Bradykinin-(1-9) mitigates autophagy through upregulating PI3K/Akt in rats with myocardial infarction.

The cardioprotective mechanisms of bradykinin-(1-9) in myocardial infarction were unclear. We investigated the effect of bradykinin-(1-9) on cardiac function, fibrosis, and autophagy induced by myocardial infarction and identified the mechanisms involved. To investigate the cardioprotective effect of bradykinin-(1-9), various doses of bradykinin-(1-9), its B2 receptor blocker HOE140, or their combination were administered to rats via subcutaneous osmotic minipump implantation before myocardial infarction. After 2 days, myocardial infarction was induced by ligation of the left anterior descending coronary artery. After 2 weeks, echocardiographic measurements and euthanasia were performed. Bradykinin-(1-9) treatment attenuated left ventricular dysfunction, fibrosis, and autophagy in rats with myocardial infarction, which was partially reversed by HOE140 administration. Moreover, the downregulatory effect of bradykinin-(1-9) on autophagy was partially reversed by combination with the PI3K inhibitor LY294002. Thus, bradykinin-(1-9) inhibits myocardial infarction-induced cardiomyocyte autophagy by upregulating the PI3K/Akt pathway.

Antioxidant protein peroxiredoxin 6 suppresses the vascular inflammation, oxidative stress and endothelial dysfunction in angiotensin II-induced endotheliocyte.

Cardiovascular disease (CVD) states are associated with endothelial dysfunction (ED) and increased production of ROS in endothelial cells. The present study aimed to explore the protective effects of antioxidant protein peroxiredoxin 6 (PRDX6) on angiotensin II (AngII)­induced human umbilical vein endothelial cell (HUVEC) dysfunction. To investigate cell viability, levels of inflammatory molecules and proteins were assayed using the CCK-8 assay and evaluated by ELISA and Western blot. NO and ROS levels were determined by Griess assay and the fluorescent probe DCFH-DA. Cell migration capacity was assessed by Transwell assay. AngII decreased cell viability and PRDX6, upregulated the expression levels of TNF-α, IL-6, IL-1ß, LDH and MDA, stimulated ROS production, and reduced NO synthase, the expressions of eNOS, MnSOD, ICAM-1, VCAM-1, and activated the MAPK family of signaling proteins. However, the stimulatory effects of AngII on HUVECs were remarkably suppressed by PRDX6. Furthermore, mercaptosuccinate (MS; PRDX6 inhibitor) had similar effects as AngII in aggravating HUVECs damage. Conversely, these adverse events caused by AngII and MS were obviously reversed by ML3404 and SP600125. The present study indicated that PRDX6 overexpression inactivated p38 MAPK and JNK pathway through decrease AngII-induced inflammation, oxidative stress and endothelial dysfunction leading to attenuation of endothelial cell damage.

Vasospastic myocardial infarction complicated with bilateral femoral arteries vasospasm.

Coronary vasospasm is an infrequent cause of acute coronary syndrome. Additionally, femoral artery spasm is not frequently encountered clinically. Here we present a case of a patient with an acute ST segment elevation myocardial infarction, secondary to a documented right coronary artery vasospasm, complicated with left coronary artery and femoral artery vasospasm. Intravenous ultrasound showed calcification at the sites of spasm. This case report indicates that coronary vasospasm should be regularly considered as part of the work up of myocardial infarction.

Correlation of echocardiographic epicardial fat thickness with severity of coronary artery disease in patients with acute myocardial infarction.

The aim of this study was to test the hypotheses that epicardial adipose tissue (EAT) can be a marker of severe coronary artery disease in patients with acute myocardial infarction. Overall, 373 cases who underwent coronary angiography were classified into 2 groups by SYNTAX score: low-score and high-score group. EAT was measured by transthoracic echocardiography. Obtained data were compared using Pearson correlation analyses and univariate and multiple logistic regression analysis. The results showed that EAT in the high-score group was significantly greater than in the normal group (5.6 ± 1.1 vs. 4.1 ± 1.0 mm, P < 0.01). EAT had a positive correlation with SYNTAX score (r = 0.61, P < 0.01). Receiver operating characteristic (ROC) curve analyses showed that EAT could reliably discriminate patients with high SYNTAX score (≥ 33) [AUC: 0.86, 95% confidence interval (CI): 0.822-0.898, P < 0.01]. Multivariate regression analyses showed that EAT was an independent predictor for major in-hospital events. These data showed an association between EAT and SYNTAX score.

Coronary angiography in dextrocardia with situs inversus and acute myocardial infarction: A case report and literature review.

We present the case of a 74-year-old man with dextrocardia and situs inversus who presented with non-ST-elevation acute myocardial infarction. The patient underwent successful coronary angiography without requiring percutaneous coronary intervention or coronary artery bypass grafting. We discuss the patient's clinical characteristics, electrocardiography findings, diagnosis, and treatment, and review the relevant literature.

Protective effect of scorpion venom oligopeptides in human umbilical vein endothelial cells under benzo(α)pyrene exposure.

Inflammation and oxidative stress play pivotal role in the process of atherosclerosis. Scorpion venom is widely used as anti-cancer agent, however, the anti-inflammatory and antioxidant activities of scorpion venom peptides (SVPs) are rarely explored. In the current study, seven novel SVPs were isolated in a protective activity tracking isolation method in a cell model of benzo(α)pyrene (BaP)-induced human umbilical vein endothelial cells (HUVECs). The current study showed that SVP-1 [Tyr-Thr-Trp-Glu-Ala] significantly attenuated BaP-induced reactive oxygen species (ROS) over-production and inflammatory cytokines (IL-6, IL-1ß, TNF-α, NO and PGE2) over-expression. Furthermore, SVP-1 attenuated BaP-induced adhesion molecules over-expression and inhibited the NF-κB and AhR signalling pathways activation. Collectively, the present study, for the first time, shows that SVPs inhibit the NF-κB and AhR signalling pathways in HUVECs under BaP-exposure, which strongly suggests the therapeutic potential of SVPs against atherosclerosis.