Catechin attenuates TNF-α induced inflammatory response via AMPK-SIRT1 pathway in 3T3-L1 adipocytes

PLoS One. 2019 May 17;14(5):e0217090. doi: 10.1371/journal.pone.0217090. eCollection 2019.

Abstract

Chronic inflammation is a fundamental symptom of many diseases. Catechin possesses anti-oxidant and anti-inflammatory properties. However, the mechanism of catechin to prevent inflammation in 3T3-L1 adipocytes caused by TNF-α remains unknown. Therefore, the effects of catechin on the gene expression of cytokines and the activation of cell signals in TNF-α induced 3T3-L1 adipocytes were investigated. The effects of catechin on adipogenesis and cell viability were detected by Oil Red O staining and CCK-8 assay, respectively. The genes expression of cytokines was determined by real-time RT-PCR. The expression of NF-κB, AMPK, FOXO3a and SIRT1 on translation level was determined by western blotting analysis. The results demonstrated that catechin significantly enhanced adipogenesis and cell viability. catechin inhibited the gene expression of pro-inflammatory cytokines including IL-1α, IL-1β, IL-6, IL-12p35, and inflammatory enzymes including iNOS and COX-2, but enhanced the gene expression of anti-inflammatory cytokines including IL-4 and IL-10. Catechin also inhibited the activation of NF-κB, AMPK, FOXO3a and SIRT1, but increased the phosphorylation level of the above factors. All these results indicated that as a potential therapeutic strategy catechin has the ability of attenuating inflammatory response triggered by TNF-α through signaling cascades involved in inflammation and cytokines.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • 3T3-L1 Cells
  • AMP-Activated Protein Kinases / genetics
  • AMP-Activated Protein Kinases / metabolism*
  • Adipocytes / drug effects*
  • Adipocytes / immunology
  • Adipocytes / metabolism
  • Adipogenesis
  • Animals
  • Catechin / pharmacology*
  • Cytokines / metabolism
  • Gene Expression Regulation / drug effects*
  • Inflammation / chemically induced
  • Inflammation / metabolism
  • Inflammation / pathology
  • Inflammation / prevention & control*
  • Mice
  • NF-kappa B / genetics
  • NF-kappa B / metabolism
  • Signal Transduction
  • Sirtuin 1 / genetics
  • Sirtuin 1 / metabolism*
  • Tumor Necrosis Factor-alpha / toxicity*

Substances

  • Cytokines
  • NF-kappa B
  • Tumor Necrosis Factor-alpha
  • Catechin
  • AMP-Activated Protein Kinases
  • Sirt1 protein, mouse
  • Sirtuin 1

Grants and funding

This research was supported by Taishan Talents Introduction Program of Shandong, China (tsxz2018) to JS, and Young Talents Training Program of Shandong Academy of Agricultural Sciences (SAAS2015-06) to AC. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.