Differential effects of olive oil, soybean oil, corn oil and lard oil on carbon tetrachloride-induced liver fibrosis in mice.

Yanan Gao,Qiang Gao,Xuguang Li,Haobin Jin,Yueping Guo,Li Fan

doi:10.1042/bsr20191913

Abstract

Olive oil could attenuate carbon tetrachloride (CCl4) induced liver fibrosis (LF) in mouse model. The present study aimed to evaluate the effects of other common oils on CCl4 induced LF. Healthy male ICR mice were administered with CCl4 intraperitoneally at 2.5 ml/kg twice a week for total 3 weeks. Mice were pre-treated with olive oil, soybean oil, corn oil or lard oil. After treatment, histopathological changes were observed using Masson trichrome staining, and alanine aminotransferase (ALT), aspartate aminotransferase (AST), malondialdehyde (MDA), hydroxyproline (HYP) and triglyceride (TG) were measured by commercial kits. The expression of LF related genes was detected by quantitative real-time PCR. We found that soybean oil or olive oil significantly reduced ALT and AST levels in serum, and MDA, HYP and TG levels in the liver, compared with corn oil or lard oil. Moreover, Masson trichrome staining and real-time PCR showed that the mice treated with CCl4 dissolved in soybean oil or olive oil had less fibrosis and apoptosis in the liver comparted to the mice treated with CCl4 dissolved in corn oil or lard oil. In conclusion, soybean oil but not corn or lard oil exerts protective effects against CCl4 induced LF in mice, possibly due to its antioxidant activity.

Highlights

The liver is important to the homeostasis in human body [1]
There was no significant difference between olive oil and soybean oil carbon tetrachloride (CCl4) groups
We demonstrated that olive oil and soybean oil had similar effects on CCl4-induced liver fibrosis (LF)

Summary

Introduction

The liver is important to the homeostasis in human body [1]. Alcohol, medicine and carbon tetrachloride (CCl4) may cause hepatotoxicity and promote liver fibrosis (LF) through the activation of hepatic stellate cells (HSCs) and extracellular matrix (ECM) [2]. Matrix metalloproteinases (MMPs) and tissue inhibitors of metalloproteinases (TIMPs) are essential to the development of LF [5]. HSCs have been shown to secrete inflammatory cytokines, TGF-β, tumor necrosis factor-α and platelet-derived growth factor (PDGF), leading to the up-regulation of α-smooth muscle actin (α-SMA) as a sign of activation [6]. Up-regulated Timp and Timp expression may contribute to ECM deposition in the liver through inhibiting the activity of MMPs [8]. MMP-9 could promote HSCs apoptosis and accelerate the recovery of LF [9]. With the progression of fibrosis, the expression of PDGF and its receptor PDGFR in the liver is increased [10]

Methods

Results

Conclusion