Therapeutic potential of bixin in PM2.5 particles-induced lung injury in an Nrf2-dependent manner.

Fine particulate matter (PM 2.5) is a well-known air pollutant threatening public health. Studies has confirmed that long-term exposure to the particles could reduce the pulmonary function, cause exacerbation of asthma and chronic obstructive pulmonary disease, and increase incidence and mortality of lung cancer. Bixin is a natural compound that is widely used as a food additive. Our previous studies demonstrated that bixin i.p. administration could protect against particles intratracheal exposure (56 days)-induced lung injury in an Nrf2-dependent manner. But the detail mechanisms are still unclarified. Our current study aimed to explore the further therapeutic potential and mechanism of bixin to slow the progression of lung injury and inflammation in vivo and in vitro. The results from the in vivo study showed that bixin treatment attenuated the accumulation of inflammatory cells, decreased the levels of tissue apoptosis, and increase the ability of cell proliferation. Besides that, bixin also could regulate the expression of MMP9, TGFβ1, and its downstream Fibronectin (FN), along with activation of Nrf2 signals. In vitro experiments in human bronchial epithelial cells demonstrated that Nrf2 activated by bixin contributes to tissue repair by alleviating oxidative stress, increasing proliferation and migration, decreasing apoptosis, which may be partially through modulating the expression of MMP9, TGFβ1, and FN. This study provides convincing experimental evidences that bixin could be used therapeutically to promote tissue repair and improve pulmonary injury induced by particles exposure.