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DCBS is a dual-functional, disubstituted curcumin-borneol prodrug synthesized via a succinate ester linkage. It was developed to address the poor solubility and low bioavailability of curcumin while leveraging the synergistic anti-inflammatory properties of borneol. DCBS functions by inhibiting the MAPK/AP-1 signaling pathway, specifically suppressing the phosphorylation of ERK and p38 and the expression of the transcription factor c-Fos. This action leads to the downregulation of matrix metalloproteinase-9 (MMP9) and pro-inflammatory cytokines such as TNF-α, IL-6, and IL-1β. Additionally, DCBS exhibits potent reactive oxygen species (ROS) scavenging activity. In preclinical studies using a collagen-induced arthritis rat model, DCBS demonstrated superior efficacy in reducing joint inflammation and destruction compared to native curcumin, while maintaining a favorable safety profile.
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