Liver injury induced in Balb/c mice by PM2.5 exposure and its alleviation by compound essential oils.

Accumulating evidence has suggested a strong link between exposure to air pollution and public health. In particular, inhaled airborne particulate matter <2.5 μm in aerodynamic diameter (PM2.5) can rapidly diffuse from the lungs to the systemic blood circulation and accumulate in the liver. In this study, we used a Balb/c mouse model to investigate liver injury caused by PM2.5 inhalation and the anti-inflammatory and antioxidant effects of compound essential oils (CEOs) in alleviating the extent of this injury. The results of serum biochemical and histopathological analyses showed that PM2.5 exposure induced inflammatory liver injury, meantime CEOs pretreatment attenuated PM2.5-induced liver inflammatory injury. Western blot and qRT-PCR assays showed that PM2.5 increased secretion of cytokines, however CEOs suppressed the production of IL-6 and TNF-α. Furthermore, heme oxygenase-1(HO-1) and superoxide dismutase-1(SOD-1) expression levels showed that PM2.5 could trigger oxidative stress-mediated liver injury, whereas CEOs pretreatment might protect against PM2.5-induced liver injury through regulation of the antioxidant system. Molecular analysis showed that the expression of TLR4, a protein which plays a key role in liver health and injury. Results showed that TLR4 was promoted by PM2.5 but inhibited by CEOs pretreatment in PM2.5-induced inflammatory liver injury. In addition, PM2.5-promoted secretion of cytokines by activating TLR4/MyD88 pathway, whereas CEOs might alleviate this type of liver inflammation inhibiting the activation of TLR4/MyD88 signaling pathway.