Department of Toxicology, School of Public Health, Medical College of Soochow University, Suzhou, Jiangsu 215123, China.
Department of Toxicology, School of Public Health, Medical College of Soochow University, Suzhou, Jiangsu 215123, China; Jiangsu Key Laboratory of Preventive and Translational Medicine for Geriatric Diseases, Soochow University, Suzhou, China.
Ecotoxicol Environ Saf. 2024 Apr 1;274:116232. doi: 10.1016/j.ecoenv.2024.116232. Epub 2024 Mar 16.
Fine particulate matter (PM) exposure is strongly associated with vascular endothelial senescence, a process implicated in cardiovascular diseases. While there is existing knowledge on the impact of Lycium barbarum polysaccharide (LBP) on vascular endothelial damage, the protective mechanism of LBP against PM-induced vascular endothelial senescence remains unclear. In this study, we investigated the impact of PM exposure on vascular endothelial senescence and explored the intervention effects of LBP in human umbilical vein endothelial cells (HUVECs). We found that PM exposure dose-dependently reduced cell viability and proliferation in HUVECs while increasing the production of reactive oxygen species (ROS), malondialdehyde (MDA), and hydrogen peroxide (HO). Additionally, PM exposure inhibited the activity of superoxide dismutase (SOD). Notably, PM exposure induced autophagy impairments and cellular senescence. However, LBP mitigated PM-induced cell damage. Further studies demonstrated that correcting autophagy impairment in HUVECs reduced the expression of the senescence markers P16 and P21 induced by PM. This suggests the regulatory role of autophagy in cellular senescence and the potential of LBP in improving HUVECs senescence. These findings provide novel insights into the mechanisms underlying PM-induced cardiovascular toxicity and highlight the potential of LBP as a therapeutic agent for improving vascular endothelial health.
细颗粒物（PM）暴露与血管内皮衰老密切相关，这是一种与心血管疾病有关的过程。虽然已有关于枸杞多糖（LBP）对血管内皮损伤影响的知识，但 LBP 对 PM 诱导的血管内皮衰老的保护机制尚不清楚。在这项研究中，我们研究了 PM 暴露对血管内皮衰老的影响，并探讨了 LBP 对人脐静脉内皮细胞（HUVEC）的干预作用。我们发现，PM 暴露以剂量依赖的方式降低了 HUVEC 的细胞活力和增殖能力，同时增加了活性氧（ROS）、丙二醛（MDA）和过氧化氢（HO）的产生。此外，PM 暴露抑制了超氧化物歧化酶（SOD）的活性。值得注意的是，PM 暴露诱导了自噬损伤和细胞衰老。然而，LBP 减轻了 PM 诱导的细胞损伤。进一步的研究表明，纠正 HUVEC 中的自噬损伤，降低了 PM 诱导的衰老标志物 P16 和 P21 的表达。这表明自噬在细胞衰老中的调节作用以及 LBP 改善 HUVEC 衰老的潜力。这些发现为 PM 诱导的心血管毒性的机制提供了新的见解，并强调了 LBP 作为改善血管内皮健康的治疗剂的潜力。
