Abstract

Ammannia baccifera Linn. is commonly used as a traditional medicine in India and China. The antioxidant potential of an ethanolic extract of A. baccifera (EEAB; 250 mg/kg and 500 mg/kg) was evaluated against CCL4-induced toxicity in rats. Antioxidant activity was assessed by measuring the enzymatic and non-enzymatic antioxidants. Phytochemical constituents of EEAB were also analyzed by using UHPLC-QTOF-MS. EEAB treatment markedly reduced CCl4 effects on lipid peroxidation, cholesterol, triacylglycerides, and protein carbonyls. It increased the levels of phospholipids, total sulfhydryl, and antioxidant enzymes, which were reduced by CCl4 intoxication. Treatment with EEAB significantly alleviated the CCl4 effect on non-enzymatic antioxidants. Isoenzyme pattern analyses revealed that significant alterations in superoxide dismutase (SOD1), glutathione peroxidase (GPx2, GPx3), and catalase (CAT) occurred in rats that were exposed to CCl4 and restored post EEAB treatment. Moreover, CCl4-induced down regulation of SOD, CAT, and GPx gene expression was conversely counteracted by EEAB. Its bioactivity may be due to its incorporation of major compounds, such as chlorogenic acid, quercetin, protocatechuic acid, lamioside, crocetin, and khayasin C. These results suggest that EEAB may be used as a potent antioxidant and hepatoprotective agent since it is a rich source of flavonoids and phenolic compounds.

Highlights

  • Carbon tetrachloride (CCl4 ) is a classical hepatotoxicant model that is often studied for xenobiotic-induced oxidative hepatotoxicity [1]

  • The results show that the positive ion chromatogram yielded significantly higher signals

  • We found a marked decrease in vitamin C and vitamin E after CCl4 treatment, which were recovered by ethanolic extract of A. baccifera (EEAB) treatment

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Summary

Introduction

Carbon tetrachloride (CCl4 ) is a classical hepatotoxicant model that is often studied for xenobiotic-induced oxidative hepatotoxicity [1]. Bio-activation of the hepatic cytochrome P450 system catabolizes CCl4 to trichloromethyl radical (CCl3 − ), which is a highly reactive metabolite. Radical further reacts with oxygen to form the most toxic reactive trichloromethyl peroxy radical, which can bind to macromolecules. This leads to cell membrane disruption and cell death [2]. Oxidative stress arises when there is an imbalance between production and scavenging of reactive oxygen species (ROS). The major cause for various degenerative diseases including some hepatopathies is oxidative stress [3]

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