Background Acute respiratory distress syndrome (ARDS) is a clinically common critical disease characterized by high mortality. There is currently a lack of more effective drug treatments. Therefore, it is particularly urgent to discover more mechanisms related to the occurrence and development of ARDS, so as to find effective therapeutic drugs.
Objective To use lipopolysaccharide (LPS) to replicate ARDS model of rabbits and then discuss the pathogenic mechanism of inflammatory mediators in the development of ARDS and the protective effect of curcumin.
Methods Twenty-eight New Zealand white rabbits were randomly divided into the control group (C), model group (M), model + vehicle group (V), and treatment group (T). The ARDS model was replicated by one-off intravenous injection of LPS (720 μg/kg). After modeling, group M was intraperitoneally injected with normal saline (0.8 mL/kg), group V was intraperitoneally injected with the same amount of dimethyl sulfoxide, and group T was intraperitoneally injected with curcumin solution (0.8 mL/kg). Contents of IL-17 and IL-22 in bronchoalveolar lavage fluid (BALF) and lung tissue were detected by ELISA at 6h after the experiment.
Results The content of IL-17 in BALF of the group M and the group V was higher than that of the group C (P<0.05), and the content of IL-17 in the group T was higher than that in the group C, but the differences were not statistically significant (P>0.05). The content of IL-22 in BALF of the group M and the group V decreased compared with that of the group C, while the content of IL-22 of group T was higher than that of the group C, but the differences were not statistically significant (P>0.05). The content of IL-17 in lung tissue of the group M and the group V was significantly higher than that of the group C (P<0.05); and it was higher in the group T than that in the group C, without significant difference (P>0.05). The content of IL-22 in lung tissue of the group T was significantly higher than that of the group C (P<0.05), however, it decreased in the group M and the group V, without significant difference (P>0.05). The pathology showed obvious lung injury in the group M and the group V, while the damage in the group T was significantly lighter than that in the group M and the group V.
Conclusion Curcumin can protect ARDS induced by LPS, which may be achieved by reducing inflammatory infiltration and the production and release of pro-inflammatory cytokines in the lung airways, and up regulating anti-inflammatory factors.
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