Liver injury induced in Balb/c mice by PM_2.5 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 (PM_2.5) 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 PM_2.5 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 PM_2.5 exposure induced inflammatory liver injury, meantime CEOs pretreatment attenuated PM_2.5-induced liver inflammatory injury. Western blot and qRT-PCR assays showed that PM_2.5 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 PM_2.5 could trigger oxidative stress-mediated liver injury, whereas CEOs pretreatment might protect against PM_2.5-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 PM_2.5 but inhibited by CEOs pretreatment in PM_2.5-induced inflammatory liver injury. In addition, PM_2.5-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.