Abstract
Studies have shown that edaravone may prevent liver injury. This study aimed to investigate the effects of edaravone on the liver injury induced by D-galactosamine (GalN) and lipopolysaccharide (LPS) in female BALB/c mice. Edaravone was injected into mice 30 min before and 4 h after GalN/LPS injection. The survival rate was determined within the first 24 h. Animals were killed 8 h after GalN/LPS injection, and liver injury was biochemically and histologically assessed. Hepatocyte apoptosis was measured by TUNEL staining; proinflammatory cytokines [tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6)] in the liver were assayed by ELISA; expression of caspase-8 and caspase-3 proteins was detected by Western blot assay; and caspase-3 activity was also determined. Results showed that GalN/LPS induced marked elevations in serum aspartate aminotransferase (AST) and alanine aminotransferase (ALT). Edaravone significantly inhibited elevation of serum AST and ALT, accompanied by an improvement in histological findings. Edaravone lowered the levels of TNF-α and IL-6 and reduced the number of TUNEL-positive cells. In addition, 24 h after edaravone treatment, caspase-3 activity and mortality were reduced. Edaravone may effectively ameliorate GalN/LPS-induced liver injury in mice by reducing proinflammatory cytokines and inhibiting apoptosis.
Highlights
Acute liver injury results from the massive death of liver cells, leading to the development of hepatic encephalopathy and severe impairment of liver function [1]
Hepatocyte apoptosis was measured by TUNEL staining; proinflammatory cytokines [tumor necrosis factor-a (TNF-a) and interleukin-6 (IL-6)] in the liver were assayed by ELISA; expression of caspase-8 and caspase-3 proteins was detected by Western blot assay; and caspase-3 activity was determined
Hepatocyte necrosis is a characteristic feature of fulminant hepatic failure, but increasing evidence indicates a dominant role of hepatocyte apoptosis in the www.bjournal.com.br pathogenesis of fulminant hepatic failure [11]
Summary
Acute liver injury results from the massive death of liver cells, leading to the development of hepatic encephalopathy and severe impairment of liver function [1]. Acute liver injury still has a high mortality rate, despite significant progress in liver support systems and liver transplantation. A variety of studies have been conducted to investigate the pathogenic mechanism of acute liver injury, and various measures have been taken to treat this disease. A free-radical scavenger, has been found to exert protective effects on injuries to the brain [2], lung [3], and liver [4]. The protective effects of edaravone are attributed to the direct scavenging of hydroxyl radicals and inhibition of lipoxygenase activity [7]
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callMore From: Brazilian Journal of Medical and Biological Research
Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
