Dendrobine has potential advantages in suppressing atherosclerosis (AS). FK506‐binding protein 1A (FKBP1A) is implicated in the regulation of autophagy, inflammation, and apoptosis. To reveal the mechanism by which dendrobine inhibits AS by modulating autophagy, oxidative stress, apoptosis, and senescence. An in vitro AS cell model was induced by culturing human umbilical vein endothelial cells (HUVECs) with oxidized low‐density lipoprotein (ox‐LDL). The cells were treated with dendrobine alone or in combination with short hairpin RNA (shRNA) targeting FKBP1A or together with 3‐methyladenine (3MA), an autophagy inhibitor. Inflammatory cytokines levels tumor necrosis factor‐α, interleukin‐6 (IL‐6), and IL‐1β were analyzed and oxidative stress levels were detected by the analysis of reactive oxygen species, malondialdehyde, and superoxide dismutase levels, followed by the analysis of apoptosis levels through terminal deoxynucleotidyl transferase dUTP nick end labeling staining. Cell senescence was evaluated by senescence‐associated β‐galactosidase and light chain 3 (LC3) levels were detected by immunofluorescence (IF) staining. The targeting relationship of dendrobine and FKBP1A was predicted by SwissTarget, PyMol, Autodock, and Open Babel software. Dendrobine reduced the levels of proinflammation factors, oxidative stress levels, apoptosis levels, and senescence phenotype in ox‐LDL‐induced HUVECs. Besides, cell viability has an opposite change. Furthermore, there was an increase in LC3 IF tensity, and LC3‐II/I and Beclin1 expressions, and a decrease in p62 expression. However, these effects of dendrobine could be markedly destroyed by shRNA silencing FKBP1A and 3MA. Dendrobine can suppress inflammatory responses, oxidative stress, apoptosis, and senescence via FKBP1A‐involved autophagy ox‐LDL‐treated HUVECs.

ObjectivesTo assess the associations of lactate level or lactate clearance at different time points with in-hospital mortality in critically ill patients with acute myocardial infarction (AMI).DesignA cohort study.SettingThe Medical Information Mart for Intensive Care III database.Participant490 AMI patients.InterventionNone.Primary and secondary outcome measuresIn-hospital mortality of patients.ResultsIn total, 120 (24.49%) patients died at the end of follow-up. After adjusting for confounders, increased risk of in-hospital mortality in patients with AMI was observed in those with high lactate level (24 hours) (HR=1.156, 95%CI: 1.002 to 1.333). Increased lactate clearance (24 hours) was correlated with a decreased risk of in-hospital mortality in patients with AMI (HR=0.995, 95% CI: 0.994 to 0.997). The area under the curves (AUCs) of lactate level (24 hours) and lactate clearance (24 hours) were 0.689 (95% CI: 0.655 to 0.723) and 0.672 (95% CI: 0.637 to 0.706), respectively. The AUC of lactate level (24 hours) and lactate clearance (24 hours) was higher than lactate level (baseline).ConclusionsIncreased lactate level (24 hours) was associated with an elevated risk of in-hospital mortality in patients with AMI and increased lactate clearance (24 hours) was correlated with a decreased risk of in-hospital mortality in patients with AMI despite the age and genders.