Guangdong Key Laboratory of Environmental Catalysis and Health Risk Control, Guangdong-Hong Kong-Macao Joint Laboratory for Contaminants Exposure and Health, School of Environmental Science and Engineering, University of Technology, Guangzhou 510006, PR China.
State Key Laboratory of Environmental and Biological Analysis, Department of Chemistry, Hong Kong Baptist University, Hong Kong, China.
Sci Total Environ. 2021 Aug 15;782:146866. doi: 10.1016/j.scitotenv.2021.146866. Epub 2021 Apr 5.
Ambient PM has been proved to be an independent risk factor for cardiovascular diseases; however, little information is available on the age-dependent effects of PM on the cardiovascular system and the underlying mechanisms following chronic exposure. In this study, multi-aged mice were exposed to PM via the newly developed real-ambient PM exposure system to investigate age-related effects on the heart after long-term exposure. First, the chemical and physical properties of PM used in the exposure system were analyzed. The heart rate of conscious mice was recorded, and results showed that exposure of aged mice to PM for 26 weeks significantly increased heart rate. Histological analysis and ELISA assays indicated that aged mice were more sensitive to PM exposure in terms of inducing cardiac oxidative stress and inflammation. Furthermore, untargeted metabolomics revealed that taurine was involved with the PM-induced cardiac dysfunction. The reduced taurine concentration in the heart was examined by LC-MS and imaging mass spectrometry; it may be due to the increased p53 expression level, ROS and inflammatory cytokines. These results emphasize the age-dependent effects of PM on the cardiovascular system and suggest that taurine may be the novel cardiac effect target for PM-induced heart dysfunction in the aged.
环境 PM 已被证明是心血管疾病的独立危险因素；然而，关于 PM 对心血管系统的年龄依赖性影响以及长期暴露后的潜在机制的信息很少。在这项研究中，多龄小鼠通过新开发的真实环境 PM 暴露系统暴露于 PM 中，以研究长期暴露后心脏的年龄相关性影响。首先，分析了暴露系统中使用的 PM 的化学和物理性质。记录了清醒小鼠的心率，结果表明，暴露于 PM 26 周的老年小鼠的心率显著增加。组织学分析和 ELISA 检测表明，老年小鼠对 PM 暴露诱导的心脏氧化应激和炎症更敏感。此外，非靶向代谢组学表明牛磺酸参与了 PM 诱导的心脏功能障碍。通过 LC-MS 和成像质谱法检测到心脏中牛磺酸浓度降低；这可能是由于 p53 表达水平、ROS 和炎症细胞因子增加所致。这些结果强调了 PM 对心血管系统的年龄依赖性影响，并表明牛磺酸可能是 PM 诱导的老年人心力衰竭的新型心脏效应靶标。
