Oleic acid ameliorates palmitic acid induced hepatocellular lipotoxicity by inhibition of ER stress and pyroptosis.

Background: Pyroptosis is a novel programmed cell death. It is identified as caspase-1 dependent and characterized by plasma-membrane rupture and release of proinflammatory intracellular contents inculuding IL-1 beta and IL-18. Pyroptosis is distinct from other forms of cell death, especially apopto...

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Published in:Nutrition & Metabolism Vol. 17; no. 1; pp. 1 - 15
Main Authors: Zeng, Xing, Zhu, Min, Liu, Xiaohong, Chen, Xuanmin, Yuan, Yujia, Li, Lan, Liu, Jingping, Lu, Yanrong, Cheng, Jingqiu, Chen, Younan
Format: letter pictorial research tables/charts Journal Article
Published: BioMed Central 1/30/2020
Online Access:View this record in EBSCOhost
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        17437075
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      jtl: Nutrition & Metabolism
      issn: 17437075
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      dt: 1/30/2020
      vid: 17
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      pub: BioMed Central
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        141474704
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        141474704
        10.1186/s12986-020-0434-8
        141474704
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        atl: Oleic acid ameliorates palmitic acid induced hepatocellular lipotoxicity by inhibition of ER stress and pyroptosis.
      aug:
        au:
          Zeng, Xing
          Zhu, Min
          Liu, Xiaohong
          Chen, Xuanmin
          Yuan, Yujia
          Li, Lan
          Liu, Jingping
          Lu, Yanrong
          Cheng, Jingqiu
          Chen, Younan
        affil: Key Laboratory of Transplant Engineering and Immunology, NHFPC
      sug:
        subj:
          Fatty Acids, Monounsaturated Pharmacodynamics
          Apoptosis Drug Effects
          Endoplasmic Reticulum Drug Effects
          Stress, Physiological Drug Effects
          Hepatocytes Drug Effects
          Lipids Metabolism
          Hepatotoxicity Prevention and Control
          Fatty Acids, Saturated Adverse Effects
          Nonalcoholic Fatty Liver Disease Pathology
          Nonalcoholic Fatty Liver Disease Prevention and Control
          Animal Studies
          Rats
          Cell Line Drug Effects
          Nucleosides Administration and Dosage
          Staining and Labeling Methods
          Interleukin 1 Drug Effects
          Tumor Necrosis Factor Drug Effects
          Enzyme-Linked Immunosorbent Assay
          Dietary Fats Adverse Effects
          Olive Oil Pharmacodynamics
          Blood Chemical Analysis
          Cell Viability
          Gene Expression Drug Effects
          RNA, Messenger Drug Effects
          Caspases Drug Effects
          Cell Membrane Drug Effects
          Biological Markers Drug Effects
          In Vitro Studies
          In Vivo Studies
          Polymerase Chain Reaction Methods
          Blotting, Western
          Fluorescent Antibody Technique
          Liver Anatomy and Histology
          Liver Metabolism
      ab: Background: Pyroptosis is a novel programmed cell death. It is identified as caspase-1 dependent and characterized by plasma-membrane rupture and release of proinflammatory intracellular contents inculuding IL-1 beta and IL-18. Pyroptosis is distinct from other forms of cell death, especially apoptosis that is characterized by nuclear and cytoplasmic condensation and is elicited via activation of a caspase cascade. In pyroptosis, gasdermin D (GSDMD) acts as a major executor, while NLRP3 related inflammasome is closely linked to caspase-1 activation. Given that pyroptosis has played a critical role in the progression of non-alcoholic steatohepatitis (NASH), here, we investigated whether the regulation of pyroptosis activation is responsible for the protective role of monounsaturated oleic acids in the context of hepatocellular lipotoxicity. Methods: Human hepatoma cell line HepG2 cells were exposed to palmitic acid (PA) with or without oleic acids (OA) or/and endoplasmic reticulum (ER) stress inhibitor tauroursodeoxycholic acid (TUDCA) for 24 h. Besides, the cells were treated with the chemical ER stressor tunicamycin (TM) with or without OA for 24 h as well. The expressions of pyroptosis and ER stress related genes or proteins were determined by real-time PCR, Western blot or immunofluorescence. The morphology of pyroptosis was detected by acridine orange and ethidium bromide (AO/EB) staining. The release of IL-1 beta and tumor necrosis factor alpha (TNF-α) was determined by ELISA. Sprague–Dawley (SD) rats were fed with high fat diet (HFD) for 16 w, then, HFD was half replaced by olive oil to observe the protective effects of olive oil. The blood chemistry were analyzed, and the liver histology and the expressions of related genes and proteins were determined in the liver tissues. Results: We demonstrated that PA impaired the cell viability and disturbed the lipid metabolism of HepG2 cells (P < 0.01), but OA robustly rescued cells from cell death (P < 0.001). More importantly, we found that instead of cell apoptosis, PA induced significant pyroptosis, evidenced by remarkably increased mRNA and protein expressions of inflammasome marker NLRP3, Caspase-1 and IL-1beta, as well as cell membrane perforation driving protein GSDMD (P < 0.05). Furthermore, we demonstrated that the PA stimulated ER stress was causally related to pyroptosis. The enhanced expressions of ER stress markers CHOP and BIP were found subcellular co-located to pyroptosis markers NLRP3 and ASC. Additionally,TM was able to induce pyroptosis like PA did, and ER stress inhibitor TUDCA was able to inhibit both PA and TM induced ER stress as well as pyroptosis. Furthermore, we demonstrated that OA substantially alleviated either PA or TM induced ER stress and pyroptosis in HepG2 cells (P < 0.01). In vivo, only olive oil supplementation did not cause significant toxicity, while HFD for 32 w obviously induced liver steatosis and inflammation in SD rats (P < 0.05). Half replacement of HFD with olive oil (a mixed diet) has remarkably ameliorated liver abnormalities, and particularly inhibited the protein expressions of either ER stress and pyroptosis markers (P < 0.05). Conclusion: Palmitic acid induced predominant pyroptosis in HepG2 cells, and ER stress may be responsible for the induction of pyroptosis and subsequent cell death. Monounsaturated oleic acids were able to ameliorate hepatocellular lipotoxicity both in vitro and in vivo, and OA mediated inhibition of ER stress and pyroptosis may be the underlying mechanisms.
      pubtype: Academic Journal
      doctype:
        letter
        pictorial
        research
        tables/charts
        Journal Article
      ougenre: Unknown
    language: English
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