Abstract

The main objective of this study is to evaluate the hepatoprotective impact of TLR9 antagonist ODN 2088 against carbon tetrachloride (CCl4)-induced acute liver injury. In this study, 24 mice were grouped into four groups. CCl4 was introduced in all groups except for the control group intraperitoneally after pretreatment with ODN 2088 and silymarin for seven days. To assess the liver injury, serum alanine Aminotransferase (ALT) and aspartate Aminotransferase (AST) were estimated and histopathological changes in the liver tissue were investigated. Expression of pro-inflammatory cytokines including TNF-α and IL-6 were measured. It was observed that the serum levels of biochemical parameters such as ALT and AST were remarkably elevated in mice treated only with CCl4 compared with the control mice (treated with corn oil). This increase in levels of ALT and AST was remarkably diminished by pretreatment with ODN 2088. The hepatoprotective impact of ODN 2088 on CCl4-intoxicated mice was verified by histopathological studies. ODN2088 pretreatment inhibited liver inflammation by diminishing the liver expression of CCl4-induced activity of TNF-α and IL-6. In conclusion, TLR9 antagonist, ODN 2088, protected the mice against CCl4-induced liver damage and inflammation by down-regulating the expression of pro-inflammatory cytokines.

Highlights

  • Acute liver injury can develop when the liver is exposed to various hepatotoxic factors such as toxic chemicals, pathogen infections and drugs

  • Necrosis and apoptosis are two processes that regenerate in the liver tissue prior to CCl4 introduction, which can result in stimulation of hepatic inflammation (Yang et al, 2015) and Extracellular Matrix (ECM) accumulation (Chiu et al, 2018)

  • Group III were administrated TLR9 antagonist ODN2088 via ip injection for seven days (50 ug/20 g body weight resuspended in endotoxin-free water), CCl4 was ip injected on the seventh day

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Summary

Introduction

Acute liver injury can develop when the liver is exposed to various hepatotoxic factors such as toxic chemicals, pathogen infections and drugs. It is strongly associated with development of oxidative stress and inflammation in the liver tissue (Lee et al, 2019). When CCl4 is introduced in the body, cytochrome P450 enzymes metabolise it, resulting in production of trichloromethyl radicals Production of these radicals involves the Kupffer cell activation and releasing of pro-inflammatory cytokines, such as Tumour Necrosis Factor-α (TNF-α) and interleukin (IL-6) (Chiu et al, 2018). CCl4 can stimulate the oxidative degradation of cellular lipids and lipid peroxidation (Chiu et al, 2018)

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