The harmful effects of acute PM2.5 exposure to the heart and a novel preventive and therapeutic function of CEOs

• Published in: Scientific reports 2019-03, Vol.9 (1), p.3495, Article 3495
• Main Authors: Dong, Lu, Sun, Wenping, Li, Fasheng, Shi, Min, Meng, Xianzong, Wang, Chunyuan, Meng, Meiling, Tang, Wenqi, Liu, Hui, Wang, Lili, Song, Laiyu
• Format: Article
• Language: English
• Subjects: 13; 13/1; 13/31; 13/51; 64/60; 692/700/478; 704/172/4081; 82/80; 96/21; Acetylcysteine; Antioxidants; Ca2+-transporting ATPase; Calcium (intracellular); Cardiovascular diseases; Cytokines; Essential oils; Heart; Humanities and Social Sciences; Inflammation; Intracellular; Morbidity; multidisciplinary; Oxidative stress; Particulate matter; Reactive oxygen species; Ryanodine receptors; Science; Science (multidisciplinary)
• ISSN: 2045-2322; 2045-2322
• DOI: 10.1038/s41598-019-40204-6

Epidemiological researches have demonstrated the relationship between PM 2.5 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 2.5 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 2.5 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 2+ channel related proteins and the increased intracellular free Ca 2+ 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 2+ and ROS induced by PM 2.5 were reduced after NAC (N-Acetyl-L-cysteine) administration. These data suggested that the acute PM 2.5 exposure would damage heart tissue by inducing the inflammatory response, oxidative stress and intracellular free Ca 2+ overload. PM 2.5 -induced oxidative stress probably increase intracellular free Ca 2+ 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 2.5 via its antioxidant function.