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Published on: October 21, 2017
Trichostatin A protects against intestinal injury in rats with acute liver failure
Qian Zhang1, Fan Yang1, Xun Li1
1Department of Infectious Diseases, Renmin Hospital of Wuhan University, Wuhan, China.
Background:
Histone deacetylase (HDAC) inhibitors have been widely applied in the clinic as anticancer drugs against multiple neoplasms and proved their anti-inflammation under different pathology recently. Trichostatin A (TSA) is an HDAC inhibitor specific in class I and II HDAC enzymes. The aim of the present study was to elucidate the protective effects of TSA on acute liver failure (ALF) in rats and its potential mechanism.
Methods:
A total of 18 female Sprague-Dawley rats were separated into control, model, and TSA groups. We used Western blotting to determine the expression of HDACs, inflammatory cytokines, and acetylation of histone in liver and small intestine. The gene expression of inflammatory factors and Cox-2 was detected by a polymerase chain reaction. Colonic motility was assessed by spatiotemporal mapping. Histologic analysis and immunohistochemistry were performed. Intestinal permeability examination and levels of alanine aminotransferase, aspartate aminotransferase, and total bilirubin were also observed.
Results:
ALF procedure caused harm to histology of liver and small intestine, increased the intestinal permeability and serum levels of alanine aminotransferase, aspartate aminotransferase, and total bilirubin. It also interrupted the normal organization of colonic motor patterns by hurting enteric nervous system and pacemaker cells. Along with the decrease of inflammatory factors in ALF rats by TSA administration, all the damage to the liver, the small intestine, and the colon was repaired.
Conclusions:
TSA alleviates the lesion in liver, as well as in small intestine and colon in ALF rats by directly inhibiting inflammatory response.
Insights
Trichostatin A (TSA), an HDAC inhibitor, effectively protected rats from acute liver failure (ALF). TSA treatment repaired liver, small intestine, and colon damage by reducing inflammation.
Area of Science:
- Pharmacology
- Hepatology
- Gastroenterology
Background:
- Histone deacetylase (HDAC) inhibitors are used as anticancer agents and show anti-inflammatory properties.
- Trichostatin A (TSA) specifically inhibits class I and II HDAC enzymes.
- Recent studies highlight the anti-inflammatory potential of HDAC inhibitors in various pathologies.
Purpose of the Study:
- To investigate the protective effects of TSA on acute liver failure (ALF) in a rat model.
- To elucidate the underlying mechanisms of TSA's protective action in ALF.
Main Methods:
- Rats were divided into control, ALF model, and TSA-treated groups.
- Evaluated liver and small intestine histology, intestinal permeability, and serum liver enzymes (ALT, AST, bilirubin).
- Assessed colonic motility, enteric nervous system, and inflammatory markers using Western blotting and PCR.
Main Results:
- ALF induced liver and small intestine damage, increased intestinal permeability, and elevated serum liver enzymes.
- ALF disrupted colonic motor patterns by affecting the enteric nervous system and pacemaker cells.
- TSA administration reduced inflammatory factors and repaired histological damage in the liver, small intestine, and colon.
Conclusions:
- TSA demonstrates significant protective effects against acute liver failure in rats.
- TSA alleviates liver, small intestine, and colon lesions by directly inhibiting inflammatory responses.
