Key Laboratory of Natural Medicine and Immuno-Engineering, Henan University, Kaifeng, Henan Province, PR China.
Key Laboratory of Natural Medicine and Immuno-Engineering, Henan University, Kaifeng, Henan Province, PR China; Biology Institute, Qilu University of Technology (Shandong Academy of Sciences), Jinan, Shandong Province, PR China.
Chemosphere. 2020 Jul;250:126288. doi: 10.1016/j.chemosphere.2020.126288. Epub 2020 Feb 22.
Particulate matter (PM10) is one of the most important indicators of the pollution that characterizes air quality. Epidemiological studies have shown that PM10 can cause cardiovascular-related diseases in the population. And, we studied the developmental toxicity of PM10 and the underlying mechanism of its effects on the cardiovascular system of zebrafish embryo/larva. Changes in cardiac morphology, sinus venosus and bulbus arteriosus (SV-BA) distance, heart rate, vascular subintestinalis, blood flow, returned blood volume, and reactive oxygen species (ROS) level were measured, and changes in the expression levels of certain genes were assessed via RT-PCR. The results showed that PM10 caused a significant increase in pericardial sac area and SV-BA distance, a decrease in heart rate, inhibition of vascular subintestinalis growth, blood flow obstruction, reduced venous return, and other cardiovascular toxicities. PM10 induced an increase in the ROS level and significant increases in the expression levels of ERS signalling pathway factors and Nrf2 signalling pathway factors. The expression levels of the Wnt pathway-related genes also showed significant changes. Furthermore, ROS inhibitor N-Acetyl-l-cysteine (NAC) could ameliorate the cardiovascular toxicity of PM10 in zebrafish larvae. It is speculated that PM10 may result in cardiovascular toxicity by inducing higher ROS levels in the body, which could then induce ERS and lead to defects in the expression of genes related to the Wnt signalling pathway. The Nrf2 signalling pathway was activated as a stress compensatory mechanism during the early stage of PM10-induced cardiovascular injury. However, it was insufficient to counteract the PM10-induced cardiovascular toxicity.
颗粒物 (PM10) 是空气质量污染的最重要指标之一。流行病学研究表明，PM10 可导致人群心血管相关疾病。本研究探讨了 PM10 的发育毒性及其对斑马鱼胚胎/幼鱼心血管系统影响的潜在机制。我们测量了心脏形态、窦房结和动脉干 (SV-BA) 距离、心率、血管下肠系膜、血流、回流血量和活性氧 (ROS) 水平的变化，并通过 RT-PCR 评估了某些基因表达水平的变化。结果表明，PM10 可导致心包囊面积和 SV-BA 距离显著增加、心率降低、血管下肠系膜生长抑制、血流阻塞、静脉回流量减少等心血管毒性。PM10 可诱导 ROS 水平升高以及 ERS 信号通路因子和 Nrf2 信号通路因子表达水平显著增加。Wnt 通路相关基因的表达水平也发生了显著变化。此外，ROS 抑制剂 N-乙酰-L-半胱氨酸 (NAC) 可改善 PM10 对斑马鱼幼鱼的心血管毒性。推测 PM10 可能通过诱导体内更高的 ROS 水平导致心血管毒性，从而诱导 ERS 并导致与 Wnt 信号通路相关基因的表达缺陷。Nrf2 信号通路在 PM10 诱导的心血管损伤早期被激活作为应激补偿机制，但不足以对抗 PM10 诱导的心血管毒性。
