"> Ahmed S. Ibrahim</a> </p> <p class="card-text"><strong>Abstract:</strong></p> Purpose: Mitochondria dysfunction is central to breaking the barrier integrity of retinal endothelial cells (RECs) in various blinding eye diseases such as diabetic retinopathy and retinopathy of prematurity. Therefore, we aimed to dissect the role of different mitochondrial components, speci铿乧ally, those of oxidative phosphorylation (OxPhos), in maintaining the barrier function of RECs. Methods: Electric cell-substrate impedance sensing (ECIS) technology was used to assess in real-time the role of different mitochondrial components in the total impedance (Z) of human RECs (HRECs) and its components; the capacitance (C) and the total resistance (R). HRECs were treated with specific mitochondrial inhibitors that target different steps in OxPhos: Rotenone for complex I; Oligomycin for ATP synthase; and FCCP for uncoupling OxPhos. Furthermore, data were modeled to investigate the effects of these inhibitors on the three parameters that govern the total resistance of cells: cell-cell interactions (Rb), cell-matrix interactions (伪), and cell membrane permeability (Cm). Results: Rotenone (1 碌M) produced the greatest reduction in the Z, followed by FCCP (1 碌M), whereas no reduction in the Z was observed after the treatment with Oligomycin (1 碌M). Following this further, we deconvoluted the effect of these inhibitors on Rb, 伪, and Cm. Firstly, rotenone (1 碌M) completely abolished the resistance contribution of Rb, as the Rb became zero immediately after the treatment. Secondly, FCCP (1 碌M) eliminated the resistance contribution of Rb only after 2.5 hours and increased Cm without considerable effect on 伪. Lastly, Oligomycin had the lowest impact among these inhibitors on Rb, which became similar to the control group at the end of the experiment without noticeable effects on Cm or 伪. Conclusion: These results demonstrate differential roles for complex I, complex V, and coupling of OxPhos in maintaining the barrier functionality of HRECs, in which complex I being the most important component in regulating the barrier functionality and the spreading behavior of HRECs. Such differences can be used in investigating gene expression as well as for screening selective agents that improve the functionality of complex I to be used in the therapeutic approach for treating REC-related retinal diseases. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=human%20retinal%20endothelial%20cells%20%28hrecs%29" title="human retinal endothelial cells (hrecs)">human retinal endothelial cells (hrecs)</a>, <a href="https://publications.waset.org/abstracts/search?q=rotenone" title=" rotenone"> rotenone</a>, <a href="https://publications.waset.org/abstracts/search?q=oligomycin" title=" oligomycin"> oligomycin</a>, <a href="https://publications.waset.org/abstracts/search?q=fccp" title=" fccp"> fccp</a>, <a href="https://publications.waset.org/abstracts/search?q=oxidative%20phosphorylation" title=" oxidative phosphorylation"> oxidative phosphorylation</a>, <a href="https://publications.waset.org/abstracts/search?q=oxphos" title=" oxphos"> oxphos</a>, <a href="https://publications.waset.org/abstracts/search?q=capacitance" title=" capacitance"> capacitance</a>, <a href="https://publications.waset.org/abstracts/search?q=impedance" title=" impedance"> impedance</a>, <a href="https://publications.waset.org/abstracts/search?q=ecis%20modeling" title=" ecis modeling"> ecis modeling</a>, <a href="https://publications.waset.org/abstracts/search?q=rb%20resistance" title=" rb resistance"> rb resistance</a>, <a href="https://publications.waset.org/abstracts/search?q=%CE%B1%20resistance" title=" 伪 resistance"> 伪 resistance</a>, <a href="https://publications.waset.org/abstracts/search?q=and%20barrier%20integrity" title=" and barrier integrity"> and barrier integrity</a> </p> <a href="https://publications.waset.org/abstracts/158792/relative-importance-of-different-mitochondrial-components-in-maintaining-the-barrier-integrity-of-retinal-endothelial-cells-implications-for-vascular-associated-retinal-diseases" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/158792.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">100</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">1</span> Anti-Obesity Effects of Pteryxin in Peucedanum japonicum Thunb Leaves through Different Pathways of Adipogenesis In-Vitro</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Ruwani%20N.%20Nugara">Ruwani N. Nugara</a>, <a href="https://publications.waset.org/abstracts/search?q=Masashi%20Inafuku"> Masashi Inafuku</a>, <a href="https://publications.waset.org/abstracts/search?q=Kensaku%20Takara"> Kensaku Takara</a>, <a href="https://publications.waset.org/abstracts/search?q=Hironori%20Iwasaki"> Hironori Iwasaki</a>, <a href="https://publications.waset.org/abstracts/search?q=Hirosuke%20Oku"> Hirosuke Oku</a> </p> <p class="card-text"><strong>Abstract:</strong></p> Pteryxin from the partially purified hexane phase (HP) of Peucedanum japonicum Thunb (PJT) was identified as the active compound related to anti-obesity. Thus, in this study we investigated the mechanisms related to anti-obesity activity in-vitro. The HP was fractionated, and effect on the triglyceride (TG) content was evaluated in 3T3-L1 and HepG2 cells. Comprehensive spectroscopic analyses were used to identify the structure of the active compound. The dose dependent effect of active constituent on the TG content, and the gene expressions related to adipogenesis, fatty acid catabolism, energy expenditure, lipolysis and lipogenesis (20 渭g/mL) were examined in-vitro. Furthermore, higher dosage of pteryxin (50渭g/mL) was tested against 20渭g/mL in 3T3-L1 adipocytes. The mRNA were subjected to SOLiD next generation sequencer and the obtained data were analyzed by Ingenuity Pathway Analysis (IPA). The active constituent was identified as pteryxin, a known compound in PJT. However, its biological activities against obesity have not been reported previously. Pteryxin dose dependently suppressed TG content in both 3T3-L1 adipocytes and HepG2 hepatocytes (P < 0.05). Sterol regulatory element-binding protein-1 (SREBP1 c), Fatty acid synthase (FASN), and acetyl-CoA carboxylase-1 (ACC1) were downregulated in pteryxin-treated adipocytes (by 18.0, 36.1 and 38.2%; P < 0.05, respectively) and hepatocytes (by 72.3, 62.9 and 38.8%, respectively; P < 0.05) indicating its suppressive effects on fatty acid synthesis. The hormone-sensitive lipase (HSL), a lipid catabolising gene was upregulated (by 15.1%; P < 0.05) in pteryxin-treated adipocytes suggesting improved lipolysis. Concordantly, the adipocyte size marker gene, paternally expressed gene1/mesoderm specific transcript (MEST) was downregulated (by 42.8%; P < 0.05), further accelerating the lipolytic activity. The upregulated trend of uncoupling protein 2 (UCP2; by 77.5%; P < 0.05) reflected the improved energy expenditure due to pteryxin. The 50渭g/mL dosage of pteryxin completely suppressed PPAR纬, MEST, SREBP 1C, HSL, Adiponectin, Fatty Acid Binding Protein (FABP) 4, and UCP鈥檚 in 3T3-L1 adipocytes. The IPA suggested that pteryxin at 20渭g/mL and 50渭g/mL suppress obesity in two different pathways, whereas the WNT signaling pathway play a key role in the higher dose of pteryxin in preadipocyte stage. Pteryxin in PJT play the key role in regulating lipid metabolism related gene network and improving energy production in vitro. Thus, the results suggests pteryxin as a new natural compound to be used as an anti-obesity drug in pharmaceutical industry. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=obesity" title="obesity">obesity</a>, <a href="https://publications.waset.org/abstracts/search?q=peucedanum%20japonicum%20thunb" title=" peucedanum japonicum thunb"> peucedanum japonicum thunb</a>, <a href="https://publications.waset.org/abstracts/search?q=pteryxin" title=" pteryxin"> pteryxin</a>, <a href="https://publications.waset.org/abstracts/search?q=food%20science" title=" food science"> food science</a> </p> <a href="https://publications.waset.org/abstracts/26176/anti-obesity-effects-of-pteryxin-in-peucedanum-japonicum-thunb-leaves-through-different-pathways-of-adipogenesis-in-vitro" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/26176.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">453</span> </span> </div> </div> </div> </main> <footer> <div id="infolinks" class="pt-3 pb-2"> <div class="container"> <div style="background-color:#f5f5f5;" class="p-3"> <div class="row"> <div class="col-md-2"> <ul class="list-unstyled"> About <li><a href="https://waset.org/page/support">About Us</a></li> <li><a href="https://waset.org/page/support#legal-information">Legal</a></li> <li><a target="_blank" rel="nofollow" href="https://publications.waset.org/static/files/WASET-16th-foundational-anniversary.pdf">WASET celebrates its 16th foundational anniversary</a></li> </ul> </div> <div class="col-md-2"> <ul class="list-unstyled"> Account <li><a href="https://waset.org/profile">My Account</a></li> </ul> </div> <div class="col-md-2"> <ul class="list-unstyled"> Explore <li><a href="https://waset.org/disciplines">Disciplines</a></li> <li><a href="https://waset.org/conferences">Conferences</a></li> <li><a href="https://waset.org/conference-programs">Conference Program</a></li> <li><a href="https://waset.org/committees">Committees</a></li> <li><a href="https://publications.waset.org">Publications</a></li> </ul> </div> <div class="col-md-2"> <ul class="list-unstyled"> Research <li><a href="https://publications.waset.org/abstracts">Abstracts</a></li> <li><a href="https://publications.waset.org">Periodicals</a></li> <li><a href="https://publications.waset.org/archive">Archive</a></li> </ul> </div> <div class="col-md-2"> <ul class="list-unstyled"> Open Science <li><a target="_blank" rel="nofollow" href="https://publications.waset.org/static/files/Open-Science-Philosophy.pdf">Open Science Philosophy</a></li> <li><a target="_blank" rel="nofollow" href="https://publications.waset.org/static/files/Open-Science-Award.pdf">Open Science Award</a></li> <li><a target="_blank" rel="nofollow" href="https://publications.waset.org/static/files/Open-Society-Open-Science-and-Open-Innovation.pdf">Open Innovation</a></li> <li><a target="_blank" rel="nofollow" href="https://publications.waset.org/static/files/Postdoctoral-Fellowship-Award.pdf">Postdoctoral Fellowship Award</a></li> <li><a target="_blank" rel="nofollow" href="https://publications.waset.org/static/files/Scholarly-Research-Review.pdf">Scholarly Research Review</a></li> </ul> </div> <div class="col-md-2"> <ul class="list-unstyled"> Support <li><a href="https://waset.org/page/support">Support</a></li> <li><a href="https://waset.org/profile/messages/create">Contact Us</a></li> <li><a href="https://waset.org/profile/messages/create">Report Abuse</a></li> </ul> </div> </div> </div> </div> </div> <div class="container text-center"> <hr style="margin-top:0;margin-bottom:.3rem;"> <a href="https://creativecommons.org/licenses/by/4.0/" target="_blank" class="text-muted small">Creative Commons Attribution 4.0 International License</a> <div id="copy" class="mt-2">© 2024 World Academy of Science, Engineering and Technology</div> </div> </footer> <a href="javascript:" id="return-to-top"><i class="fas fa-arrow-up"></i></a> <div class="modal" id="modal-template"> <div class="modal-dialog"> <div class="modal-content"> <div class="row m-0 mt-1"> <div class="col-md-12"> <button type="button" class="close" data-dismiss="modal" aria-label="Close"><span aria-hidden="true">×</span></button> </div> </div> <div class="modal-body"></div> </div> </div> </div> <script src="https://cdn.waset.org/static/plugins/jquery-3.3.1.min.js"></script> <script src="https://cdn.waset.org/static/plugins/bootstrap-4.2.1/js/bootstrap.bundle.min.js"></script> <script src="https://cdn.waset.org/static/js/site.js?v=150220211556"></script> <script> jQuery(document).ready(function() { /*jQuery.get("https://publications.waset.org/xhr/user-menu", function (response) { jQuery('#mainNavMenu').append(response); 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