College of Medical Laboratory, Dalian Medical University, Dalian, 116044, Liaoning Province, People's Republic of China.
Department of Clinical Laboratory, Xinyi People's Hospital, Xinyi, 221400, Jiangsu Province, People's Republic of China.
Sci Rep. 2019 Mar 5;9(1):3495. doi: 10.1038/s41598-019-40204-6.
Epidemiological researches have demonstrated the relationship between PM exposure and increased morbidity and mortality of cardiovascular injury. However, no effective therapeutic method was established. The purpose of this study is to investigate the effect of acute PM exposure on the mice heart tissue and explore the therapeutic effects of compound essential oils (CEOs) in this model. In this study, after mice were exposed to PM intratracheally, some obvious histopathological changes as well as some great alterations of proinflammatory cytokines were observed in the heart tissue. The imbalance of oxidative stress, the altered Ca channel related proteins and the increased intracellular free Ca were all involved in the heart impairment and would also be investigated in this model. The CEOs alleviated the heart impairment via its antioxidant effect rather than its anti-inflammatory function because our results revealed that oxidative stress related indicators were restored after CEOs administration. At the same time, increased concentration of intracellular free Ca and ROS induced by PM were reduced after NAC (N-Acetyl-L-cysteine) administration. These data suggested that the acute PM exposure would damage heart tissue by inducing the inflammatory response, oxidative stress and intracellular free Ca overload. PM-induced oxidative stress probably increase intracellular free Ca via RYR2 and SERCA2a. CEOs have the potential to be a novel effective and convenient therapeutic method to prevent and treat the acute heart impairment induced by PM via its antioxidant function.
流行病学研究表明,PM 暴露与心血管损伤发病率和死亡率的增加之间存在关联。然而,目前尚未建立有效的治疗方法。本研究旨在探讨急性 PM 暴露对小鼠心脏组织的影响,并探索复方精油(CEOs)在该模型中的治疗效果。
在本研究中,通过气管内滴注 PM 使小鼠暴露于 PM 后,观察到心脏组织中出现明显的组织病理学变化和促炎细胞因子的大量改变。氧化应激失衡、钙通道相关蛋白改变以及细胞内游离钙增加都参与了心脏损伤,这在该模型中也将进行研究。
通过抗氧化作用而非抗炎作用,CEOs 缓解了心脏损伤,因为我们的研究结果表明,CEOs 给药后氧化应激相关指标得到了恢复。同时,NAC(N-乙酰-L-半胱氨酸)给药后,PM 诱导的细胞内游离 Ca 和 ROS 浓度增加得到了降低。这些数据表明,急性 PM 暴露通过诱导炎症反应、氧化应激和细胞内游离钙过载来损伤心脏组织。PM 诱导的氧化应激可能通过 RYR2 和 SERCA2a 增加细胞内游离 Ca。
CEOs 有可能通过其抗氧化功能成为一种预防和治疗 PM 诱导的急性心脏损伤的新型有效且方便的治疗方法。