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This brief action is heavily dependent on the plasma pseudocholinesterase pathway, as butyrylcholinesterase in the blood hydrolyzes roughly 90% of the drug before it ever reaches the neuromuscular junction

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found that Receptor-interacting protein 2 (RIP2) can regulate cartilage degradation and oxidative stress in IL-1 β-treated chondrocytes by regulating TRAF3 expression and p38-MAPK pathway activation (Pan et al., 2021)