Mechanism of Curcumin Inhibiting NLRP3 Inflammatory Body and Improving Atherosclerotic Endothelial Cell Injury

Discov Med. 2024 Jan;36(180):121-128. doi: 10.24976/Discov.Med.202436180.11.

Abstract

Background: Curcumin is a kind of natural hydrophobic polyphenol isolated from the stem of the Curcuma plant. To investigate regulatory curcumin effect on atherosclerotic endothelial cell injury.

Methods: 30 male ApoE-/- mice were selected and divided into the control group, model group, and curcumin group (n = 10). The curcumin group was treated with curcumin by gavage. Body weight, atherosclerotic plaque area, plaque cap thickness, blood lipid levels, total cholesterol (TC), triacylglycerol (TG), low-density lipoprotein cholesterol (LDL-C) content, nitric oxide (NO) content, interleukin-1β (IL-1β), tumor necrosis factor-α (TNF-α) content and circulating endothelial cell number of mice in each group were detected. Western blot detected NACHT, LRR, and receptor family pyrin domain-containing 3 (NLRP3) and Asc-type amino acid transporter protein 1 (ASC) protein level in mice. Human aortic endothelial cells (HAEC) were cultured to establish an atherosclerotic endothelial cell injury model in vivo. Cell counting kit-8 (CCK-8) detected the cell viability of each group.

Results: Body weight, atherosclerotic plaque area, plaque cap thickness, TC, TG, and LDL-C content of blood lipid levels of the curcumin group were obviously reduced as compared with the model group (p < 0.05), the content of NO and the number of circulating endothelial cells in curcumin group were obviously decreased (p < 0.05). The cell viability of the curcumin group was obviously higher than that of the model group (p < 0.05). The NO content of the curcumin group was lower than the model group (p < 0.05). The content of IL-1β and TNF-α in the curcumin group was obviously lower than in the model group (p < 0.05). Compared with the model group, the expression of receptor family pyrin domain-containing 3 (NLRP3) and ASC protein in the curcumin group was decreased obviously (p < 0.05).

Conclusion: Curcumin improves endothelial cell injury in atherosclerosis by inhibiting the expression of NLRP3 inflammatory bodies.

Keywords: NLRP3 inflammatory body; atherosclerosis; curcumin; endothelial cell injury.

MeSH terms

  • Animals
  • Atherosclerosis* / drug therapy
  • Atherosclerosis* / metabolism
  • Body Weight
  • Cholesterol, LDL / metabolism
  • Curcumin* / metabolism
  • Curcumin* / pharmacology
  • Curcumin* / therapeutic use
  • Endothelial Cells
  • Humans
  • Inflammasomes / metabolism
  • Lipids
  • Mice
  • NLR Family, Pyrin Domain-Containing 3 Protein / metabolism
  • Plaque, Atherosclerotic* / metabolism
  • Tumor Necrosis Factor-alpha

Substances

  • NLR Family, Pyrin Domain-Containing 3 Protein
  • Curcumin
  • Tumor Necrosis Factor-alpha
  • Cholesterol, LDL
  • Lipids
  • Inflammasomes