Objective：To investigate the effect of hepatic ischemia-reperfusion（I/R） on bile canalicular F-actin microfilaments in rats. Methods： A rat model of hepatic ischemia-reperfusion was employed and the ischemia time ...Objective：To investigate the effect of hepatic ischemia-reperfusion（I/R） on bile canalicular F-actin microfilaments in rats. Methods： A rat model of hepatic ischemia-reperfusion was employed and the ischemia time was 35 min. The activity of serum alanine aminotransferase （ALT）, aspartate aminotransferase（AST）, γ-glutamyl transferase（GGT） and the level of total bilirubin（TBIL） were measured. Changes in the bile canaliculi were observed by transmission electron microscope. The modification of F-actin microfilaments was quantified by using FITC-Phalloidin and analyzed by confocal laser scanning microscopy imaging. Results：Modifications of F-actin staining were consistent with the observations made by transmission electron microscopy. The staining of F-actin was normal in hepatocytes before reperfusion but decreased significantly after reperfusion, and there was a marked loss of canalicular microvilli after reperfusion, which coincided with abnormal serum GGT and TBIL levels. Conclusion：Reperfusion, not short-term ischemia, induced a disruption of F-actin microfilaments and a loss of microvilli. These modifications could lead to the impaired bile secretion by damaging canalicular contraction, and could be the main mechanisms of cholestasis after hepatic ischemia-reperfusion in rats.展开更多
基金supported by National Natural Science Foundation of China(30571765)
文摘Objective：To investigate the effect of hepatic ischemia-reperfusion（I/R） on bile canalicular F-actin microfilaments in rats. Methods： A rat model of hepatic ischemia-reperfusion was employed and the ischemia time was 35 min. The activity of serum alanine aminotransferase （ALT）, aspartate aminotransferase（AST）, γ-glutamyl transferase（GGT） and the level of total bilirubin（TBIL） were measured. Changes in the bile canaliculi were observed by transmission electron microscope. The modification of F-actin microfilaments was quantified by using FITC-Phalloidin and analyzed by confocal laser scanning microscopy imaging. Results：Modifications of F-actin staining were consistent with the observations made by transmission electron microscopy. The staining of F-actin was normal in hepatocytes before reperfusion but decreased significantly after reperfusion, and there was a marked loss of canalicular microvilli after reperfusion, which coincided with abnormal serum GGT and TBIL levels. Conclusion：Reperfusion, not short-term ischemia, induced a disruption of F-actin microfilaments and a loss of microvilli. These modifications could lead to the impaired bile secretion by damaging canalicular contraction, and could be the main mechanisms of cholestasis after hepatic ischemia-reperfusion in rats.
