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  • Title: Protective effects and mechanism of curcumin on myocardial injury induced by coronary microembolization.
    Author: Liu Y, Liu Y, Huang X, Zhang J, Yang L.
    Journal: J Cell Biochem; 2019 Apr; 120(4):5695-5703. PubMed ID: 30324684.
    Abstract:
    OBJECTIVE: Coronary microembolization (CME) is a common complication during the percutaneous coronary intervention (PCI). CME-induced local myocardial inflammation and myocardial apoptosis are the primary causes of progressive cardiac dysfunction. Curcumin exerts a protective role in various cardiovascular diseases; however, its effects in CME are yet to be clarified. Therefore, the current study investigated the effects of curcumin on myocardial inflammatory responses, myocardial apoptosis, and cardiac dysfunctions induced by CME in rats. METHODS: A total of 40 Sprague-Dawley rats were randomly divided into the following groups: Sham operation (sham group), CME group, curcumin, and control with 10 rats in each group. The ascending aortas were clamped, and the CME-model group was established by injecting microspheres into the apex of the left ventricle. An equivalent amount of normal saline was injected to establish the sham group. The cardiac functions, serum c-troponin I level, and apoptotic index was examined. Also, the levels of Toll-like receptor 4 (TLR4), myeloid differentiation primary response 88 (MYD88), nuclear factor κB (NF-κB) p65, BCL2-associated X protein (Bax), B-cell lymphoma 2 (Bcl-2), cleaved caspase-3, tumor necrosis factor α (TNF-α), and interleukin-1β (IL-1β) were detected. RESULTS: Myocardial dysfunction enhanced serum c-troponin I, and apoptotic index were induced following CME. Moreover, CME elevated the expression of TLR4, MyD88, NF-κB p65, cleaved caspase-3, TNF-α, and IL-1β, while the Bcl-2/Bax ratio decreased. Curcumin reversed these effects by CME, while the gastric lavage control did not exert any effect. CONCLUSION: Curcumin was responsible for the anti-CME-induced myocardial injury. The effector mechanism might be related to the reduction of cardiomyocyte apoptosis and inhibition of myocardial inflammatory responses mediated by TLR4/MyD88/NF-κB signaling pathway.
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