Tea Polyphenols Attenuates Inflammation via Reducing Lipopolysaccharides Level and Inhibiting TLR4/NF-κB Pathway in Obese Mice

Plant Foods Hum Nutr. 2022 Mar;77(1):105-111. doi: 10.1007/s11130-021-00937-0. Epub 2022 Feb 9.

Abstract

Obesity is a worldwide epidemic and increases the risk of metabolic syndrome through chronic inflammation. Tea polyphenols (TP), the major functional component of tea, has shown preventive effects on obesity and obesity-related disease, but the underlying mechanism is complicated and remains obscure. The present study was aimed to elucidate the anti-inflammation effect of TP in high-fat-diet (HFD)-induced obese mice. Results showed that TP reduced obesity-induced inflammation and systemic lipopolysaccharides (LPS) level. The decrease of LPS level in circulation was followed by the downregulation of LPS specific receptor, toll-like receptor 4 (TLR4), and its co-receptor cluster of differentiation 14 (CD14) and adaptor protein differentiation factor 88 (MyD88) in hepatic and adipose tissues. That further inhibited the activation of nuclear factor κB (NF-κB). The serum levels of tumor necrosis factor-alpha (TNF-α), interleukin-1-beta (IL-1β) and interleukin-6 (IL-6) were significantly decreased by TP in HFD-fed mice. TP also maintained the intestinal barrier integrity by increasing intestinal tight junction proteins and reversed gut dysbiosis in obese mice. These results suggested that TP attenuated obesity-induced inflammation by reducing systemic LPS level and inhibiting LPS-activated TLR4/NF-κB pathway.

Keywords: Gut microbiota; Lipopolysaccharides; Obesity; Tea polyphenols.

MeSH terms

  • Animals
  • Inflammation / drug therapy
  • Inflammation / prevention & control
  • Interleukin-6
  • Lipopolysaccharides
  • Mice
  • Mice, Obese
  • NF-kappa B* / metabolism
  • Obesity / drug therapy
  • Polyphenols / pharmacology
  • Tea
  • Toll-Like Receptor 4* / metabolism

Substances

  • Interleukin-6
  • Lipopolysaccharides
  • NF-kappa B
  • Polyphenols
  • Tea
  • Tlr4 protein, mouse
  • Toll-Like Receptor 4