Original article

BioMedicine

, 4:5

First online:

Open Access This content is freely available online to anyone, anywhere at any time.

Protective effects from Houttuynia cordata aqueous extract against acetaminophen-induced liver injury

  • Wei-ting ChenAffiliated withDepartment of Nutrition, China Medical University
  • , Chieh-ling YangAffiliated withDepartment of Nutrition, China Medical University
  • , Mei-chin YinAffiliated withDepartment of Nutrition, China Medical University Email author 

Abstract

Background

Protective effects of Houttuynia cordata aqueous extract (HCAE) against acetaminophen-induced hepatotoxicity in Balb/cA mice were examined.

Methods

HCAE, at 1 or 2 g/L, was added into the drinking water for 4 weeks. Acute liver injury was induced by acetaminophen treatment intraperitoneally (350 mg/kg body weight).

Results

Acetaminophen treatment significantly depleted hepatic glutathione (GSH) content, increased hepatic malonyldialdehyde (MDA), reactive oxygen species (ROS) and oxidized glutathione (GSSG) levels, and decreased hepatic activity of glutathione peroxidase (GPX), catalase and superoxide dismutase (SOD) (p<0.05). The pre-intake of HCAE alleviated acetaminophen-induced oxidative stress by retaining GSH content, decreasing MDA, ROS and GSSG production, and maintaining activity of GPX, catalase and SOD in liver (p<0.05). The pre-intake of HCAE also significantly lowered acetaminophen-induced increase in cytochrome P450 2E1 activity (p<0.05). Acetaminophen treatment increased hepatic release of interleukin (IL)-6, IL-10, tumor necrosis factor (TNF)-alpha and monocyte chemoattractant protein-1 (p<0.05). HCAE intake significantly diminished acetaminophen-induced elevation of these cytokines (p<0.05).

Conclusion

These results support that HCAE could provide hepato-protection

Keywords

Hepatotoxicity Houttuynia cordata Acetaminophen MCP-1 CYP2E1