Effect of zinc nanoparticles seed priming and foliar application on the growth and physio-biochemical indices of spinach (Spinacia oleracea L.) under salt stress.

Salt stress is the major risk to the seed germination and plant growth via affecting physiological and biochemical activities in plants. Zinc nanoparticles (ZnNPs) are emerged as a key agent in regulating the tolerance mechanism in plants under environmental stresses. However, the tolerance mechanisms which are regulated by ZnNPs in plants are still not fully understood. Therefore, the observation was planned to explore the role of ZnNPs (applied as priming and foliar) in reducing the harmful influence of sodium chloride (NaCl) stress on the development of spinach (Spinacia oleracea L.) plants. Varying concentrations of ZnNPs (0.1%, 0.2% & 0.3%) were employed to the spinach as seed priming and foliar, under control as well as salt stress environment. The alleviation of stress was observed in ZnNPs-applied spinach plants grown under salt stress, with a reduced rise in the concentration hydrogen peroxide, melondialdehyde and anthocyanin contents. A clear decline in soluble proteins, chlorophyll contents, ascorbic acid, sugars, and total phenolic contents was observed in stressed conditions. Exogenous ZnNPs suppressed the NaCl generated reduction in biochemical traits, and progress of spinach plants. However, ZnNPs spray at 0.3% followed by priming was the most prominent treatment in the accumulation of osmolytes and the production of antioxidant molecules in plants.

Flavanone metabolites decrease monocyte adhesion to TNF-α-activated endothelial cells by modulating expression of atherosclerosis-related genes.

Flavanones are found specifically and abundantly in citrus fruits. Their beneficial effect on vascular function is well documented. However, little is known about their cellular and molecular mechanisms of action in vascular cells. The goal of the present study was to identify the impact of flavanone metabolites on endothelial cells and decipher the underlying molecular mechanisms of action. We investigated the impact of naringenin and hesperetin metabolites at 0·5, 2 and 10 µM on monocyte adhesion to TNF-α-activated human umbilical vein endothelial cells (HUVEC) and on gene expression. Except hesperetin-7-glucuronide and naringenin-7-glucuronide (N7G), when present at 2 µM, flavanone metabolites (hesperetin-3'-sulphate, hesperetin-3'-glucuronide and naringenin-4'-glucuronide (N4'G)) significantly attenuated monocyte adhesion to TNF-α-activated HUVEC. Exposure of both monocytes and HUVEC to N4'G and N7G at 2 µM resulted in a higher inhibitory effect on monocyte adhesion. Gene expression analysis, using TaqMan Low-Density Array, revealed that flavanone metabolites modulated the expression of genes involved in atherogenesis, such as those involved in inflammation, cell adhesion and cytoskeletal organisation. In conclusion, physiologically relevant concentrations of flavanone metabolites reduce monocyte adhesion to TNF-α-stimulated endothelial cells by affecting the expression of related genes. This provides a potential explanation for the vasculoprotective effects of flavanones.