Effect of triptolide on the regulation of ATP-binding cassette transporter A1 expression in lipopolysaccharide-induced acute lung injury of rats

Abstract

The aim of this study was to investigate the effect of triptolide on ATP-binding cassette transporter A1 (ABCA1) expression in lipopolysaccharide (LPS)-induced acute lung injury (ALI) in rats. Thirty male Sprague Dawley rats weighing 200-250 g were randomly divided into six groups: Normal (N, n=5), Control (C, n=5), LPS (L, n=5), Triptolide 25 μg (TP1, n=5), Triptolide 50 μg (TP2, n=5) and Triptolide 100 μg (TP3, n=5). The N group was not administered anything; the C group was administered 5 ml/kg normal saline intravenously and 7.5 ml/kg 1% dimethylsulfoxide (DMSO) intraperitoneally; the L group was administered 5 mg/kg 0.1% LPS and 1% DMSO; and the TP1, TP2 and TP3 groups were separately injected with 0.1% LPS and 25, 50 or 100 μg/kg triptolide, respectively. All groups had the same liquid-injection volume. Arterial blood gases, tumor necrosis factor-α (TNF-α) and ABCA1 expression and general pathology were examined following the treatments. It was found that increasing the triptolide dose in the TP1-3 groups resulted in an increase in the expression of ABCA1 mRNA and protein. As compared with the L group, the ABCA1 expression showed a significant increase in TP2 and TP3 groups (P<0.05). In addition, the expression level of TNF-α was significantly increased in the L and TP1 groups, as compared with that in the N or C groups (P<0.05). Conversely, a marked decrease in TNF-α expression was detected in the TP2 and TP3 groups, as compared with the L or TP1 groups (P<0.05). In conclusion, this study found that triptolide could promote the expression of ABCA1 mRNA and protein and inhibit other inflammatory factors during LPS-induced ALI in rats. Regulating the expression of ABCA1 may be one of the protective mechanisms of triptolide. Furthermore, triptolide-induced increases in ABCA1 expression occurred in a dose-dependent manner between 25 and 100 μg/kg.