Yuzhu Zhang1,2, Zhenzhen Chen2, Nianhai Feng2, Junxia Tang2, Xingbo Zhao3, Chengxiao Liu1, Hongyu Xu1,2, Mengyuan Zhang1. 1. Department of Anesthesiology, Shandong Provincial Hospital Affiliated to Shandong University, Jinan 250021, China. 2. Department of Anesthesiology, Zibo Central Hospital, Zibo 255000, China. 3. Department of Gynaecology, Shandong Provincial Hospital Affiliated to Shandong University, Jinan 250021, China.
Abstract
BACKGROUND: Blood reperfusion after ischemia is the main measure to restore cell function. This study was aimed to explore the effect of propofol on rat and cell models of liver ischemia-reperfusion (I/R) injury, and to investigate its possible mechanism. METHODS: Wistar rats were divided into four groups: control group, sham group, I/R group, and propofol group. Human hepatocyte HL7702 was divided into six groups: control group, I/R group and propofol (5, 10, 20 and 40 µmol/L) groups. After the animal and cell models were established, the alanine aminotransferase (ALT), aspartate aminotransferase (AST), malondialdehyde (MDA) and adenosine triphosphate (ATP) levels in liver tissues and hepatocytes were measured. Cell viability and apoptosis of hepatocytes were respectively determined by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay and flow cytometry. Furthermore, the expressions of apoptosis-related proteins in hepatocytes were determined by Western blot analysis. RESULTS: ALT, AST and MDA levels were all decreased significantly, and the ATP level was increased significantly in propofol group compared with that in I/R group in both liver tissues and hepatocytes. Additionally, cell viability of hepatocytes in propofol group was higher than that in I/R group, while the percentage of apoptotic cells in propofol group was less than that in I/R group. Moreover, the expression of caspase-3 decreased and the expression of Bcl-2 increased significantly after propofol preconditioning. CONCLUSIONS: Our findings suggested that propofol preconditioning might be an effective strategy for protecting the liver from I/R injury, which might provide a scientific basis for clinical application.
BACKGROUND: Blood reperfusion after ischemia is the main measure to restore cell function. This study was aimed to explore the effect of propofol on rat and cell models of liver ischemia-reperfusion (I/R) injury, and to investigate its possible mechanism. METHODS:Wistar rats were divided into four groups: control group, sham group, I/R group, and propofol group. Human hepatocyte HL7702 was divided into six groups: control group, I/R group and propofol (5, 10, 20 and 40 µmol/L) groups. After the animal and cell models were established, the alanine aminotransferase (ALT), aspartate aminotransferase (AST), malondialdehyde (MDA) and adenosine triphosphate (ATP) levels in liver tissues and hepatocytes were measured. Cell viability and apoptosis of hepatocytes were respectively determined by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay and flow cytometry. Furthermore, the expressions of apoptosis-related proteins in hepatocytes were determined by Western blot analysis. RESULTS: ALT, AST and MDA levels were all decreased significantly, and the ATP level was increased significantly in propofol group compared with that in I/R group in both liver tissues and hepatocytes. Additionally, cell viability of hepatocytes in propofol group was higher than that in I/R group, while the percentage of apoptotic cells in propofol group was less than that in I/R group. Moreover, the expression of caspase-3 decreased and the expression of Bcl-2 increased significantly after propofol preconditioning. CONCLUSIONS: Our findings suggested that propofol preconditioning might be an effective strategy for protecting the liver from I/R injury, which might provide a scientific basis for clinical application.
Authors: Sophia M Schmitz; Henriette Dohmeier; Christian Stoppe; Patrick H Alizai; Sandra Schipper; Ulf P Neumann; Mark Coburn; Tom F Ulmer Journal: Int J Mol Sci Date: 2020-07-30 Impact factor: 5.923