Changes and significance of serum monocyte chemoattractant protein-1 and Lp-PLA2 in patients with hypertension and coronary heart disease.

OBJECTIVE: To explore the combined application value of serum monocyte chemoattractant protein-1 and lipoprotein-associated phospholipase A2 in the diagnosis of hypertension and coronary heart disease. METHODS: The cross-sectional case-control study was conducted at Baoji Hospital of Traditional Chinese medicine, Shaanxi, China, from April 2018 to May 2020, and comprised patients with suspected hypertension and coronary heart disease. Patients with both hypertension and coronary heart disease formed Group A, and those with simple hypertension formed Group B. Healthy individuals formed the control Group C. Receiver operating characteristic curve was used to evaluate the value of serum monocyte chemoattractant protein-1 combined with lipoprotein-associated phospholipase A2 in the diagnosis of hypertension complicated with coronary heart disease. Data was analysed using SPSS 25. RESULTS: Of the 306 subjects, there were 122(40%) in Group A; 68(55.7%) males and 54(44.3%) females with mean age 68.77±5.76 years. There were 92(30%) cases in Group B; 51(55.4%) males and 41(44.6%) females with mean age 68.80±5.28 years. Group C had 92(30%) cases; 50(54.3%) males and 42(45.7%) females with mean age 67.85±5.29 years. Serum monocyte chemoattractant protein-1 and lipoprotein-associated phospholipase A2 levels were higher in Group A than the other two groups (p<0.001), and the levels in patients with carotid plaque total score <2 were lower than those with carotid plaque total score >2 (p<0.001). Area under receiver operating characteristic curve of the combination of the serum markers was 0.883 (95% confidence interval: 0.837-0.929, p<0.001), which was greater than that of two serum markers alone (p<0.05). CONCLUSIONS: Monocyte chemoattractant protein-1 and lipoprotein-associated phospholipase A2 may be involved in pathogenesis of elevated blood pressure and coronary artery disease. Combined detection of the two serum markers can provide a certain basis for the diagnosis and treatment of hypertension and coronary heart disease.

U0126 attenuates ischemia/reperfusion-induced apoptosis and autophagy in myocardium through MEK/ERK/EGR-1 pathway.

Myocardial ischemia is one of the main causes of sudden cardiac death worldwide. Depending on the cell type and stimulus, ERK activity mediates different anti-proliferative events, such as apoptosis, autophagy, and senescence. The aim of this study was to determine the protective effect of 1,4-diamino-2,3-dicyano-1,4-bis[2-aminophenylthio] butadiene (U0126), an ERK kinase inhibitor, on myocardial ischemia/reperfusion (I/R) injury and the mechanisms involved. An I/R model was established in vivo in C57BL/6 mice and in vitro using mouse cardiomyocytes, respectively. To evaluate the protective effects of U0126 on I/R injury, we measured the myocardial infarct area, apoptosis, and autophagy. Our data indicated that pretreatment with U0126 significantly reduced the infarct area caused by I/R. Moreover, U0126 reduced the caspase-3 activity and the number of TUNEL-positive cardiomyocytes, which together indicate decreased apoptosis. Additionally, U0126 remarkable reduced the level of Beclin-1 and LC3 and increased p62 expression, which indicates that U0126 suppressed H/R-induced autophagy. Furthermore, the relationship between U0126 and MEK/ERK pathway activation in H/R-induced cardiomyocytes was also investigated. U0126 ameliorated H/R injury through inhibition of the MEK/ERK pathway and by suppressing in the downstream EGR-1 expression. Together, our research suggests that U0126 may protect against H/R injury by preventing H/R-induced myocardium apoptosis and autophagy via the MEK/ERK/EGR-1 pathway, and may be a potential therapeutic approach for attenuating myocardial I/R injury.