Pinolenic acid ameliorates oleic acid-induced lipogenesis and oxidative stress via AMPK/SIRT1 signaling pathway in HepG2 cells
- Publication type:
- Journal article
- Metadata:
-
- Autoren
- Jing Zhang
- Sun-dong Zhang
- Peng Wang
- Na Guo
- Wei Wang
- Li-ping Yao
- Qing Yang
- Thomas Efferth
- Jiao Jiao
- Yu-jie Fu
- Autoren-URL
- https://www.webofscience.com/api/gateway?GWVersion=2&SrcApp=fis-test-1&SrcAuth=WosAPI&KeyUT=WOS:000483936600018&DestLinkType=FullRecord&DestApp=WOS_CPL
- DOI
- 10.1016/j.ejphar.2019.172618
- eISSN
- 1879-0712
- Externe Identifier
- Clarivate Analytics Document Solution ID: IU9YM
- PubMed Identifier: 31430456
- ISSN
- 0014-2999
- Zeitschrift
- EUROPEAN JOURNAL OF PHARMACOLOGY
- Schlüsselwörter
- Pinolenic acid
- Lipogenesis
- NAFLD
- AMPK
- Oxidative stress
- Artikelnummer
- ARTN 172618
- Datum der Veröffentlichung
- 2019
- Status
- Published
- Titel
- Pinolenic acid ameliorates oleic acid-induced lipogenesis and oxidative stress <i>via</i> AMPK/SIRT1 signaling pathway in HepG2 cells
- Sub types
- Article
- Ausgabe der Zeitschrift
- 861
Data source: Web of Science (Lite)
- Other metadata sources:
-
- Autoren
- Jing Zhang
- Sun-dong Zhang
- Peng Wang
- Na Guo
- Wei Wang
- Li-ping Yao
- Qing Yang
- Thomas Efferth
- Jiao Jiao
- Yu-jie Fu
- DOI
- 10.1016/j.ejphar.2019.172618
- ISSN
- 0014-2999
- Zeitschrift
- European Journal of Pharmacology
- Sprache
- en
- Artikelnummer
- 172618
- Paginierung
- 172618 - 172618
- Datum der Veröffentlichung
- 2019
- Status
- Published
- Herausgeber
- Elsevier BV
- Herausgeber URL
- http://dx.doi.org/10.1016/j.ejphar.2019.172618
- Datum der Datenerfassung
- 2022
- Titel
- Pinolenic acid ameliorates oleic acid-induced lipogenesis and oxidative stress via AMPK/SIRT1 signaling pathway in HepG2 cells
- Ausgabe der Zeitschrift
- 861
Data source: Crossref
- Abstract
- Pinolenic acid (PLA), a natural compound isolated from pine nut oil, has been reported to exert bioactivity against lipid anabolism. Nonetheless, the underlying mechanisms still poorly elucidated. The aim of this study is to comprehensively demonstrate the effects of PLA on oleic acid (OA)-induced non-alcoholic fatty liver disease (NAFLD) and their relationship with the lipid metabolic regulation. The results demonstrated that treatment with PLA dramatically inhibited lipid accumulation, oxidative stress as well as inflammatory responses induced by oleic acid in HepG2 cells. PLA also obviously decreased the levels of cellular triglyceride (TG), total cholesterol (TC), malondialdehyde (MDA), reactive oxygen species (ROS) and nitric oxide (NO). As well as PLA stilled promoted the antioxidant enzymes activity including superoxide dismutase (SOD) and glutathione peroxidase (GPX). Furthermore, PLA could increase the expressions of nuclear factor erythroid-2-related factor 2 (Nrf2) and heme oxygenase1 (HO-1) to alleviate oxidative damage. It also could reduce lipogenesis-related transcription factors expression, such as sterol regulatory element-binding protein 1 (SREBP1c), fatty acid synthase (FASN) and stearoyl-CoA desaturase 1 (SCD1). PLA treatment resulted in increasing phosphorylation of AMP-activated protein kinase (AMPK) and peroxisome proliferator-activated receptor-α (PPARα) expression. However, pretreatment with compound C (inhibitor of AMPK) inhibited the effect of PLA on promoting the expression of p-AMPK, SIRT1 and PPARα for lipolysis. Taken together, these results demonstrated that PLA possessed the potential to prevent lipid accumulation in OA-induced HepG2 cells via upregulating the AMPK/SIRT1 signaling pathway, which supported the development of new drug candidate against non-alcoholic steatohepatitis.
- Addresses
- Key Laboratory of Forest Plant Ecology, Ministry of Education, Northeast Forestry University, Harbin, 150040, China.
- Autoren
- Jing Zhang
- Sun-Dong Zhang
- Peng Wang
- Na Guo
- Wei Wang
- Li-Ping Yao
- Qing Yang
- Thomas Efferth
- Jiao Jiao
- Yu-Jie Fu
- DOI
- 10.1016/j.ejphar.2019.172618
- eISSN
- 1879-0712
- Externe Identifier
- PubMed Identifier: 31430456
- Funding acknowledgements
- National Key Research and Development Program of China: 2016YFD0600805
- Fundamental Research Funds for the Central Universities: 2572017AA10
- Harbin Medical University:
- Fundamental Research Funds for the Central Universities: 2572017ET03
- Ministry of Education of the People&apos;s Republic of China: KF201620
- Key Laboratory of Myocardial Ischemia, Ministry of Education:
- Fundamental Research Funds for the Central Universities: 2572017EA03
- Open access
- false
- ISSN
- 0014-2999
- Zeitschrift
- European journal of pharmacology
- Schlüsselwörter
- Humans
- Nitric Oxide
- Linolenic Acids
- Oleic Acid
- PPAR alpha
- Signal Transduction
- Gene Expression Regulation
- Oxidative Stress
- Lipogenesis
- AMP-Activated Protein Kinases
- Sirtuin 1
- Hep G2 Cells
- Sprache
- eng
- Medium
- Print-Electronic
- Online publication date
- 2019
- Paginierung
- 172618
- Datum der Veröffentlichung
- 2019
- Status
- Published
- Datum der Datenerfassung
- 2019
- Titel
- Pinolenic acid ameliorates oleic acid-induced lipogenesis and oxidative stress via AMPK/SIRT1 signaling pathway in HepG2 cells.
- Sub types
- Journal Article
- Ausgabe der Zeitschrift
- 861
Data source: Europe PubMed Central
- Abstract
- Pinolenic acid (PLA), a natural compound isolated from pine nut oil, has been reported to exert bioactivity against lipid anabolism. Nonetheless, the underlying mechanisms still poorly elucidated. The aim of this study is to comprehensively demonstrate the effects of PLA on oleic acid (OA)-induced non-alcoholic fatty liver disease (NAFLD) and their relationship with the lipid metabolic regulation. The results demonstrated that treatment with PLA dramatically inhibited lipid accumulation, oxidative stress as well as inflammatory responses induced by oleic acid in HepG2 cells. PLA also obviously decreased the levels of cellular triglyceride (TG), total cholesterol (TC), malondialdehyde (MDA), reactive oxygen species (ROS) and nitric oxide (NO). As well as PLA stilled promoted the antioxidant enzymes activity including superoxide dismutase (SOD) and glutathione peroxidase (GPX). Furthermore, PLA could increase the expressions of nuclear factor erythroid-2-related factor 2 (Nrf2) and heme oxygenase1 (HO-1) to alleviate oxidative damage. It also could reduce lipogenesis-related transcription factors expression, such as sterol regulatory element-binding protein 1 (SREBP1c), fatty acid synthase (FASN) and stearoyl-CoA desaturase 1 (SCD1). PLA treatment resulted in increasing phosphorylation of AMP-activated protein kinase (AMPK) and peroxisome proliferator-activated receptor-α (PPARα) expression. However, pretreatment with compound C (inhibitor of AMPK) inhibited the effect of PLA on promoting the expression of p-AMPK, SIRT1 and PPARα for lipolysis. Taken together, these results demonstrated that PLA possessed the potential to prevent lipid accumulation in OA-induced HepG2 cells via upregulating the AMPK/SIRT1 signaling pathway, which supported the development of new drug candidate against non-alcoholic steatohepatitis.
- Date of acceptance
- 2019
- Autoren
- Jing Zhang
- Sun-Dong Zhang
- Peng Wang
- Na Guo
- Wei Wang
- Li-Ping Yao
- Qing Yang
- Thomas Efferth
- Jiao Jiao
- Yu-Jie Fu
- Autoren-URL
- https://www.ncbi.nlm.nih.gov/pubmed/31430456
- DOI
- 10.1016/j.ejphar.2019.172618
- eISSN
- 1879-0712
- Zeitschrift
- Eur J Pharmacol
- Schlüsselwörter
- AMPK
- Lipogenesis
- NAFLD
- Oxidative stress
- Pinolenic acid
- AMP-Activated Protein Kinases
- Gene Expression Regulation
- Hep G2 Cells
- Humans
- Linolenic Acids
- Lipogenesis
- Nitric Oxide
- Oleic Acid
- Oxidative Stress
- PPAR alpha
- Signal Transduction
- Sirtuin 1
- Sprache
- eng
- Country
- Netherlands
- Paginierung
- 172618
- PII
- S0014-2999(19)30570-9
- Datum der Veröffentlichung
- 2019
- Status
- Published
- Datum, an dem der Datensatz öffentlich gemacht wurde
- 2020
- Titel
- Pinolenic acid ameliorates oleic acid-induced lipogenesis and oxidative stress via AMPK/SIRT1 signaling pathway in HepG2 cells.
- Sub types
- Journal Article
- Ausgabe der Zeitschrift
- 861
Data source: PubMed
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- Property of