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. 2019 Nov 21;13:3949–3961. doi: 10.2147/DDDT.S203094

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© 2019 Zuo et al.

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Schematic representation of the potential mechanism of ICA in Nrf2 activation and ROS elimination in IL-1β-induced chondrocytes. IL-1β causes excess ROS generation, whereas ICA treatment activates the redox-sensitive transcription factor Nrf2. ICA can disrupt the formation of Keap1-Nrf2 dipolymer by directly inhibiting the expression of Keap1, thereby interdicting the combination of Nrf2 and Keap1 protein and leading to activation and nuclear importation of Nrf2. Thus, activation of the Nrf2 pathway leads to transcription of the downstream genes SOD-1, SOD-2, NQO-1 and HO-1. The activation of ARE results in the reduction of ROS, consequently reducing the IL-1β-induced matrix-degrading proteases and ECM degradation.