Abstract
Xuebijing (XBJ) is a Chinese herbal preparation. Previous studies have demonstrated that XBJ injection is able to inhibit the uncontrolled release of endogenous inflammatory mediators, attenuate inflammation, and alleviate organ damage. However, there are no relevant reports on the protective effect of XBJ against left ventricular ischemia/reperfusion (I/R)-induced acute lung injury (ALI). Therefore, the aim of the present study was to evaluate the protective effect of XBJ on ALI induced by left ventricular I/R, and provide evidence for the clinical application of XBJ. In the present study, 120 healthy rabbits of mixed gender were randomly assigned to a normal control group, ischemia group, I/R group (I/RG) and XBJ-injection treatment group (TG). In addition, each group was further divided into three subgroups (n=10/subgroup), namely, 30 min pre-ischemia, 30 min post-ischemia and 30 min post-reperfusion subgroups. Blood samples (5 ml) were collected from the jugularis externa and carotis communis of the rabbits at the three time points, and a blood gas analyzer was used to measure the arterial partial pressure of oxygen (PaO(2)) and carbon dioxide (PaCO(2)). Following sacrifice, the lungs of the rabbits were removed and a bronchoalveolar lavage (BAL) was immediately performed. An enzyme-linked immunosorbent assay was used to measure the expression levels of tumor necrosis factor-α (TNF-α) in the BAL fluid (BALF) and peripheral blood. In addition, the lower lobe of the right lung was removed in order to measure the protein expression levels of intercellular adhesion molecule-1 (ICAM-1) and TNF-α. The results demonstrated that in the rabbits of the TG PaO(2) was increased, PaCO(2) was decreased, the lung tissue congestion edema was attenuated, the expression levels of TNF-α in the peripheral blood and BALF were reduced and the protein expression levels of ICAM-1 and TNF-α in the lung tissue samples were decreased, as compared with those in the I/RG rabbits. These results suggest that XBJ may protect against left ventricular I/R-induced ALI by regulating the expression of the inflammatory mediators TNF-α and ICAM-1.