In coronary arteries, plaque disruption, the major acute clinical manifestations of atherosclerosis, leads to a subsequent cardiac event, such as acute myocardial infarction (AMI) and unstable angina pectoris (UA). Numerous reports have shown that high expression of MMP-9 (matrix metalloproteinase-9), MMP-13 (matrix metalloproteinase-13) and EMMPRIN (extracellular matrix metalloproteinase induce) in monocyte/macrophage results in the plaque progression and destabilization. Curcumin exerts well-known anti-inflammatory and antioxidant effects and probably has a protective role in the atherosclerosis. The purpose of our study was to investigate the molecular mechanisms by which curcumin affects MMP-9, MMP13 and EMMPRIN in PMA (phorbol 12-myristate 13-acetate) induced macrophages. Human monocytic cells (THP-1 cells) were pretreated with curcumin or compound C for 1 h, and then induced by PMA for 48 h. Total RNA and proteins were collected for real-time PCR and Western blot analysis, respectively. In the present study, the exposure to curcumin resulted in attenuated JNK, p38, and ERK activation and decreased expression of MMP-9, MMP-13 and EMMPRIN in PMA induced macrophages. Moreover, we demonstrated that AMPK (AMP-activated protein kinase) and PKC (Protein Kinase C) was activated by PMA during monocyte/macrophage differentiation. Furthermore, curcumin reversed PMA stimulated PKC activation and suppressed the chronic activation of AMPK, which in turn reduced the expression of MMP-9, MMP-13 and EMMPRIN. Therefore, it is suggested that curcumin by inhibiting AMPK-MAPK (mitogen activated protein kinase) and PKC pathway may led to down-regulated EMMPRIN, MMP-9 and MMP-13 expression in PMA-induced THP-1 cells.

Background. Acute myocardial infarction (AMI) is a disease with high morbidity and mortality. Some new biomarkers can help us to improve the life quality and prognosis of AMI patients. Objective. We therefore performed a systematic review and meta-analysis on the use of galectin-3 (gal3) for assessing prognosis of AMI patients. Methods. We searched Medline, Embase, Web of Science, Cochrane Library, SinoMed, China National Knowledge Infrastructure (CNKI), and Wanfang database up to June 2019. Trials included using galectin-3 to estimate prognosis in myocardial infarction (MI) patients. Results. We identified 10 trails with a total of 2809 participants. The negative correlation between galectin-3 and left ventricular ejection fraction (LVEF) was significant in 505 AMI patients (Fisher's Z −0.22, 95% CI: −0.34, −0.09). The correlation between galectin-3 and infarct size was not significant in 119 patients (Fisher's Z 0.12, 95% CI: −0.36, 0.60). Higher galectin-3 was associated with increased all-cause mortality in 2343 AMI patients (Fisher's Z 1.58, 95% CI: 1.23, 2.03). Conclusion. The limited evidence suggests that galectin-3 is likely to predict the adverse outcomes in MI patients, but it is not significantly correlated with infarct size after MI. More high-quality trials with longer-term follow-up are still needed to confirm this finding.

Aim: To explore potential value of inter-alpha-trypsin inhibitor heavy chain-4 (ITIH4) for coronary artery disease (CAD) diagnosis. Patients & methods: We recruited the patients who received coronary arteriography (CAG) examination. The enzyme-linked immunosorbent assay was used to detect plasma ITIH4. Results: ITIH4 level was lower expression in CAD patients than that in patients of control group, and was negatively correlated with C-reactive protein (CRP). ITIH4 level is no differences between ST-elevated myocardial infarction (STEMI) and non-ST-elevated myocardial infarction (NSTEMI) patients. However, its expression was significantly correlated with D-Dimer and thrombin time, and the logistic analysis confirmed predictive value of ITIH4 for visible thrombus in coronary. Conclusion: ITIH4 may be a useful biomarker in CAD diagnosis, and to predict visible thrombus in coronary.

Objectives. To study the predictive value for coronary artery calcification (CAC) of plasma galectin‐3 and brachial‐ankle pulse wave velocity (BaPWV) in coronary arteriography (CAG) patients. Methods. Patients who received coronary arteriography (CAG) examination were recruited. The level of plasma galectin‐3 was measured by the enzyme‐linked immunosorbent assay. The arterial stiffness was analyzed by BaPWV and ankle‐brachial index (ABI) which were measured using a volume‐plethysmographic device. Receiver operating characteristic (ROC) curve was used to analyze the prognostic value of galectin‐3 or BaPWV for coronary artery calcification (CAC). Results. The level of galectin‐3 and BaPWV was significantly higher in CAC patients compared with that in control (p < 0.01). The level of plasma galectin‐3 was positively correlated with BaPWV (r = −0.296, p < 0.01) and negatively correlated with ABI (r = −0.296, p < 0.01). ROC curve analysis revealed that galectin‐3 ≥5.90 ng/ml was the most powerful predictor for CAC with sensitivity of 85.5% and specificity of 83.5%. The area under the curve (AUC) was 0.916. When the level of BaPWV was more than 1909 m/s, the sensitivity and specificity were 61.8% and 69.6%, respectively, for predicting CAC. The AUC was 0.646. Conclusions. The level of plasma galectin‐3 increases significantly in CAC patients compared to control, and its level is related to BaPWV and ABI. Galectin‐3 and BaPWV can be used to predict CAC, and the diagnosis value (sensitivity and specificity) of galectin‐3 for CAC is better than that of BaPWV.

Allicin is an active component of garlic that exerts protective effects against cardiovascular diseases. Vascular contraction and relaxation are the essential capacities of the vascular system to maintain its normal function. Endothelial cells (ECs) and vascular smooth muscle cells (VSMCs) are the main types of cells that control vascular function. This study was aimed at assessing the effects of allicin on vascular function and exploring its potential regulatory mechanisms. Mass spectrometry analysis was used to identify potential downstream targets of allicin in the artery. A primary culture of mouse VSMCs and ECs was established via enzymatic digestion of the aorta. Small interfering RNA (siRNA) was used to knock down the expression of the target gene, and a vector was used to upregulate specific protein expressions. Protein levels were determined using western blotting. Our results showed that allicin treatment increased both endothelium-dependent and endothelium-independent relaxation in aortic rings. Based on mass spectrometry analysis, we proposed that ATP-binding cassette transporter G1 (ABCG1), ryanodine receptor 2 (RyR2), and peroxisome proliferator-activated receptor γ (PPAR γ) might be the downstream targets of allicin. In ECs, Allicin increased ABCG1 expression and nitric oxide (NO) production, ABCG1 siRNA decreased allicin-induced NO production. RyR2 expression and Ca²⁺ spark were inhibited by allicin in VSMCs; RyR2 overexpression partly reversed the allicin-induced Ca²⁺ spark decrease in VSMCs. PPAR γ siRNA significantly inhibited the effects of allicin in ECs and VSMCs. These results indicated that allicin treatment exerted vasorelaxation effects by increasing ABCG1 expression and NO production in ECs and reducing RyR2 expression and Ca²⁺ spark in VSMCs. The PPAR γ signaling pathway was confirmed to mediate these processes.