[Protective effect of human amnion epithelial cells through endotracheal instillation against lipopolysaccharide-induced acute lung injury in mice].

Objective To investigate the therapeutic effect of human amnion epithelial cells (hAECs) through endotracheal instillation on acute lung injury (ALI) induced by lipopolysaccharide (LPS) in mice and its underlying mechanism. Methods Male C57BL/6 mice were randomly divided into normal control group, hAECs control group, LPS-induced ALI group and hAECs treatment group (n=10 each group). In the latter two groups, mice were subjected to LPS (5 mg/kg) by oral insertion, and 1 hour later, PBS (50 μL) and hAECs (1×107/mL, 50 μL) were administered by oral insertion in the two groups, respectively. The normal control group and hAECs control group were injected with the same amount of PBS and hAECs by oral insertion, respectively. Twenty-four hours after LPS administration, the mice were sacrificed to collect blood and lung tissues. Cytoplasmic and nuclear proteins were extracted from the lung tissues, and other lung tissues were embedded in paraffin and cut into sections. The wet mass and dry mass of lung tissues were obtained to calculate the wet/dry mass ratios. Concentrations of interleukin (IL)-10, IL-6, IL-1β and tumor necrosis factor (TNF)-α in sera were measured by ELISA. Pulmonary histological changes were evaluated by HE staining. The nuclear transcription factor-kappaBp65 (NF-κBp65) activation in lung tissues was detected by Western blotting. Results Compared with the control group, the lung wet/dry mass ratios and the serum concentrations of TNF-α, IL-1β and IL-6 in the LPS-induced model group increased, while the level of IL-10 decreased. Under a light microscope, the lung tissues from LPS-induced model group showed serious pulmonary edema, haemorrhagia in stroma, alveolar wall thickness, alveolus collapse and obvious inflammatory cell infiltration. LPS administration also increased the activation of NF-κBp65 in lung tissues. hAECs administration significantly decreased LPS-induced lung histopathological changes, lung wet/dry mass ratios and the serum levels of IL-6, IL-1β and TNF-α, and inhibited the activation of NF-κBp65 in lung tissues. Conclusion hAECs can inhibit the activation of NF-κBp65 in lung tissues and significantly attenuat lipopolysaccharide-induced ALI.