{"title":"肝缺血再灌注对大鼠胆管f -肌动蛋白微丝的影响","authors":"Yiming Li, Hua Li, Jidong Liu, Hong Ji","doi":"10.1016/S1007-4376(09)60042-3","DOIUrl":null,"url":null,"abstract":"<div><h3>Objective</h3><p>To investigate the effect of hepatic ischemia-reperfusion(I/R) on bile canalicular F-actin microfilaments in rats.</p></div><div><h3>Methods</h3><p>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.</p></div><div><h3>Results</h3><p>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.</p></div><div><h3>Conclusion</h3><p>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.</p></div>","PeriodicalId":100807,"journal":{"name":"Journal of Nanjing Medical University","volume":"23 2","pages":"Pages 137-142"},"PeriodicalIF":0.0000,"publicationDate":"2009-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/S1007-4376(09)60042-3","citationCount":"0","resultStr":"{\"title\":\"Effect of hepatic ischemia-reperfusion on bile canalicular F-actin microfilaments in rats\",\"authors\":\"Yiming Li, Hua Li, Jidong Liu, Hong Ji\",\"doi\":\"10.1016/S1007-4376(09)60042-3\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<div><h3>Objective</h3><p>To investigate the effect of hepatic ischemia-reperfusion(I/R) on bile canalicular F-actin microfilaments in rats.</p></div><div><h3>Methods</h3><p>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.</p></div><div><h3>Results</h3><p>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.</p></div><div><h3>Conclusion</h3><p>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.</p></div>\",\"PeriodicalId\":100807,\"journal\":{\"name\":\"Journal of Nanjing Medical University\",\"volume\":\"23 2\",\"pages\":\"Pages 137-142\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2009-03-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://sci-hub-pdf.com/10.1016/S1007-4376(09)60042-3\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Journal of Nanjing Medical University\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://www.sciencedirect.com/science/article/pii/S1007437609600423\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of Nanjing Medical University","FirstCategoryId":"1085","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S1007437609600423","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
Effect of hepatic ischemia-reperfusion on bile canalicular F-actin microfilaments in rats
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.
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