Objective To explore the potential mechanisms of curcumin on myocardial inflammatory responses following coronary microembolization (CME) in rats.

Methods Thirty-two SD rats were randomly divided into a sham group, a CME group (model group), a CME + curcumin group (curcumin group), and a CME + curcumin + Foxy-5 group (agonist group), with 8 rats in each group. The CME model in rats was established by clamping the ascending aorta and injecting inert polystyrene microspheres into the left ventricle. Real-time fluorescent quantitative PCR (RT-qPCR) and western blotting (WB) were employed to detect the transcription and translation levels of interleukin-1β (IL-1β), tumor necrosis factor-α (TNF-α), Wnt family member 5a (Wnt5a), and β-catenin in the myocardium.

Results Compared with the sham group, rats in the model group exhibited significantly decreased cardiac function, along with significantly elevated transcription and translation levels of TNF- α, IL-1β, and Wnt5a, while β-catenin expression levels showed a decrease (all P < 0.05). Compared with the model group, rats in the curcumin group showed an increasing trend in cardiac function, with significantly decreased transcription and translation levels of TNF-α, IL-1β, and Wnt5a, and an increase in β-catenin expression levels (all P < 0.05). The agonist Foxy-5 significantly reversed the effects of curcumin on the above indexes (P < 0.05).

Conclusion Curcumin can alleviate myocardial inflammatory responses by inhibiting the Wnt5a/β-catenin pathway following CME in rats.