Sirtuin 6 protects human retinal pigment epithelium cells from LPS-induced inflammation and apoptosis partly by regulating autophagy

Biosci Biotechnol Biochem. 2020 Oct;84(10):2062-2068. doi: 10.1080/09168451.2020.1788377. Epub 2020 Jul 3.

Abstract

Lipopolysaccharides (LPS)-induced retinal inflammation is an important factor in retinal diseases. This study was aimed to investigate the effect of Sirt6 on LPS-induced retinal injury. ARPE-19 cells were incubated with LPS to induce inflammation. The cell viability was determined using CCK-8 assay. The mRNA level and protein expression of corresponding genes was detected using qRT-PCR and western blot, respectively. The production of inflammatory cytokines was measured using ELISA kit. The levels of oxidative stress-related factors were measured using their detection kits. Cell apoptosis was observed using TUNEL assay. The results showed that Sirt6 was downregulated after LPS treatment. Sirt6 strengthened LPS-induced autophagy by promoting the expression of LC3II/I, beclin1 and ATG5. Sirt6 treatment significantly inhibited LPS-induced inflammation, oxidative stress and cell apoptosis, which was then partly abolished by 3 MA. These results suggest Sirt6 to be an important regulator for LPS-induced inflammation, oxidative stress, and apoptosis partly by regulating cell autophagy.

Keywords: Sirtuin 6; apoptosis; autophagy; human retinal pigment epithelium cells; inflammation.

MeSH terms

  • Apoptosis / drug effects*
  • Autophagy / drug effects*
  • Cell Line
  • Humans
  • Inflammation / chemically induced
  • Inflammation / metabolism
  • Lipopolysaccharides / pharmacology*
  • Oxidative Stress / drug effects
  • Retinal Pigment Epithelium / cytology*
  • Sirtuins / metabolism*

Substances

  • Lipopolysaccharides
  • SIRT6 protein, human
  • Sirtuins