Abstract

Nepeta cataria L. has long been used in folk food and medicine for several functions. Essential oils (EOs) were extracted from Nepeta cataria L. by supercritical fluid extraction. The results of animal experiments showed that EOs from Nepeta cataria L. significantly attenuated acetaminophen-induced liver damage. Further study confirmed that EOs were able to increase mRNA expression of uridine diphosphate glucuronosyltransferases (UGTs) and sulfotransferases (SULTs), as well as inhibit CYP2E1 activities, and thereby suppressed toxic intermediate formation. Nrf-2 activation might be involved in EOs-induced up-regulation of Phase II enzymes. Collectively, our data provide evidence that EOs protect the liver against acetaminophen-induced liver injury mainly by accelerating acetaminophen harmless metabolism, implying that EOs can be considered as a potential natural resource to develop hepatoprotective agent.

Highlights

  • Nepeta cataria L. is a fragrant annual herb, widely distributed in Asia, Europe and North America since the Eastern Han Dynasty

  • The levels of alanine aminotransferase (ALT) and aspartate aminotransferase (AST) have no significant difference in essential oil (EO)-APAP and NAC-APAP treatment group, suggestion EOs can prevent APAP-induced liver injury

  • The activated nuclear factor erythroid 2-related factor 2 (Nrf2) was transfer from cytoplasm into nuclear, the nuclear/cytosolic relative expression was significantly increased in EOs treatment group, suggestion EOs were induced Nrf2 transfer from cytoplasm to nucleus, it leads to transcriptional activation of antioxidant enzymes, such as heme oxygenase-1 (HO-1), Superoxide dismutase (SOD), CAT (Figures 2 and 3) and Phase II metabolic enzyme, such as uridine diphosphate glucuronosyltransferases (UGTs), SULT (Figure 4)

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Summary

Introduction

Nepeta cataria L. is a fragrant annual herb, widely distributed in Asia, Europe and North America since the Eastern Han Dynasty. It has been traditionally and popularly used as both food and medicine for thousands of years [1]. Most of APAP is metabolized by Phase II conjugating enzymes, mainly sulfotransferase (SULT) and UDP-glucuronosyltransferase (UGT), converting it to nontoxic compounds which are excreted with the urine. When Phase II metabolizing enzymes are saturated after APAP overdose, excessive NAPQ1 deplete GSH, leading to covalent binding of sulfhydryl groups in cellular proteins, this results liver oxidative stress [8,9]

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