ObjectiveTo explore the vascular endothelial injury in male mice caused by exposure to polystyrene microplastics （PS-MPs） and the intervention effect of luteolin on vascular remodeling. Additionally， to investigate the mechanism through the oxidative system and metabolomics. MethodsThirty-two C57BL/6 mice （6-8 weeks old） were randomly divided into the saline group （saline group）， the 0.1 mg/kg PS-MPs exposure group （0.1PS-MPs group）， the 1 mg/kg PS-MPs exposure group （1PS-MPs group）， and the 1 mg/kg PS-MPs + luteolin treatment group （1PS-MPs + Lut group）， with 8 mice in each group. After 8 weeks of intervention， the body weight， blood pressure， aortic organ coefficient， and aortic histopathological changes of mice in each group were detected； the total cholesterol （TC）， triglyceride （TG）， and high-density lipoprotein cholesterol （HDL-C） lipid metabolism-related indicators in the aorta of mice were detected； the reactive oxygen species （ROS）， glutathione （GSH）， and malondialdehyde （MDA） oxidative stress-related indicators were detected； the endothelin （ET-1）， nitric oxide （NO）， vascular endothelial growth factor A （VEGF-A）， vascular cell adhesion molecule-1 （VCAM-1/CD106）， and intercellular adhesion molecule-1 （ICAM-1/CD54） endothelial function-related indicators and serum metabolomics were detected. ResultsCompared to the saline group， exposure to PS-MPs resulted in pathological thickening of the mouse aorta， increased aortic organ coefficient， and elevated blood pressure. Lipid metabolism-related indicators， including TC and TG， were elevated， while HDL-C was reduced， indicating lipid metabolism disorder in mice. Oxidative stress markers such as ROS and MDA increased， whereas GSH decreased， demonstrating oxidative damage. Vascular endothelial inflammation and injury markers， including ET-1， VEGF-A， VCAM-1， and ICAM-1， were upregulated， while the vasodilatory substance NO was downregulated， confirming endothelial injury. Furthermore， serum metabolomics results revealed that PS-MPs exposure induced endothelial damage by disrupting metabolic pathways such as the citrate cycle. Compared to the PS-MPs group， luteolin significantly reversed these effects， attenuating oxidative stress and lipid metabolism disorders， and effectively repairing endothelial injury. ConclusionPS-MPs induce vascular toxicity through oxidative stress and lipid metabolism. Luteolin effectively alleviates endothelial damage and vascular remodeling.

Granulocytic myeloid-derived suppressor cells(G-MDSCs)are the principal subsets of myeloid-derived suppressor cells(MDSCs),which involved in development and progression of a variety of tumor and non-tumor diseases.G-MDSCs mediated disfunction of immune effector cells(such as T cells and NK cells)through producing Arg-1,ROS,iNOS,etc.is major cause of its immunosuppressive function.To date,a large number of studies have focused on tumor-promoting effects of G-MDSCs.However,their complex immunomodulatory functions,especially their positive effects in diseases such as autoimmune arthritis,are often overlooked.Besides,G-MDSCs share the same origin and phenotype with neutrophils,but their immune functions are heterogeneous.Therefore,precision of G-MDSCs targeted therapy will be largely improved if the two can be accurately distinguished,though this field is still under exploration.At present,there are abundant experimental studies on G-MDSCs at home and abroad,mainly in tumors,but there are no domestic reports on the immunomodulatory function of G-MDSCs in tumors and non-tumor diseases.Therefore,in this review,we summarizes the different roles played by G-MDSCs in tumor and non-tumor diseases,in order to reveal the important and complex functions of G-MDSCs in immune regulation.

Granulocytic myeloid-derived suppressor cells(G-MDSCs)are the principal subsets of myeloid-derived suppressor cells(MDSCs),which involved in development and progression of a variety of tumor and non-tumor diseases.G-MDSCs mediated disfunction of immune effector cells(such as T cells and NK cells)through producing Arg-1,ROS,iNOS,etc.is major cause of its immunosuppressive function.To date,a large number of studies have focused on tumor-promoting effects of G-MDSCs.However,their complex immunomodulatory functions,especially their positive effects in diseases such as autoimmune arthritis,are often overlooked.Besides,G-MDSCs share the same origin and phenotype with neutrophils,but their immune functions are heterogeneous.Therefore,precision of G-MDSCs targeted therapy will be largely improved if the two can be accurately distinguished,though this field is still under exploration.At present,there are abundant experimental studies on G-MDSCs at home and abroad,mainly in tumors,but there are no domestic reports on the immunomodulatory function of G-MDSCs in tumors and non-tumor diseases.Therefore,in this review,we summarizes the different roles played by G-MDSCs in tumor and non-tumor diseases,in order to reveal the important and complex functions of G-MDSCs in immune regulation.