4.6 Article

The Inhibitory Effects of Purple Sweet Potato Color on Hepatic Inflammation Is Associated with Restoration of NAD+ Levels and Attenuation of NLRP3 Inflammasome Activation in High-Fat-Diet-Treated Mice

Journal

MOLECULES
Volume 22, Issue 8, Pages -

Publisher

MDPI
DOI: 10.3390/molecules22081315

Keywords

purple sweet potato color; hepatic inflammation; NAD(+); NLRP3 inflammasome; high-fat diet

Funding

  1. Priority Academic Program Development of Jiangsu Higher Education Institutions (PAPD)
  2. National Natural Science Foundation of China [81570531, 81571055]
  3. China Agriculture Research System-sweetpotato [CARS-10]
  4. Key Research and Development Plan of Jiangsu Province [BE2015313]
  5. Scientific Research Support Project for Teachers with Doctor's Degrees [15XLR005]
  6. Natural Science Foundation of Jiangsu Province [BK20131127]
  7. Graduate Student Innovation Program of Jiangsu Province [KYZZ_0395, KYZZ16_0467]

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Purple sweet potato color (PSPC), a class of naturally occurring anthocyanins, exhibits beneficial effects on metabolic syndrome. Sustained inflammation plays a crucial role in the pathogenesis of metabolic syndrome. Here we explored the effects of PSPC on high-fat diet (HFD)-induced hepatic inflammation and the mechanisms underlying these effects. Mice were divided into four groups: Control group, HFD group, HFD + PSPC group, and PSPC group. PSPC was administered by daily oral gavage at doses of 700 mg/kg/day for 20 weeks. Nicotinamide riboside (NR) was used to increase NAD(+) levels. Our results showed that PSPC effectively ameliorated obesity and liver injuries in HFD-fed mice. Moreover, PSPC notably blocked hepatic oxidative stress in HFD-treated mice. Furthermore, PSPC dramatically restored NAD(+) level to abate endoplasmic reticulum stress (ER stress) in HFD-treated mouse livers, which was confirmed by NR treatment. Consequently, PSPC remarkably suppressed the nuclear factor-kappa B (NF-kappa B) p65 nuclear translocation and nucleotide oligomerization domain protein1/2 (NOD1/2) signaling in HFD-treated mouse livers. Thereby, PSPC markedly diminished the NLR family, pyrin domain containing 3 (NLRP3) inflammasome activation, ultimately lowering the expressions of inflammation-related genes in HFD-treated mouse livers. In summary, PSPC protected against HFD-induced hepatic inflammation by boosting NAD(+) level to inhibit NLRP3 inflammasome activation.

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