关键词: 肝肺综合征(HPS), 白细胞介素-6(IL-6), JAK2, STAT3

Abstract: Objective To establish a rat model of hepatopulmonary syndrome(HPS), isolate and culture pulmonary endothelium, and elucidate the role and mechanism of IL-6 in the pathogenesis of hepatopulmonary syndrome in rats.Methods We established a rat model of Hepatopulmonary Syndrome, isolated and cultured rat lung Endothelium, and studied the effects of IL-6 on cell proliferation and related signaling pathways by PCR and Western blot. Results HPS rat model was established by common bile duct ligation. Liver cirrhosis and HPS were induced in 4~6 weeks. The manifestations of HPS were listlessness, yellowing of urine, bradykinesia, dyspnea, hypoxemia and increased concentration of plasma nitric oxide, ultrasound showed that the bile duct was dilated and the membrane of the liver was uneven. 6w rats were sacrificed to observe the formation of hepatic fibrous bands and the dilatation of hepatic pseudolobule and pulmonary microvessels; The expression of IL-6 in HPS was significantly higher than that in tumor necrosis factor-α, IL-8 and IL-1, P<0.05; The results showed that IL-6 could promote the proliferation of lung endothelium and inhibit the apoptosis of PMVECs induced by lipopolysaccharide (LPS), the main mechanism is through activating JAK2/STAT3 signal pathway.Conclusion IL-6 can activate JAK2/STAT3 signal transduction pathway, promote the proliferation of PMVECs, and then affect the occurrence of HPS.

Key words: Hepatopulmonary syndrome, IL-6, JAK2, STAT3