Objective:

2

To explore the effect of bear bile powder (BBP) on acute lung injury (ALI) and the underlying mechanism.

Methods:

2

The chemical constituents of BBP were analyzed by ultra-high-pressure liquid chromatography-mass spectrometry (UPLC-MS). After 7 days of adaptive feeding

50 mice were randomly divided into 5 groups by a random number table (

n

=10): normal control (NC)

lipopolysaccharide (LPS)

dexamethasone (Dex)

low-

and high-dose BBP groups. The dosing cycle was 9 days. On the 12th and 14th days

20 μL of

Staphylococcus aureus

solution (bacterial concentration of 1×10

-7

CFU/mL) was given by nasal drip after 1 h of intragastric administration

and the mice in the NC group was given the same dose of phosphated buffered saline (PBS) solution. On the 16th day

after 1 h intragastric administration

100 μL of LPS solution (1 mg/mL) was given by tracheal intubation

and the same dose of PBS solution was given to the NC group. Lung tissue was obtained to measure the myeloperoxidase (MPO) activity

the lung wet/dry weight ratio and expressions of CD14 and other related proteins. The lower lobe of the right lung was obtained for pathological examinatio

n. The concentrations of inflammatory cytokines including interleukin (IL)-6

tumour necrosis factor α (TNF-α) and IL-1β in the bronchoalveolar lavage fluid (BALF) were detected by enzyme linked immunosorbent assay

and the number of neutrophils was counted. The colonic contents of the mice were analyzed by 16 sRNA technique and the contents of short-chain fatty acids (SCFAs) were measured by gas chromatograph-mass spectrometer (GC-MS).

Results:

2

UPLC-MS revealed that the chemical components of BBP samples were mainly tauroursodeoxycholic acid and taurochenodeoxycholic acid sodium salt. BBP reduced the activity of MPO

concentrations of inflammatory cytokines

and inhibited the expression of CD14 protein

thus suppressing the activation of NF-κB pathway (

P

<

0.05). The lung histopathological results indicated that BBP significantly reduced the degree of neutrophil infiltration

cell shedding

necrosis

and alveolar cavity depression. Moreover

BBP effectively regulated the composition of the intestinal microflora and increased the production of SCFAs

which contributed to its treatment effect (

P

<

0.05).

Conclusions:

2

BBP alleviates lung injury in ALI mouse through inhibiting activation of NF-κB pathway and decreasing expression of CD14 protein. BBP may promote recovery of ALI by improving the structure of intestinal flora and enhancing metabolic function of intestinal flora.