Your browser doesn't support javascript.
loading
Relationships of ?-AR and GRK2 in lung,lung injury in rats with severe acute pancreatitis and therapeutic effect by methlyprednisolone / 中国病理生理杂志
Article in Zh | WPRIM | ID: wpr-531518
Responsible library: WPRO
ABSTRACT
AIM: To investigate the variation of ?-AR in pulmonary microvascular endothelial cells and variation of GRK2 in lung and to explore the therapeutic effect of methlyprednisolone in severe acute pancreatitis-associated lung injury model in rats.METHODS: 36 rats were divided into three groups randomly: the control group,the experimental group,and the intervention group.In the experimental group,severe acute pancreatitis-associated lung injury model was induced in SD rats by retrograde injection of 5% sodium taurocholate into biliopancreatic duct.In the control group,laparotomy was performed,duodenum and pancreas were flipped only.In the intervention group,methlyprednisolone(30 mg/kg) was injected into rump muscle of rats after model developed.At 6 and 12 h after model was developed,the maximum binding capacity(Bmax) and the Kd value of ?-AR were detected in lung by means of radioactive ligand binding assay.GRK2 expression was detected in lung by means of immunofluorescence.RESULTS: The scores of the severity of pancreatitis and the severity of lung injury in the experimental group were obviously higher than those in control group.In the experimental group,Bmax was obviously lower,Kd and GRK2 were obviously higher than those in control group and the intervention group.CONCLUSION: The ?-AR in lung is lower down and GRK2 expression in lung is up-regulated in severe acute pancreatitis-associated lung injury model in rats.The therapeutic effect of methlyprednisolone to severe acute pancreatitis-associated lung injury is positive.
Key words
Full text: 1 Index: WPRIM Type of study: Prognostic_studies Language: Zh Journal: Chinese Journal of Pathophysiology Year: 2000 Type: Article
Full text: 1 Index: WPRIM Type of study: Prognostic_studies Language: Zh Journal: Chinese Journal of Pathophysiology Year: 2000 Type: Article