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Thus, in the cerebral arterioles, arachidonic acid promoted vasodilation that was dependent on hydrogen peroxide, and excess antioxidant enzymes, including GPx1, attenuated hydrogen peroxide-mediated vasodilation [74]

[Google Scholar] Pasternak T, Palme K, Paponov IA

The key events involved in this MOA are: Key Event 1: Accumulation of parent compound due to metabolic saturation

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Grouping: Control group (physiological saline intra-articular injection), AOD 9604 group (0.25mg/joint), hyaluronic acid (HA) group (0.5mg/joint), AOD 9604+HA combination group