Damage effects of bisphenol A against sepsis induced acute lung injury.

In addition to oxidative damage, sepsis can cause multiple organ dysfunction and poses a life-threatening threat. In addition to severe tissue damage, hypotension, and multiple organ failure, sepsis can cause high morbidity and mortality. It is the lungs that are most vulnerable in abdominal sepsis, with impaired oxygen and nutrient exchange occurring in the pulmonary microcirculation. However, the etiology of sepsis and the link between sepsis and lung injury has not been elucidated. In this work, by exploring the data from the GEO and CTD database, a gene association study was conducted to determine whether sepsis-induced lung injury is caused by BPA. Further analysis demonstrated that MMP9, CEBPA, CYP1B1, CTSD, FKBP5, DGAT2, HP, TIMP2, ARG1 and MGST1 may play an important role in sepsis-induced lung injury. Finally, the single-cell RNA sequence demonstrated that CEBPA is mainly enriched in lung epithelial cells and epithelial cells, whereas CYP1B1 is closely related to basal cells, macrophages, and interstitial cells. In order to maintain lung function, epithelial and alveolar macrophages as well as other lung cells are important. When the lung epithelium is activated for a prolonged period of time, barrier function may be compromised and tissue damage may result, aggravating the lung injury. By using the animal model, we successfully simulated the model of sepsis lung injury. The HE staining demonstrated the rats with BPA-treated septic lung injury showed more alveolar structure to be disordered, pulmonary interstitial edema to be evident, and red blood cells as well as inflammatory cells. For PCR assay, the results demonstrated that the expression level of CEBPA is higher in the lung samples with sepsis compared with the normal samples of the lung. In order to evaluate the expression level of CEBPA and CYP1B1 in lung tissue, we then performed the PCR assay. For CYP1B1, the results demonstrated that the expression level of CYP1B1 in lung samples with sepsis is lower than in normal lung samples. In total, BPA may be a potential contributing factor to sepsis-induced lung injury.