Kidney and lung tissue modifications after BDL-induced liver injury in mice are associated with increased expression of IGFBPrP1 and activation of the NF-κB inflammation pathway.

BACKGROUND: Hepatorenal and hepatopulmonary syndrome are common clinical diseases; however, their mechanisms have not been fully elucidated. Our aim was to determine whether liver injury by bile duct ligation (BDL) causes modifications in kidney and lung tissue in mice, and to explore the possible mechanism of these changes. METHODS: BDL in mice was used as a research model. Pathologic changes of liver, kidney, and lung tissue were observed by hematoxylin-eosin (H&E) staining. The expression of IGFBPrP1, NF-κB, TNF-α, and IL-6 were investigated in liver, kidney, and lung tissue by immunohistochemical staining and western blot. The correlation between IGFBPrP1 and NF-κB, TNF-α, and IL-6 protein expression in liver, kidney, and lung tissues of each group was analyzed by the Pearson method. RESULTS: H&E staining showed, after BDL administration in mice, different degrees of inflammatory change in liver, kidney, and lung tissues of mice in each group. The results of immunohistochemical staining and western blot analysis showed increased expressions of IGFBPrP1, NF-κB, TNF-α, and IL-6 after BDL. Pearson correlation analysis showed that IGFBPrP1 positively correlated with the expressions of NF-κB, TNF-α, and IL-6. CONCLUSION: Liver injury caused by bile duct ligation can lead to kidney and lung tissue injury in mice. The mechanism of injury may be related to the high expression of liver injury factor IGFBPrP1, transcription factor NF-κB, proinflammatory cytokine TNF-α, and IL-6 in kidney and lung tissue. Moreover, an increased expression level of IGFBPrP1 may be accompanied by the activation of the NF-κB inflammatory pathway.