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Given that the degradation of KEAP1 encompasses two distinct pathways, namely autophagy 29 and proteasomal degradation 30 , we employed the protein synthesis inhibitor cycloheximide (CHX), the proteasome inhibitor MG132, and the autophagy inhibitor chloroquine (Chlq) to further explore the underlying mechanism in macrophages (Fig

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down-regulating TNF-, IL-6, IL-1 and cyclooxygenase [COX] expression, etc.) and excitoneurotoxicity (e.g