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

Wei-Ting Chen,Chieh-Ling Yang,Mei-Chin Yin

doi:10.7603/s40681-014-0005-2

Abstract

BackgroundProtective effects of Houttuynia cordata aqueous extract (HCAE) against acetaminophen-induced hepatotoxicity in Balb/cA mice were examined.MethodsHCAE, 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).ResultsAcetaminophen 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).ConclusionThese results support that HCAE could provide hepato-protection

Highlights

Acetaminophen is an antipyretic and analgesic drug, and metabolized by cytochrome P450 system, which leads to the formation of. n-acetyl-pbenzoquinoneimine (NAPQI) [1,2] A large dose of this drug causes depletion of cellular glutathione (GSH) in liver because NAPQI reacts rapidly with GSH, which enhances oxidation stress in conjunction with mitochondrial dysfunction, and leads to massive hepatocyte necrosis, liver failure or death [3,4]
Our present study further found that the pre-intake of Houttuynia cordata aqueous extract (HCAE) markedly protected liver against subsequent acetaminophen-induced oxidative and inflammatory injury via decreasing ALT and AST levels, increasing GSH retention, suppressing cytochrome P450 2E1 (CYP2E1) activity, lowering IL-6 and MCP-1 release
We found that the pre-intake of HCAE effectively alleviated acetaminophen-induced GSH depletion and GSSG increase in liver

Summary

Introduction

Acetaminophen is an antipyretic and analgesic drug, and metabolized by cytochrome P450 system, which leads to the formation of. n-acetyl-pbenzoquinoneimine (NAPQI) [1,2] A large dose of this drug causes depletion of cellular glutathione (GSH) in liver because NAPQI reacts rapidly with GSH, which enhances oxidation stress in conjunction with mitochondrial dysfunction, and leads to massive hepatocyte necrosis, liver failure or death [3,4]. Our previous study found that Houttuynia cordata aqueous extract (HCAE) was rich in phenolic acids and flavonoids; and HCAE intake at 1 and 2% suppressed high fat diet induced oxidative and inflammatory stress in heart and liver via reducing malondialdehyde level, retaining GSH content and glutathione peroxidase activity, declining TNF-alpha, IL-1beta and IL-6 production [16]. Those previous studies suggest that HCAE may provide nutritional benefit for liver. The influence of this extract upon CYP2E1 activity, associated antioxidant enzymes activities, and cytokines were evaluated

Materials

Animals and diets

Cytokines measurements

Results

Determination of lipid oxidation and ROS

Discussion