7-hydroxyflavone and Inflammation

Inflammation is the primary pathological process of myocardial ischemia/reperfusion injury (MI/RI). 7-Hydroxyflavone (HF), a natural flavonoid with a variety of bioactivities, plays a crucial role in various biological processes. However, its cardioprotective effects and the underlying mechanisms of MI/RI have not been investigated. This study aimed to explore whether pretreatment with HF could attenuate MI/RI-induced inflammation in rats and investigate its potential mechanisms. The results showed that pretreatment with HF could significantly improve the anatomic data and electrocardiograph parameters, reduce the myocardial infarct size, decrease markers of myocardial injury (aspartate transaminase, creatine kinase, lactate dehydrogenase, and cardiac troponin I), inhibit inflammatory cytokines (IL-1β, IL-6, and TNF-α), suppress oxidative stress, and recover the architecture of the cardiomyocytes. The cardioprotective effect of HF was connected with the regulation of the MAPK/NF-κB signaling pathway. What is more, molecular docking was carried out to prove that HF could be stably combined with p38, ERK1/2, JNK, and NF-κB. In summary, this is a novel study demonstrating the cardioprotective effects of HF against MI/RI in vivo. Consequently, these results demonstrate that HF can be considered a promising potential therapy for MI/RI.

Topics: Animals; Apoptosis; Flavonoids; Inflammation; Molecular Docking Simulation; Myocardial Reperfusion Injury; NF-kappa B; Rats; Rats, Sprague-Dawley

Flavonoids are a class of compounds that having the benzo-γ-pyrone skeleton, which possess anti-inflammatory properties in vitro and in vivo. The aim of this study was to investigate the inhibition of two flavonoids 7-hydroxyflavone (HF) and 7,8-dihydroxyflavone (DHF) on the production of pro-inflammatory mediators in RAW264.7 cells activated by lipopolysaccharides (LPS).. For this purpose, we selected four pro-inflammatory mediators including nitric oxide (NO), prostaglandin E. In this regard, we showed that HF and DHF dose-dependently reduced the production of NO, PGE. Consider together, these findings suggest that DHF and HF can inhibit LPS-induced inflammation via attenuating the production of NO, PGE

Topics: Animals; Anti-Inflammatory Agents; Dinoprostone; Dose-Response Relationship, Drug; Down-Regulation; Flavones; Flavonoids; Inflammation; Inflammation Mediators; Interleukin-6; Lipopolysaccharides; Mice; Nitric Oxide; Nitric Oxide Synthase Type II; RAW 264.7 Cells; RNA, Messenger; Tumor Necrosis Factor-alpha

This protocol describes microsphere-based protease assays for use in flow cytometry and high-throughput screening. This platform measures a loss of fluorescence from the surface of a microsphere due to the cleavage of an attached fluorescent protease substrate by a suitable protease enzyme. The assay format can be adapted to any site or protein-specific protease of interest and results can be measured in both real time and as endpoint fluorescence assays on a flow cytometer. Endpoint assays are easily adapted to microplate format for flow cytometry high-throughput analysis and inhibitor screening.

Topics: Animals; Biotinylation; Flow Cytometry; Fluorescence Resonance Energy Transfer; Green Fluorescent Proteins; High-Throughput Screening Assays; Humans; Inflammation; Kinetics; Microspheres; Peptide Hydrolases; Peptides; Reproducibility of Results; Temperature