We can't find the internet
Attempting to reconnect
Something went wrong!
Hang in there while we get back on track
Ginsenoside Rh1 ameliorates polystyrene nanoplastics-caused vascular injury by regulating HSP70 to suppress endoplasmic reticulum stress and pyroptosis.
AI summary Read the abstract
Tiny plastic particles called nanoplastics—the kind increasingly found in our environment and bodies—can damage the cells lining our blood vessels, potentially contributing to heart disease. In this study on cells and animals, researchers found that a natural compound from ginseng called Rh1 helped protect blood vessels from this plastic-induced damage by calming down stress responses and inflammation inside cells. While these are early lab and animal findings rather than proof it works in humans, the research points to a promising natural approach for protecting cardiovascular health against everyday plastic pollution exposure.
INTRODUCTION: The vascular toxicity of polystyrene nanoparticles (PS-Nps) via the circulatory system has emerged as novel critical health risk factors. However, the specific mechanisms underlying PS-Nps-induced vascular endothelial injury and corresponding protective strategies remain poorly understood. OBJECTIVES: This work seeks to assess the vascular toxicity of PS-Nps and the function and mechanism of rare ginsenoside Rh1 derived from ginseng in alleviating vascular endothelial injury caused by PS-Nps. METHODS: To dissect the protective mechanisms of Rh1 against PS-Nps-triggered vascular endothelial injury across in vitro and in vivo models, we employed an integrated approach including western blot, immunofluorescence, histopathological staining, siRNA-mediated gene silencing, molecular docking, molecular dynamics simulations, co-immunoprecipitation (Co-IP), surface plasmon resonance (SPR) and cellular thermal shift assay (CETSA). Furthermore, transcriptome sequencing (RNA-seq) was performed to validate the key regulatory pathways involved. RESULTS: Rh1 inhibited the caspase-1-dependent pyroptosis pathway and NLRP3 inflammasome activation. Importantly, Rh1 exerted its endothelial protective effects by targeting HSP70, thereby suppressing NF-κB p65 nuclear translocation and downregulating endoplasmic reticulum stress (ERS) signaling via GRP78-ATF4-CHOP. Moreover, we further verified that Rh1 effectively alleviates atherosclerosis, reinforcing its translational value in classical cardiovascular disease settings. CONCLUSION: This research provides the first comprehensive investigation of the protective efficacy of ginsenoside Rh1 for preventing cardiovascular damage induced by the new environmental pollutant PS-Nps. This study provides an innovative theoretical basis for the prevention of cardiovascular diseases related to environmental pollutants by ginseng.
More Papers Like This
Intravenous Exposure to Amino-polystyrene Induces Excessive Autophagy and Apoptosis in Myocardium Through ROS Driven PI3K/AKT/mTOR Axis
AI summary Read the abstract
Scientists injected mice with tiny plastic particles similar to those that could come from medical devices touching your blood, and found that a specific type, positively charged nanoplastics, damaged heart cells by causing stress that triggers cell death. The good news: antioxidant compounds like NAC and ginsenoside Rb1 reversed much of the damage, hinting at possible protective treatments as we learn more about plastic exposure risks.
Baicalein Inhibited Amino‐modified Polystyrene Nanoplastics Induced Human Umbilical Vein Endothelial Cells Pyroptosis by Reducing the Expression of NLRP3/Caspase‐1/Gasdermin D Pathway‐related Proteins
AI summary Read the abstract
Researchers tested whether baicalein, a natural plant compound with anti-inflammatory properties, could protect blood vessel cells from damage caused by nanoplastics. They found that baicalein significantly reduced the inflammatory cell death triggered by amino-modified polystyrene nanoplastics by blocking a key inflammatory pathway. The study suggests that natural anti-inflammatory compounds may help mitigate some of the vascular damage associated with nanoplastic exposure.
Attenuative Effects of Ginkgetin Against Polystyrene Microplastics-Induced Renal Toxicity in Rats
AI summary Read the abstract
Researchers found that ginkgetin, a natural flavonoid, significantly reduced polystyrene microplastic-induced kidney damage in rats by restoring antioxidant enzyme activity and reducing oxidative stress and inflammation markers.
Palliative potential of robinetin to avert polystyrene microplastics instigated pulmonary toxicity in rats
AI summary Read the abstract
Researchers investigated whether the flavonoid compound robinetin could protect against lung damage caused by polystyrene microplastic exposure in rats. They found that robinetin supplementation reduced oxidative stress markers and inflammatory responses in lung tissue that had been damaged by microplastic ingestion. The study suggests that certain natural compounds may help mitigate some of the harmful effects of microplastic exposure on respiratory tissues.
Sinensetin mitigates polystyrene nanoplastics induced hepatotoxicity in albino rats: A biochemical and histopathological study
AI summary Read the abstract
Exposure to polystyrene nanoplastics caused significant liver damage in rats, including oxidative stress, inflammation, and cell death, along with elevated liver enzymes that are markers of liver injury in clinical settings. Treatment with sinensetin — a natural plant flavonoid — substantially reversed these effects, restoring antioxidant enzyme activity and reducing inflammatory markers. The findings establish a potential protective role for natural compounds against nanoplastic-induced organ toxicity and illuminate the mechanisms by which nanoplastics harm the liver.
Research digests by email
When a large batch of papers lands in the Atlas, we read through it and send a short write-up of what stood out.