F-53B stimulated vascular smooth muscle cell phenotypic switch and vascular remodeling via ferroptosis-related pathway.

The compound 6:2 chlorinated polyfluorinated ether sulfonate (F53B), an alternative to perfluorooctane sulfonate (PFOS), has been widely utilized in China. Although the connection between the exposure and toxicity of F53B is established, the role and mechanisms of the compound in promoting vascular remodeling are yet to be elucidated. Thus, the present study investigated the impact of F53B on the function of vascular smooth muscle cells (VSMCs) and vascular remodeling.

Polystyrene nanoplastics induce vascular stenosis via regulation of the PIWI-interacting RNA expression profile.

Nanoplastics (NPs) have become common worldwide and attracted increasing attention due to their serious toxic effects. Owing to their higher surface area and volume ratios and ability to easily enter tissues, NPs impose more serious toxic effects than microplastics. However, the effect of NP exposure on vascular stenosis remains unclear.

A novel tiRNA-Glu-CTC induces nanoplastics accelerated vascular smooth muscle cell phenotypic switching and vascular injury through mitochondrial damage.

Nanoplastics pose several health hazards, especially vascular toxicity. Transfer RNA-derived small RNAs (tsRNAs) are novel noncoding RNAs associated with different pathological processes. However, their biological roles and mechanisms in aberrant vascular smooth muscle cell (VSMC) plasticity and vascular injury are unclear.

Effects of seed size and bract of on germination and seedling growth under drought stress.

Drought is a crucial factor affecting seed germination and seedling growth of desert plants. In the study, we examined the effects of seed size (large, small) and bract (without bracts, with bracts) on seed germination and seedling growth of , a perennial super xerophyte semi-shrub, under different drought levels (0, 100, 200, 300 and 400 g·L PEG6000). The results showed that drought stress significantly inhibited seed germination and reduced shoot length of seedlings.

Analysis of the risk factors for contrast-induced nephropathy in over-aged patients receiving coronary intervention.

Contrast-induced nephropathy has been the common cause of hospital-acquired acute kidney injury in the elderly patients. This study aimed to analyze the risk factors for contrast-induced nephropathy in over-aged patients undergoing coronary angiography or percutaneous coronary intervention. A total of 470 over-aged patients (≥80 years old) were judged as the contrast-induced nephropathy group ( n = 46) and non-contrast-induced nephropathy group ( n = 424) according to the postoperative 48-h serum creatinine levels.

Allicin Decreases Lipopolysaccharide-Induced Oxidative Stress and Inflammation in Human Umbilical Vein Endothelial Cells through Suppression of Mitochondrial Dysfunction and Activation of Nrf2.

Background: Allicin, a major component of garlic, is regarded as a cardioprotective agent and is associated with increased endothelial function.

Methods: The effects of allicin on lipopolysaccharide (LPS)-induced vascular oxidative stress and inflammation in cultured human umbilical vein endothelial cells (HUVECs) and the mechanisms underlying these effects were studied. The protective effects were measured using cell viability, a lactate dehydrogenase (LDH) assay and cell apoptosis as indicators, and the anti-oxidative activity was determined by measuring reactive oxygen species (ROS) generation, oxidative products and endogenous antioxidant enzyme activities.

Epigallocatechin-3-gallate attenuates microcystin-LR induced oxidative stress and inflammation in human umbilical vein endothelial cells.

Epigallocatechin-3-gallate (EGCG) has been shown to possess anti-inflammatory effects. Microcystin-LR (MC-LR) is a potent toxin and our past research suggested that it also mediated human umbilical vein endothelial cell (HUVEC) injury. The aim of this study was to investigate the effects of EGCG on MC-LR-induced oxidative stress and inflammatory responses in HUVECs.