In this experiment, it was observed that after 24 h of sepsis-induced lung injury in mice, the expression of the anti-apoptotic protein Bcl-2 decreased in the lung tissue, and the expression of pro-apoptotic protein Bax increased, while the treatment of lidocaine could increase the expression level of Bcl-2 protein in the lung tissue and reduce the expression level of Bax protein and the ratio of Bax/Bcl-2, which also corroborated the findings presented in previous studies that the anti-inflammatory effect of lidocaine might be closely related to anti-apoptosis. Here, BCL2 is linked to Sepsis.