Impact of Camellia japonica Bee Pollen Polyphenols on Hyperuricemia and Gut Microbiota in Potassium Oxonate-Induced Mice

Nutrients. 2021 Jul 30;13(8):2665. doi: 10.3390/nu13082665.

Abstract

Camellia japonica bee pollen is one of the major types of bee pollen in China and exhibits antioxidant and anti-inflammatory activities. The aims of our study were to evaluate the effects and the possible mechanism of Camellia japonica bee pollen polyphenols on the treatment of hyperuricemia induced by potassium oxonate (PO). The results showed that Camellia japonica bee pollen ethyl acetate extract (CPE-E) owned abundant phenolic compounds and strong antioxidant capabilities. Administration with CPE-E for two weeks greatly reduced serum uric acid and improved renal function. It inhibited liver xanthine oxidase (XOD) activity and regulated the expression of urate transporter 1 (URAT1), glucose transporter 9 (GLUT9), organic anion transporter 1 (OAT1), organic cation transporter 1 (OCT1) and ATP-binding cassette superfamily gmember 2 (ABCG2) in kidneys. Moreover, CPE-E suppressed the activation of the toll-like receptor 4/myeloid differentiation factor 88/nuclear factor-κB (TLR4/MyD88/NF-κB) signaling pathway and nucleotide-binding oligomerization domain-like receptor family pyrin domain-containing 3 (NLRP3) inflammasome in PO-treated mice, and related inflammatory cytokines were reduced. CPE-E also modulated gut microbiota structure, showing that the abundance of Lactobacillus and Clostridiaceae increased in hyperuicemic mice. This study was conducted to explore the protective effect of CPE-E on hyperuricemia and provide new thoughts for the exploitation of Camellia japonica bee pollen.

Keywords: Camellia japonica bee pollen polyphenols; NLRP3 inflammasome; TLR4/MyD88/NF-κB; gut microbiota; hyperuricemia; kidney inflammation.

MeSH terms

  • ATP Binding Cassette Transporter, Subfamily G, Member 2 / metabolism
  • Animals
  • Anti-Inflammatory Agents
  • Antioxidants
  • Bees*
  • Camellia / chemistry*
  • China
  • Disease Models, Animal
  • Glucose Transport Proteins, Facilitative
  • Humans
  • Hyperuricemia / chemically induced
  • Hyperuricemia / drug therapy*
  • Inflammasomes / metabolism
  • Kidney / metabolism
  • Liver / metabolism
  • Mice
  • Myeloid Differentiation Factor 88 / metabolism
  • NF-kappa B / metabolism
  • Octamer Transcription Factor-1
  • Organic Anion Transport Protein 1 / metabolism
  • Organic Anion Transporters
  • Oxonic Acid / adverse effects*
  • Pollen / chemistry*
  • Polyphenols / pharmacology*
  • Signal Transduction / drug effects
  • Toll-Like Receptor 4
  • Uric Acid

Substances

  • ATP Binding Cassette Transporter, Subfamily G, Member 2
  • Abcg2 protein, mouse
  • Anti-Inflammatory Agents
  • Antioxidants
  • Glucose Transport Proteins, Facilitative
  • Inflammasomes
  • Myeloid Differentiation Factor 88
  • NF-kappa B
  • Octamer Transcription Factor-1
  • Organic Anion Transport Protein 1
  • Organic Anion Transporters
  • Polyphenols
  • Pou2f1 protein, mouse
  • Slc22a12 protein, mouse
  • Slc22a6 protein, mouse
  • Slc2a9 protein, mouse
  • Tlr4 protein, mouse
  • Toll-Like Receptor 4
  • Uric Acid
  • potassium oxonate
  • Oxonic Acid