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2018 ; 10
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Zinc Protects Articular Chondrocytes through Changes in Nrf2-Mediated
Antioxidants, Cytokines and Matrix Metalloproteinases
#MMPMID29641501
Nutrients
2018[Apr]; 10
(4
): ä PMID29641501
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Osteoarthritis (OA) is an age-related degenerative joint disease characterized by
high oxidative stress, chondrocyte death and cartilage damage. Zinc has been
implicated in the antioxidant capacity of the cell, and its deficiency might
inhibit chondrocyte proliferation. The present study examined the potential of
zinc as a preventive supplement against OA using the in vitro chondrosarcoma cell
line SW1353 and an in vivo Wistar rat model to mimic OA progress induced by
monosodium iodoacetate (MIA). The results demonstrated that, in SW1353 cells, 5
?M MIA exposure increased oxidative stress and decreased the expression of GPx1
and Mn-SOD but still increased GSH levels and HO-1 expression and enhanced the
expression of interleukin (IL)-10, IL-1?, and matrix metalloproteinase (MMP)-13.
Zinc addition could block these changes. Besides, the expression of Nrf2 and
phosphorylated (p)-Akt was dramatically increased, implicating the p-Akt/Nrf2
pathway in the effects of zinc on MIA-treated cells. A rat model achieved similar
results as those of cell culture, and 1.6 mg/kg/day of zinc supplementation is
sufficient to prevent OA progress, while 8.0 mg/kg/day of zinc supplementation
does not have a better effect. These findings indicate that zinc supplementation
exerts a preventive effect with respect to MIA-induced OA progress.