Sirtuin 1 modulation in rat model of acetaminophen-induced hepatotoxicity

Title:

Sirtuin 1 modulation in rat model of acetaminophen-induced hepatotoxicity

Creator:

Wojnarová, L., Nikolína Kutinová-Canová, Hassan Farghali, and Tomáš Kučera

Identifier:

https://cdk.lib.cas.cz/client/handle/uuid:c132cddc-d270-4147-b17e-7512378fdfd8
uuid:c132cddc-d270-4147-b17e-7512378fdfd8
issn:0862-8408

Subject:

Fyziologie člověka a srovnávací fyziologie, fyziologie, játra, physiology, liver, SIRT1, resveratrol, acetaminophen, CAY10591, 14, and 612

Type:

article, články, model:article, and TEXT

Format:

print, bez média, and svazek

Description:

Sirtuin 1 (SIRT1) is involved in important biological processes such as energy metabolism and regulatory functions of the cell cycle, apoptosis, and inflammation. Our previous studies have shown hepatoprotective effect of polyphenolic compound resveratrol, which is also an activator of SIRT1. Therefore, the aim of our present study was to clarify the role of SIRT1 in process of hepatoprotection in animal model of drug-induced liver damage. Male Wistar rats were used for both in vivo and in vitro studies. Hepatotoxicity was induced by single dose of acetaminophen (APAP). Some rats and hepatocytes were treated by resveratrol or synthetic selective activator of sirtuin 1 (CAY10591). The degree of hepatotoxicity, the activity and expression of the SIRT1 were determined by biochemical, histological and molecular-biological assessments of gained samples (plasma, liver tissue, culture media and hepatocytes). Resveratrol and CAY attenuated APAP-induced hepatotoxicity in vivo and in vitro. Moreover, both drugs enhanced APAPreduced SIRT1 activity. Our results show that modulation of the SIRT1 activity plays a role in hepatoprotection. Synthetic activators of SIRT1 would help in understanding the role of SIRT1 and are therefore a major boost towards the search for specific treatment of liver disease., L. Wojnarová, N. Kutinová Canová, H. Farghali, T. Kučera., and Obsahuje bibliografii

Language:

English

Rights:

http://creativecommons.org/publicdomain/mark/1.0/
policy:public

Source:

Physiological research | 2015 Volume:64 | Number:Suppl 4

Harvested from:

CDK

Metadata only:

false