Association between joint physical activity and healthy dietary patterns and hypertension in US adults: cross-sectional NHANES study.

BACKGROUND: Lack of physical activity (PA), poor dietary habits, or other unhealthy lifestyle behaviors are potential modifiable risk factors for hypertension. It has been sufficiently demonstrated in previous studies that physical activity or healthy dietary patterns can reduce the risk of hypertension. However, no research focused on the joint effects of PA and healthy dietary patterns on hypertension in a representative sample of adults. METHODS: We used data collected from the 2007-2018 National Health and Nutrition Examination Survey. Healthy dietary patterns were assessed with the Healthy Eating Index 2015 (HEI-2015), and PA was measured using the metabolic equivalent minutes per week reported in questionnaires. We created four lifestyle categories based on the HEI-2015 and PA: (1) unhealthy diet and physically inactive (less than recommended PA), (2) healthy diet but physically inactive, (3) unhealthy diet but physically active (recommended PA), (4) healthy diet and physically active. Logistic regression was used to evaluate the association between joint PA and HEI-2015 and hypertension. RESULTS: A total of 24,453 participants were enrolled in the study. Compared with unhealthy diet and physically inactive individuals, only healthy diet and physically active participants (adjusted odds ratio [AOR]: 0.77, 95% CI 0.65-0.9) were negatively associated with hypertension, while healthy diet but physically inactive participants (AOR: 0.89, 95% CI 0.76-1.03) and unhealthy diet but physically active participants (AOR: 0.9, 95% CI 0.76-1.06) were not associated with hypertension. CONCLUSION: In a representative sample of US adults, our findings suggest that individuals with recommended PA and healthy dietary patterns have a lower risk of hypertension than those with an unhealthy diet or less than recommended PA. Healthy eating habits and regular PA are potential preventive precautions against hypertension.

Transcriptome Profiles Reveal the Promoting Effects of Exogenous Melatonin on Fruit Softening of Chinese Plum.

In this study, we investigated the effect of exogenous melatonin (MT) on cell wall metabolism leading to Chinese plum (Prunus salicina Lindl.) fruit softening. Exogenous MT treatment increased the endogenous MT content in plum fruits before fruit ripening. However, in mature plum fruits, exogenous MT treatment decreased the fruit hardness, pulp hardness, fruit elasticity, contents of ion-bound pectin, covalently-bound pectin, hemicellulose, and cellulose, and activities of xyloglucan endotransglycosylase/hydrolase and endo-ß-1,4-glucanase, and increased the water-soluble pectin content, and activities of pectin methyl esterase, pectin lyase, polygalacturonase, ß-galactopyranosidase, and α-L-arabinofuranosidase. Transcriptome analysis revealed that the differentially expressed genes (DEGs) associated with cell wall metabolism in the exogenous MT-treated plum fruits were mainly enriched in the pentose and glucuronate interconversions, phenylpropanoid biosynthesis, cyanoamino acid metabolism, and galactose metabolism pathways. Analysis of these DEGs revealed that exogenous MT treatment affected the expression of genes regulating the cell wall metabolism. Overall, exogenous MT treatment promotes the fruit softening of Chinese plum.

Resveratrol Inhibits High Glucose-Induced H9c2 Cardiomyocyte Hypertrophy and Damage via RAGE-Dependent Inhibition of the NF-κB and TGF-ß1/Smad3 Pathways.

Hyperglycaemia is associated with the development of cardiac vascular disease. Resveratrol (RES) is a naturally occurring polyphenolic compound that possesses many biological properties, including anti-inflammatory properties and antioxidation functions. Our study aimed to explore the RES's protective roles on high glucose (HG)-induced H9c2 cells and the underlying mechanisms. Small-molecule inhibitors, western blotting (WB), as well as reverse-transcription PCR (RT-PCR) were employed to investigate the mechanisms underlying HG-induced damage in H9c2 cells. RES (40 µg/mL) treatment significantly alleviated HG-induced cardiac hypertrophy and cardiac dysfunction. RES abated the HG-induced increase in the levels of extracellular matrix (ECM) components and inflammatory cytokines, reducing ECM accumulation and inflammatory responses. Additionally, RES administration prevented HG-induced mitochondrion-mediated cardiac apoptosis of myocardial cells. In terms of mechanisms, we demonstrated that RES ameliorated the HG-induced overexpression of receptor for advanced glycation endproducts (RAGE) and downregulation of NF-κB signalling. Moreover, RES inhibited HG-induced cardiac fibrosis by inhibiting transforming growth factor beta 1 (TGF-ß1)/Smad3-mediated ECM synthesis in cultured H9c2 cardiomyocytes. Further studies revealed that the effects of RES against HG-induced upregulation of NF-κB and TGF-ß1/Smad3 pathways were similar to those of FPS-ZM1, a RAGE inhibitor. Collectively, the results implied that RES might help alleviate HG-induced cardiotoxicity via RAGE-dependent downregulation of the NF-κB and TGF-ß/Smad3 pathways. This study provided evidence that RES can be developed as a promising cardioprotective drug.