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  Indian J Med Microbiol
 

Figure 2: Potential mechanism of action of oxygen-ozone therapy Note: Oxidative stress is involved in NF-κB pathways activation. NF-κB signaling induces the release of proinflammatory cytokines (IL-1β, IL-6, TNF-α, COX-2), implicated in the inhibition of extracellular matrix components synthesis and in matrix metalloproteinase activation causing cartilage damage, disturbance of the metabolic balance of the cartilage matrix, until apoptosis. Oxygen-ozone mixture attenuates inflammatory responses by inhibiting the activation of NF-κB pathway, resulting in cell proliferation and survival. ATP: Adenosine triphosphate; COX-2: cyclooxygenase-2; IκB: inhibitor of nuclear factor-κB; IL: interleukin; NF-κB: nuclear factor-κB; TNF-α: tumor necrosis factor-α.

<b>Figure 2: Potential mechanism of action of oxygen-ozone therapy</b>
Note: Oxidative stress is involved in NF-κB pathways activation. NF-κB signaling induces the release of proinflammatory cytokines (IL-1β, IL-6, TNF-α, COX-2), implicated in the inhibition of extracellular matrix components synthesis and in matrix metalloproteinase activation causing cartilage damage, disturbance of the metabolic balance of the cartilage matrix, until apoptosis. Oxygen-ozone mixture attenuates inflammatory responses by inhibiting the activation of NF-κB pathway, resulting in cell proliferation and survival. ATP: Adenosine triphosphate; COX-2: cyclooxygenase-2; IκB: inhibitor of nuclear factor-κB; IL: interleukin; NF-κB: nuclear factor-κB; TNF-α: tumor necrosis factor-α.