Regulation by resveratrol of the cellular factors mediating liver damage and regeneration after acute toxic liver injury. Issue 3 (March 2014)
- Record Type:
- Journal Article
- Title:
- Regulation by resveratrol of the cellular factors mediating liver damage and regeneration after acute toxic liver injury. Issue 3 (March 2014)
- Main Title:
- Regulation by resveratrol of the cellular factors mediating liver damage and regeneration after acute toxic liver injury
- Authors:
- Chan, Che‐Chang
Lee, Kuei‐Chuan
Huang, Yi‐Hsiang
Chou, Chung‐Kai
Lin, Han‐Chieh
Lee, Fa‐Yauh - Abstract:
- <abstract abstract-type="main"> <title>Abstract</title> <sec id="jgh12366-sec-0001" sec-type="section"> <title>Background and Aim</title> <p>Acute liver injury is manifested by different degree of hepatocyte necrosis and may recover via the process of hepatocyte regeneration once the injury is discontinued. Most of the liver injury is associating with inflammatory cytokines. Resveratrol (RSV) is a natural phytoalexin with powerful anti‐inflammatory effects.</p> </sec> <sec id="jgh12366-sec-0002" sec-type="section"> <title>Aim</title> <p>The effects of RSV on cellular factors mediating liver damage and regeneration in acute carbon tetrachloride (CCl<sub>4</sub>) liver injury were investigated.</p> </sec> <sec id="jgh12366-sec-0003" sec-type="section"> <title>Results</title> <p>RSV decreased alanine aminotransferase, aspartate aminotransferase, necrosis, and 4‐hydroxynonenal in the CCl<sub>4</sub>‐injured liver. RSV decreased hepatocyte apoptosis by reducing caspase 8 and caspase 3 but not Bax and Bcl‐xL. RSV reduced Kupffer cells recruitment, the expressions of tumor necrosis factor‐α and interleukin‐6, but not interleukin‐10. RSV lowered the numbers of anti‐5‐bromon‐2'‐deoxyuridine and anti‐Ki67‐positive hepatocytes. Hepatic hepatocyte growth factor, c‐Met and transforming growth factor‐α expressions were reduced by RSV, while transforming growth factor‐β1 and hepatic stellate cells activation were not changed. RSV reduced the injury‐induced CXCL10 elevations in serum and<abstract abstract-type="main"> <title>Abstract</title> <sec id="jgh12366-sec-0001" sec-type="section"> <title>Background and Aim</title> <p>Acute liver injury is manifested by different degree of hepatocyte necrosis and may recover via the process of hepatocyte regeneration once the injury is discontinued. Most of the liver injury is associating with inflammatory cytokines. Resveratrol (RSV) is a natural phytoalexin with powerful anti‐inflammatory effects.</p> </sec> <sec id="jgh12366-sec-0002" sec-type="section"> <title>Aim</title> <p>The effects of RSV on cellular factors mediating liver damage and regeneration in acute carbon tetrachloride (CCl<sub>4</sub>) liver injury were investigated.</p> </sec> <sec id="jgh12366-sec-0003" sec-type="section"> <title>Results</title> <p>RSV decreased alanine aminotransferase, aspartate aminotransferase, necrosis, and 4‐hydroxynonenal in the CCl<sub>4</sub>‐injured liver. RSV decreased hepatocyte apoptosis by reducing caspase 8 and caspase 3 but not Bax and Bcl‐xL. RSV reduced Kupffer cells recruitment, the expressions of tumor necrosis factor‐α and interleukin‐6, but not interleukin‐10. RSV lowered the numbers of anti‐5‐bromon‐2'‐deoxyuridine and anti‐Ki67‐positive hepatocytes. Hepatic hepatocyte growth factor, c‐Met and transforming growth factor‐α expressions were reduced by RSV, while transforming growth factor‐β1 and hepatic stellate cells activation were not changed. RSV reduced the injury‐induced CXCL10 elevations in serum and liver <italic>in vivo</italic>. Besides, RSV inhibited CXCL10 release from CCl<sub>4</sub>‐injured hepatocytes <italic>in vitro</italic>. In contrast, recombinant CXCL10 improved the viability of CCl<sub>4</sub>‐injured hepatocytes.</p> </sec> <sec id="jgh12366-sec-0004" sec-type="section"> <title>Conclusions</title> <p>RSV therapy can be beneficial for acute toxic liver injury. RSV reduced hepatocyte apoptosis but limited hepatocyte regeneration possibly through reducing the hepatomitogenic signaling and the release of CXCL10.</p> </sec> </abstract> … (more)
- Is Part Of:
- Journal of gastroenterology and hepatology. Volume 29:Issue 3(2014:Mar.)
- Journal:
- Journal of gastroenterology and hepatology
- Issue:
- Volume 29:Issue 3(2014:Mar.)
- Issue Display:
- Volume 29, Issue 3 (2014)
- Year:
- 2014
- Volume:
- 29
- Issue:
- 3
- Issue Sort Value:
- 2014-0029-0003-0000
- Page Start:
- 603
- Page End:
- 613
- Publication Date:
- 2014-03
- Subjects:
- Gastroenterology -- Periodicals
Digestive organs -- Diseases -- Periodicals
Liver -- Diseases -- Periodicals
Gastroenterology -- Periodicals
Liver Diseases -- Periodicals
616.33 - Journal URLs:
- http://onlinelibrary.wiley.com/journal/10.1111/(ISSN)1440-1746 ↗
http://onlinelibrary.wiley.com/ ↗
http://www.blackwell-synergy.com/loi/jgh ↗ - DOI:
- 10.1111/jgh.12366 ↗
- Languages:
- English
- ISSNs:
- 0815-9319
- Deposit Type:
- Legaldeposit
- View Content:
- Available online (eLD content is only available in our Reading Rooms) ↗
- Physical Locations:
- British Library DSC - 4987.615000
British Library DSC - BLDSS-3PM
British Library HMNTS - ELD Digital store - Ingest File:
- 4317.xml