1,25-Vitamin D3 protects against cooking oil fumes-derived PM2.5-induced cell damage through its anti-inflammatory effects in cardiomyocytes.

The functional role of 1,25-vitamin D3 in cooking oil fumes (COFs)-derived PM2.5-induced cell damage is largely unexplored. The present study investigated the protective role of 1,25-vitamin D3 against cell injury by possible involvement of JAK/STAT and NF-κB signaling pathways in cardiomyocytes. Cell viability was measured using CCK-8 assay, and cell apoptosis was analyzed by flow cytometry, qRT-PCR and Western blot in cultured rat neonatal cardiomyocytes treated with 1,25-vitamin D3 and COFs-derived PM2.5. Expressions of JAK/STAT and NF-κB signaling pathway were measured by Western blot. The results suggested that treatment with COFs-derived PM2.5 significantly decreased cell viability and increased apoptosis and oxidative stress in cultured rat neonatal cardiomyocytes. 1,25-vitamin D3 pretreatment alleviated the cell injury by increasing cell viability and decreasing apoptosis in the cardiomyocytes. 1,25-vitamin D3 pretreatment also decreased the ROS level and inflammation in the cardiomyocytes. Furthermore, 1,25-vitamin D3 pretreatment alleviated COFs-derived PM2.5-evoked elevation of JAK/STAT and NF-κB signaling pathways. Our study showed that 1,25-vitamin D3 pretreatment protected cardiomyocytes from COFs-derived PM2.5-induced injury by decreasing ROS, apoptosis and inflammation level via activations of the JAK/STAT and NF-κB signaling pathways.

Comparison of clinical outcomes after drug-eluting stent implantation in diabetic versus nondiabetic patients in China: A retrospective study.

Diabetes mellitus (DM) has been proved to be a predictor of adverse outcomes after percutaneous coronary intervention (PCI). Drug-eluting stents (DESs) could reduce the adverse events in DM patients. In this study, we aimed to analyze the clinical outcome after DES implantation in diabetic versus nondiabetic patients in China. Totally, 200 Chinese DM patients and 400 Chinese non-DM patients were enrolled in this retrospective study. Compared with non-DM patients, DM patients were more likely to have a higher incidence of cardiac death (3.5% vs. 1.0%, P = .048), stent thrombosis (2.5% vs. 0.5%, P = .044), target lesion revascularization (6.0% vs. 1.8%, P = .005), target vessel failure (15.5% vs. 8.0%, P < .001), target lesion failure (14.0% vs. 4.3%, P < .001), myocardial infarction (4.5% vs. 1.5%, P = .030), and major adverse cardiac events (12.5% vs. 5.0%, P = .001) at 2-year follow-up. However, the incidence of target vessel revascularization (7.5% vs. 5.5%, P = .340) was similar between DB and non-DB patients. Patients with DB (hazard ratio [HR] = 2.54, P = .001), older than 80 years (HR = 1.33, P = .027) with hypercholesterolemia (HR = 1.03, P < .001), serum creatinine >177 µmol/L (HR = 3.04, P = .011), a history of cerebral vascular accident (HR = 4.29, P = .010), or a history of myocardial infarction (HR = 31.4, P < .001) were more likely to experience adverse events. In China, DM could also be served as an independent predictor of adverse outcomes after DES implantation. These patients should be reexamined more frequently.