Hu Zhi-Hui, Kong Yang-Yang, Ren Jun-Jie, Huang Ting-Juan, Wang Yan-Qin, Liu Li-Xin
Department of Gastroenterology and Hepatology, The First Hospital of Shanxi Medical University Taiyuan 030001, China.
Experimental Center of Science and Research, The First Hospital of Shanxi Medical University Taiyuan 030001, China.
Int J Clin Exp Pathol. 2020 Feb 1;13(2):192-202. eCollection 2020.
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.
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.
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.
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.
肝肾综合征和肝肺综合征是常见的临床疾病；然而，它们的发病机制尚未完全阐明。我们的目的是确定胆管结扎（BDL）所致的肝损伤是否会引起小鼠肾和肺组织的改变，并探讨这些变化的可能机制。
采用小鼠胆管结扎作为研究模型。通过苏木精-伊红（H&E）染色观察肝、肾和肺组织的病理变化。采用免疫组织化学染色和蛋白质印迹法研究肝、肾和肺组织中IGFBPrP1、NF-κB、TNF-α和IL-6的表达。采用Pearson法分析各组小鼠肝、肾和肺组织中IGFBPrP1与NF-κB、TNF-α和IL-6蛋白表达之间的相关性。
H&E染色显示，小鼠胆管结扎后，各组小鼠肝、肾和肺组织均出现不同程度的炎症变化。免疫组织化学染色和蛋白质印迹分析结果显示，胆管结扎后IGFBPrP1、NF-κB、TNF-α和IL-6表达增加。Pearson相关性分析显示，IGFBPrP1与NF-κB、TNF-α和IL-6的表达呈正相关。
胆管结扎所致的肝损伤可导致小鼠肾和肺组织损伤。损伤机制可能与肾和肺组织中肝损伤因子IGFBPrP1、转录因子NF-κB、促炎细胞因子TNF-α和IL-6的高表达有关。此外，IGFBPrP1表达水平的升高可能伴随着NF-κB炎症通路的激活。
