Sudden cardiac death (SCD) is one of the most common causes of death in the world. Coronary heart disease (CHD) is the root cause of most patients with SCD, and myocardial infarction (MI) is the main cause of SCD among all types of CHD. Early identification of high-risk patients after an MI, and the application of related prevention strategies and disease-specific treatments will be the key to reduce SCD. The mechanism of SCD after MI varies over time, and the relevant risk prediction indicators are also dynamic and different. In the existing guidelines for MI patients, the static and slightly single stratification of primary (PP) and secondary (SP) prevention has significant room for improvement. The 1.5 primary prevention (1.5PP) is defined as patients with PP who also had the following risk factors: non-sustained ventricular tachycardia (NSVT), frequent premature ventricular contractions (PVCs), severe heart failure (left ventricular ejection fraction, LVEF <25%), and syncope or pre-syncope. The emergence of 1.5PP has provided a new method for the stratification and management of SCD after an MI.

Background and objective: Abnormal activation of Janus kinase 2 (JAK2) promotes the pathogenesis and progress of inflammatory bowel disease (IBD) by stimulating the cytokine traffic. Based on docking studies, arbutin, a natural product extracted from a traditional medicinal plant bearberry, was found to bind to JAK2. The study aimed to investigate the effects and mechanisms of regulating JAK2 by arbutin on colitis in mice.Methods: A mice colitis model was established to mimic human IBD. The mice freely drank water containing dextran sulfate sodium. Inflammation in epithelial (IEC6) and immune (RAW264.7) cells was analyzed following treatment with lipopolysaccharides (LPS).Results: Colitis symptoms, including body weight loss, increased disease activity index, and increased colon weight/length ratio, were significantly alleviated by arbutin. Mediators of colonic pro-inflammatory cytokines as well as apoptosis markers in colitis were suppressed by the glycoside. High expression of phosphorylated JAK2 in colitis was significantly reversed by arbutin. The effects of arbutin treatment on colitis were considerably inhibited by the JAK2 inhibitor AG490. LPS-induced inflammatory responses were also suppressed by arbutin, which was notably inhibited by the JAK2 inhibitor AG490.Conclusion: The findings obtained herein suggest the protective role of arbutin and provide novel insights into alternative colitis treatments, which involve inhibition of the JAK2 signaling pathway.