Objective: To study the effect of Chuankezhi injection on lipopolysaccharide (LPS)-induced acute lung injury (ALI) in mice and its mechanism. Method: The 48 SPF grade female C57BL/6J mice were randomly divided into normal group

model group

dexamethasone group

and Chuankezhi group

a total of 4 groups

12 mice in each group. Each mouse was intraperitoneally injected with 0.2 mL · d-1 in Chuankezhi group

once a day for 7 days. The mice in the dexamethasone group were injected intraperitoneally at 1 mg · kg-1 per day for 3 days before modeling. The mice in model group were injected with equal dose of normal saline while the normal group had no treatment. Except in the normal group

LPS 0.1 mL (0.5 g · L-1) was injected intraperitoneally on the 8 day

and the mice received 25 μL (0.5 g · L-1) by nasal drops after ether inhalation for anesthesia to establish ALI models. Detection was conducted after 24 h. The expression levels of tumor necrosis factor (TNF)-α

interleukin (IL)-1β and IL-18 were detected by enzyme-linked immunosorbent assay (ELISA). The expression level of nuclear factor-kappa B (NF-κB) p65 protein was detected by immunohistochemistry. Western blot was used to detect the expression levels of p65

Toll-like receptor4 (TLR4)

Nod-like receptor protein 3 (NLRP3) and cysteine aspartate protease-1 (Caspase-1) protein in lung tissues

and Real-time polymerase chain reaction (Real-time PCR) was used to detect the expression of p65 and TLR4 mRNA in lung tissues. Result: As compared with the normal group

the levels of TNF-α

IL-1β and IL-18 in serum in the model group were increased (P<0.01); the expression of p65

TLR4

NLRP3 and Caspase-1 were increased; p65 and TLR4 mRNA were increased (P<0.05). As compared with the model group

the levels of TNF-α

IL-1β and IL-18 in serum in Chuankezhi group were significantly decreased (P<0.01)

and the levels of p65

TLR4

NLRP3 and Caspase-1 protein and expression levels of p65 and TLR4 mRNA were also decreased (P<0.05). Conclusion: Chuankezhi injection can effectively improve the injury of lung tissues induced by LPS in mice with acute lung injury. The mechanism may be associated with inhibiting TLR4/NF-κB/NLRP3 signaling pathway to protect the lung tissues.