0
Article ? AI-assigned paper type based on the abstract. Classification may not be perfect — flag errors using the feedback button. Tier 2 ? Original research — experimental, observational, or case-control study. Direct primary evidence. Detection Methods Human Health Effects Nanoplastics Remediation Sign in to save

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

Chemistry & Biodiversity 2025 3 citations ? Citation count from OpenAlex, updated daily. May differ slightly from the publisher's own count. Score: 58 ? 0–100 AI score estimating relevance to the microplastics field. Papers below 30 are filtered from public browse.
Junliang Chen, Ziqi Ren, Xiaodan Sun, Le Wang, Dan Liu, Xiangyu Cao, Yiqing Chen, Xiangyu Cao

Summary

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.

Polymers

Amino-modified polystyrene nanoplastics (NH2-NPs), generated through ultraviolet aging and photocatalytic processes, can lead to vascular damage. Baicalein is a flavonoid compound with anti-inflammatory properties that exerts a protective effect on blood vessels. However, whether baicalein can inhibit vascular damage induced by NH2-NPs remains to be investigated. In this study, cell viability assay, fluorescence staining observation, and western blot techniques were used to evaluate the mechanisms after NH2-NPs and baicalein exposure. The results showed that baicalein at concentrations of 12.5, 25, and 50 µM effectively inhibited the toxicity induced by NH2-NPs. Besides, baicalein reduced reactive oxygen species levels to 226.63 ± 25.65%, 168.13 ± 14.45%, and 124.70 ± 18.04% at 12.5, 25, and 50 µM, respectively. The results of Hoechst/propidium iodide (PI) staining showed that 50 µM baicalein reduced the PI-positive rate to 12.42 ± 1.16%. Additionally, co-incubation with baicalein significantly reduced the expression of proteins in the pyroptosis pathway, including NLRP3, Cleaved Caspase-1, ASC, and Gasdermin D, effectively inhibiting the activation of pyroptosis induced by NH2-NPs in human umbilical vein endothelial cells (HUVECs). This study elucidated the mechanism by which baicalein inhibited NH2-NPs-induced pyroptosis in HUVECs, providing a reference for the prevention of vascular injury and utilization of natural product resources.

Sign in to start a discussion.

More Papers Like This

Article Tier 2

Effects of Baicalein Pretreatment on the NLRP3/GSDMD Pyroptosis Pathway and Neuronal Injury in Pilocarpine-Induced Status Epilepticus in the Mice

This study tested whether baicalein pretreatment could protect against microplastic-induced neuroinflammation by blocking the NLRP3/GSDMD pyroptosis pathway. Baicalein suppressed pyroptotic cell death and reduced neuroinflammatory markers in exposed animals, suggesting a potential protective mechanism.

Article Tier 2

Polystyrene Microplastics Induce Injury to the Vascular Endothelial Through NLRP3 ‐Mediated Pyroptosis

Researchers found that polystyrene microplastics caused blood vessel damage in rats by triggering a type of inflammatory cell death called pyroptosis through the NLRP3 pathway. The microplastics activated this destructive immune response in the cells lining blood vessels, leading to inflammation and tissue injury. This study provides a specific mechanism by which microplastic exposure could contribute to cardiovascular disease in humans.

Article Tier 2

Hepatoprotective effects of astragalin against polystyrene microplastics induced hepatic damage in male albino rats by modulating Nrf-2/Keap-1 pathway

Researchers investigated whether astragalin, a natural plant compound, could protect against liver damage caused by polystyrene microplastics in rats. They found that microplastic exposure triggered oxidative stress and inflammation in the liver, but astragalin treatment restored antioxidant enzyme activity and reduced damage. The study suggests that natural compounds may help counteract some of the harmful effects microplastics have on liver health.

Article Tier 2

Evaluation of Possible Ameliorative Role of Robinetin to Counteract Polystyrene Microplastics Instigated Renal Toxicity in Rats

Researchers tested whether robinetin, a plant-derived compound, could protect rat kidneys from damage caused by polystyrene microplastic exposure. They found that microplastics caused significant kidney harm through oxidative stress, inflammation, and cell death, but robinetin supplementation substantially reversed these effects. The study suggests that natural antioxidant compounds may offer a protective strategy against microplastic-related organ damage.

Article Tier 2

Sinensetin mitigates polystyrene nanoplastics induced hepatotoxicity in albino rats: A biochemical and histopathological study

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.

Share this paper