Zinc decreases C-reactive protein, lipid peroxidation, and inflammatory cytokines in elderly subjects: a potential implication of zinc as an atheroprotective agent.

Article Details

Citation

Bao B, Prasad AS, Beck FW, Fitzgerald JT, Snell D, Bao GW, Singh T, Cardozo LJ

Zinc decreases C-reactive protein, lipid peroxidation, and inflammatory cytokines in elderly subjects: a potential implication of zinc as an atheroprotective agent.

Am J Clin Nutr. 2010 Jun;91(6):1634-41. doi: 10.3945/ajcn.2009.28836. Epub 2010 Apr 28.

PubMed ID
20427734 [ View in PubMed
]
Abstract

BACKGROUND: Chronic inflammation and oxidative stress are common risk factors for atherosclerosis. Zinc is an essential micronutrient that can function as an antiinflammatory and antioxidative agent, and as such, it may have atheroprotective properties. OBJECTIVE: We hypothesized that zinc down-regulates the production of atherosclerosis-related cytokines/molecules in humans. DESIGN: To examine these effects, we conducted a randomized, double-blinded, placebo trial of zinc supplementation in elderly subjects. We recruited 40 healthy elderly subjects (aged 56-83 y) and randomly assigned them to 2 groups. One group was given an oral dose of 45 mg zinc/d as a gluconate for 6 mo. The other group was given a placebo. Cell culture models were conducted to study the mechanism of zinc as an atheroprotective agent. RESULTS: After 6 mo of supplementation, the intake of zinc, compared with intake of placebo, increased the concentrations of plasma zinc and decreased the concentrations of plasma high-sensitivity C-reactive protein (hsCRP), interleukin (IL)-6, macrophage chemoattractant protein 1 (MCP-1), vascular cell adhesion molecule 1 (VCAM-1), secretory phospholipase A2, and malondialdehyde and hydroxyalkenals (MDA+HAE) in elderly subjects. Regression analysis showed that changes in concentrations of plasma zinc were inversely associated with changes in concentrations of plasma hsCRP, MCP-1, VCAM-1, and MDA+HAE after 6 mo of supplementation. In cell culture studies, we showed that zinc decreased the generation of tumor necrosis factor-alpha, IL-1beta, VCAM-1, and MDA+HAE and the activation of nuclear transcription factor kappaB and increased antiinflammatory proteins A20 and peroxisome proliferator-activated receptor-alpha in human monocytic leukemia THP-1 cells and human aortic endothelial cells compared with zinc-deficient cells. CONCLUSION: These findings suggest that zinc may have a protective effect in atherosclerosis because of its antiinflammatory and antioxidant functions.

DrugBank Data that Cites this Article

Pharmaco-proteomics
DrugDrug GroupsGeneGene IDChangeInteractionChromosome
ZincApproved InvestigationalCRP1401
decreased
Zinc results in decreased expression of CRP protein1q23.2
ZincApproved InvestigationalIL1B3553
decreased
Zinc results in decreased expression of IL1B protein2q14.1
ZincApproved InvestigationalIL63569
decreased
Zinc results in decreased expression of IL6 protein7p15.3
ZincApproved InvestigationalVCAM17412
decreased
Zinc results in decreased expression of VCAM1 protein1p21.2
ZincApproved InvestigationalPPARA5465
increased
Zinc results in increased expression of PPARA protein22q13.31
ZincApproved InvestigationalTNFAIP37128
increased
Zinc results in increased expression of TNFAIP3 protein6q23.3