Objective: To investigate the effect of Radix Paeoniae Rubra (RPR) on the expression of heme oxygenase ( HO-1 ) and induced nitric oxide synthase (iNOS) in endotoxininduced acute lung injury in rats and its protective mechanism.Methods: Forty Wistar rats were divided randomly into 5 groups with 8 rats in each group: saline control group ( NS group ), lipopolysaccharide group ( LPS group), RPR-treatment group, RPR-prevention group and Herin group. The effect of RPR on protein content, the ratio of neutrophiles in bronchoalveolar lavage fluid,malondialdehyde (MDA) content in the lung and the activity of serum NO were observed. Arterial blood was drawn for blood-gas analysis. The expression of HO-1 and iNOS in lung tissues was detected by immunohistochemitry and morphometry computer image analysis. The histological changes of the lung were observed under light microscope.Results: Compared with that in NS group, the expression of HO-1 and iNOS was markedly increased in LPS group (P ＜ 0.01). In RPR-treatment, RPR-prevention, and Hemin groups, the expression of iNOS was significantly lower, while the expression of HO-1 was higher than that in LPS group (P ＜0.05). The protein content,the ratio of neutrophiles in bronchoalveolar lavage fluid,the content of MDA and the activity of serum NO in LPS group were significantly higher than those in NS group (P ＜ 0.01 ). There was a significant decrease in the level of arterial bicarbonate and partial pressure of oxygen in the LPS group (P＜0.01); these parameters of lung injury however, were significantly lower in RPR-treatment, RPR-prevention, and Hemin groups than LPS group (P ＜0.05or P ＜ 0.01). The pathologic changes of lung tissues were substantially attenuated in RPR-treatment, RPR-prevention, and Hemin groups than LPS group.Conclusions : The high expression of HO-1 reflects an important protective function of the body during lipopolysaccharide-induced acute lung injury. The protective effect of RPR on lipopolysaccharide-induced acute lung injury is related to the inhibition of iNOS expression and the induction of HO-1 expression.