Xuebijing injection is a complex herbal medicine, and clinical and experimental studies have shown that it has a significant effect on
acute respiratory distress syndrome and
multiple organ dysfunction syndrome. However, the majority of studies regarding
Xuebijing injection have focused on serum inflammatory factors, and few studies have been carried out from the perspective of the
protein and
mRNA expression of inflammatory
cytokines. In this study, 60 healthy rabbits of mixed gender were randomly assigned to a normal control group (CG),
oleic acid group (model group; MG) and
oleic acid +
Xuebijing injection group (treatment group; TG). Rabbits of the CG were treated with
normal saline through the ear vein, rabbits of the MG were injected with
oleic acid (0.4 ml/kg) and rabbits of the TG received 0.4 ml/kg
oleic acid + 10 ml/kg
Xuebijing injection. Blood samples were collected from the common carotid artery of all rabbits of all groups 1 h after the ear vein was injected with the corresponding
reagent, and was used to measure the arterial partial pressure of
oxygen (PaO2) and of
carbon dioxide (PaCO2). The activity of
myeloperoxidase (MPO) was tested, and the
protein and
mRNA expression levels of
interleukin (IL)-6 and
IL-10 were determined. Rabbits of the MG exhibited evident respiratory dysfunction (PaO2 and PaCO2 were low), histopathological lung damage and overactive inflammatory responses (the expression of the proinflammatory
cytokine IL-6 and the anti-inflammatory
cytokine IL-10 was increased at the
protein and
mRNA levels). Following the administration of the
Xuebijing injection, the inflammatory response of the rabbits was significantly reduced.
Xuebijing injection raised PaO2 and PaCO2, weakened the activity of MPO in the lung tissue, downregulated the expression of the proinflammatory
cytokine IL-6 and further increased the expression of the anti-inflammatory
cytokine IL-10. These results demonstrated that
Xuebijing injection improved the respiratory function of rabbits with acute
oleic acid-induced
lung injury by inhibiting
IL-6 expression and promoting
IL-10 expression.