Lutein prevents osteoarthritis through Nrf2 activation and downregulation of inflammation
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Submission date: 2015-09-29
Final revision date: 2016-02-04
Acceptance date: 2016-02-11
Online publication date: 2016-05-12
Publication date: 2018-04-13
Arch Med Sci 2018;14(3):617–624
Osteoarthritis is an inflammatory disorder associated with oxidative stress and apoptosis leading to cartilage destruction and impairment of cartilage formation. In the present study, we studied the protective effect of lutein against monosodium iodoacetate (MIA)-induced osteoarthritis in primary chondrocyte cells.

Material and methods:
Oxidative stress was determined through testing antioxidant status, reactive oxygen species levels and lipid peroxide content. Also, Nrf2 expression and its downstream target genes HO-1 and NQO-1 were determined. Inflammation was analyzed through NF-κB, COX-2 and pro-inflammatory cytokines (IL-6, TNF-α, IL-1β). In addition, the effects of MIA and lutein on mitochondrial membrane potential and caspase-3 levels were analyzed.

The results showed that lutein treatment significantly increased the cell viability of chondrocytes and offered significant cytoprotection by enhancing the antioxidant defense mechanisms and reducing oxidative stress (reactive oxygen species and lipid peroxidation). Lutein treatment showed anti-inflammatory effects by downregulating inflammatory proteins (NF-κB, COX-2) and pro-inflammatory cytokines (IL-6, TNF-α, IL-1β). Lutein reduced MIA-induced apoptosis through maintaining mitochondrial membrane potential and downregulating caspase-3 activity.

The present study shows significant cytoprotection offered by lutein against MIA-induced oxidative stress, inflammation and apoptosis by the modulatory effect of NF-κB and Nrf2 activation.