Theaflavin 3,3′‐digallate (TF3), is reported to protect cardiomyocytes from lipotoxicity and reperfusion injury. However, the role of TF3 in the protection of high‐glucose injury is still poorly understood. This study investigated the protective effects of TF3 on gap junctions and autophagy in neonatal cardiomyocytes (NRCMs). NRCMs preincubated with high glucose were coincubated with TF3. The expression of connexins and autophagy‐related proteins was determined. The functioning of gap‐junctional intercellular communication (GJIC) was measured by a dye transfer assay. Adenosine monophosphate‐activated protein kinase (AMPK) activity was determined by western blot. Moreover, AMPK was activated with aminoimidazole‐4‐carboxamide‐1‐β‐d‐ribofuranoside (AICAR) or inhibited by AMPKα small interfering RNA (siRNA) to explore the role of AMPK in the modulation of connexin 43 (Cx43) and autophagy. Meanwhile, autophagy was activated or blocked to observe the change in Cx43 expression. It was found that the protein expression of Cx43 and autophagy‐related proteins was increased in a TF3 dose‐ and time‐dependent manner under high glucose. TF3 also recovered the reduced GJIC function induced by high glucose concentrations. TF3 activated phosphorylated AMPK in a time‐dependent way. AMPKα siRNA abrogated the protection of TF3, while AICAR showed similar results compared to the TF3 treatment. Meanwhile, autophagy activation caused decreased Cx43, while cotreatment with baf A1 enhanced Cx43 expression further compared with the TF3 treatment alone under high glucose. We concluded that TF3 partly reversed the inhibition of Cx43 expression and autophagy induced by high glucose in NRCMs, partly by restoring AMPK activity. Inhibition of autophagy might be protective by preserving Cx43 expression in NRCMs stimulated by high glucose.

Background: Although coronary artery bypass graft (CABG) surgery is the main method to revascularize the occluded coronary vessels in coronary artery diseases, the full benefits of the operation are mitigated by ischemia-reperfusion (IR) injury. Although many studies have been devoted to reducing IR injury in animal models, the translation of this research into the clinical field has been disappointing. Our study aimed to explore the underlying hub genes and mechanisms of IR injury.Methods: A weighted gene co-expression network analysis (WGCNA) was executed based on the expression profiles in patients undergoing CABG surgery (GSE29396). Functional annotation and proteinprotein interaction (PPI) network construction were executed within the modules of interest. Potential hub genes were predicted, combining both intramodular connectivity (IC) and degrees. Meanwhile, potential transcription factors (TFs) and microRNAs (miRNAs) were predicted by corresponding bioinformatics tools.Results: A total of 336 differentially expressed genes (DEGs) were identified. DEGs were mainly enriched in neutrophil activity and immune response. Within the modules of interest, 5 upregulated hub genes (IL-6, CXCL8, IL-1β, MYC, PTGS-2) and 6 downregulated hub genes (C3, TIMP1, VSIG4, SERPING1, CD163, and HP) were predicted. Predicted miRNAs (hsa-miR-333-5p, hsa-miR-26b-5p, hsa-miR-124-3p, hsa-miR-16-5p, hsa-miR-98-5p, hsa-miR-17-5p, hsa-miR-93-5p) and TF (STAT1) might have regulated gene expression in the most positively related module, while hsa-miR-333-5p and HSF-1 were predicted to regulate the genes within the most negatively related module.Conclusions: Our study illustrates an overview of gene expression changes in human atrial samples from patients undergoing CABG surgery and might help translate future research into clinical work.

ObjectivesA lower relative handgrip strength (HGS) may disrupt metabolic homeostasis and then lead to metabolic syndrome (MetS). There is a paucity of longitudinal studies to examine whether relative HGS at baseline is linked to incident MetS. Thus, the purpose of the present study was to explore the association between relative HGS and new-onset MetS.DesignThis is an observational and longitudinal research.A nationally representative sample of population in China.ParticipantsA total of 3350 subjects without MetS were selected for analysis in the present study. Data are from the China Health and Retirement Longitudinal Study (2011–2015).Outcome measuresWe calculated the relative HGS by dividing the HGS by body weight. Participants were divided into gender-specific quartiles. We estimated HRs for MetS and its components using Cox proportional hazard models according to the relative HGS categories.ResultsAfter multiple adjustment, the risk of MetS increased with the lower quartile of relative HGS in both sexes. Using the highest quartile (Q4) as a reference, the HR for quartile Q3–1 was 1.49 (0.95, 2.34), 1.67 (1.08, 2.59) and 1.76 (1.12, 2.78), respectively, in men, and 1.14 (0.82, 1.58), 1.30 (1.02, 1.57) and 1.28 (1.03, 1.55), respectively, in women. Additionally, we observed that relative HGS was negatively or inversely associated with the risk of abdominal obesity in both sexes.ConclusionsThe current study demonstrated that relative HGS was inversely and independently associated with an increased risk of MetS and abdominal obesity, suggesting a possible role of relative HGS as a useful and simple index for muscle strength in the prediction of occurrence of MetS.