Breviscapine reduces acute lung injury induced by left heart ischemic reperfusion in rats by inhibiting the expression of ICAM-1 and IL-18

摘要

It has been demonstrated that breviscapine is able to treat coronary disease and reduce the inflammatory response; however, there are no relevant reports concerning its effects on the expression of inflammatory factors in acute lung injury induced by left heart ischemic reperfusion and the underlying mechanisms. In this study, we created a left heart ischemia-reperfusion model in rats to investigate the effects of breviscapine on the expression of interleukin 18 (IL-18) and intercellular adhesion molecule-1 (ICAM-1), as well as to determine the possible mechanisms involved in the protective effects of breviscapine on respiratory function. The left heart ischemia-reperfusion model was created by ligating the anterior descending branch of the coronary artery for 30 mins followed by reperfusion. Rats in the treatment group (TG) were treated with breviscapine (10 mg/kg) and the rats in the control group (CG) received normal saline. Ten rats in the two groups were sacrificed at three points: 30 min after ligating (T1), 30 min after reperfusion (T2) and 60 min after reperfusion (T3). A respiration curve was produced and the arterial partial pressure of oxygen (PaO2) was measured for all rats. Additionally, the expression levels of IL-18 and ICAM-1 were determined and the correlation between IL-18 and ICAM-1 expression in lung tissue was analyzed. The level of IL-18 in peripheral blood and bronchialalveolar lavage fluid (BALF) was also measured. The respiration amplitude was lower and the duration time was shorter in the TG rats than in the CG rats at T1, T2 and T3. The expression levels of IL-18 and ICAM-1 in the TG group were clearly reduced. The level of IL-18 in the peripheral blood and BALF was downregulated following the administration of breviscapine. These results demonstrate that breviscapine inhibits the expression of IL-18 and ICAM-1, thereby protecting the lungs from inflammatory cascade responses.