Angelicin, a furocoumarin found in Psoralea corylifolia L. fruit, has been reported to have anti-inflammatory activity. The purpose of this study was to determine the protective effects of angelicin on allergic asthma induced by ovalbumin (OVA) in mice. Mice were sensitized to OVA (on days 0 and 14) and challenged with OVA three times (on days 21 to 23). Angelicin (2.5, 5, 10 mg/kg) was given intraperitoneally 1 h before OVA treatment after the initial OVA sensitization. The production of IL-4, IL-5, and IL-13 in BALF and IgE in the serum were measured by ELISA. Lung histological changes were detected by using hematoxylin and eosin (H&E) stain. The results showed that angelicin significantly inhibited inflammatory cells infiltration into the lungs. Histological studies showed that angelicin significantly attenuated OVA-induced lung injury. Meanwhile, treatment of angelicin dose-dependently inhibited OVA-induced the production of IL-4, IL-5, and IL-13 in BALF and IgE in the serum. Furthermore, angelicin was found to inhibit airway hyperresponsiveness and NF-kB activation. In conclusion, our results suggested that angelicin inhibited allergic airway inflammation and hyperresponsiveness by inhibiting NF-kB activation.

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Background Catechin protects heart from myocardial ischaemia/reperfusion (MI/R) injury. However, whether catechin inhibits H/R‐induced myocardial cell apoptosis is largely unknown. Objective This study aims to investigate the underlying mechanism of catechin in inhibiting the apoptosis of H/R‐induced myocardial cells. Methods LncRNA MIAT expression was detected by qRT‐PCR. Cell viability of H9C2 cells was detected using CCK‐8 assay. The apoptosis of H9C2 cells was detected by flow cytometry. The interaction between CREB and MIAT promoter regions was confirmed by dual‐luciferase reporter gene assay and ChIP assay. Results In MI/R rats, catechin improved heart function and down‐regulated lncRNA MIAT expression in myocardial tissue. In H/R‐induced H9C2 cells, catechin protected against cell apoptosis, and lncRNA MIAT overexpression attenuated this protective effect of catechin. We confirmed that transcription factor CREB could bind to MIAT promoter region, and catechin suppressed lncRNA MIAT expression through up‐regulating CREB. Catechin improved mitochondrial function and relieved apoptosis through promoting Akt/Gsk‐3β activation. In addition, MIAT inhibited Akt/Gsk‐3β activation and promoted cell apoptosis in H/R‐induced H9C2 cells. Finally, we found catechin promoted Akt/Gsk‐3β activation through inhibiting MIAT expression in H/R‐induced H9C2 cells. Conclusion Catechin relieved H/R‐induced myocardial cell apoptosis through regulating CREB/lncRNA MIAT/Akt/Gsk‐3β pathway.

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Cardiac fibroblasts (CFs) could be activated after myocardial infarction (MI). Thus, it is necessary to explore effective drugs to suppress the activation of CFs following MI. This study was designed to investigate the impacts of ellagic acid on CFs and the underlying mechanisms. The expression of histone deacetylases (HDACs) and fibrosis-related genes was detected by qRT-PCR and western blot. The Masson's Trichrome Staining assay was used to evaluate the area of cardiac fibrosis. The proliferation and migration of CFs were measured by CCK8 Kit and Transwell assay, respectively. Our results showed that ellagic acid significantly reduced protein expression of HDAC1, mRNA expression of collagen I, collagen III, MMP-2 and MMP-9 and the area of cardiac fibrosis in MI rats. In Ang II-stimulated CFs, ellagic acid (60 μmol/L) decreased the protein expression of HDAC1, collagen I, collagen III, MMP-2 and MMP-9, and inhibited cell proliferation and migration. Further, HDAC1 over-expression reversed the inhibitor effects of ellagic acid on proteins expression (collagen I, collagen III, MMP-2 and MMP-9) and proliferation and migration of CFs. The present results suggested that ellagic acid suppressed proliferation and migration of CFs by down-regulating expression of HDAC1.

Although the mechanism of sudden cardiac death (SCD) in heart failure is not completely known, genetic variations are known to play key roles in this process. Increasing numbers of mutations and variants are being discovered through genome-wide association studies. The genetic variations involved in the mechanisms of SCD have aroused widespread concern. Comprehensive understanding of the genetic variations involved in SCD may help prevent it. To this end, we briefly reviewed the genetic variations involved in SCD and their associations and interactions, and observed that cardiac ion channels are the core molecules involved in this process. Genetic variations involved in cardiac structure, cardiogenesis and development, cell division and differentiation, and DNA replication and transcription are all speculated to be loci involved in SCD. Additionally, the systems involved in neurohumoral regulation as well as substance and energy metabolism are also potentially responsible for susceptibility to SCD. They form an elaborate network and mutually interact with each other to govern the fate of SCD-susceptible individuals.