Artemisia has long been used in traditional medicine and as a food source for different functions in eastern Asia. Artemisia vulgaris L. (AV) is a species of the genus Artemisia. Essential oils (EOs) were extracted from AV by subcritical butane extraction. EO contents were detected by electronic nose and headspace solid-phase microextraction coupled with gas chromatography (HS-SPME-GC-MS). To investigate the hepatoprotective effects, mice subjected to liver injury were treated intragastrically with EOs or eucalyptol for 3 days. Acetaminophen (APAP) alone caused severe liver injury characterized by significantly increased serum AST and ALT levels, ROS and hepatic malondialdehyde (MDA), as well as liver superoxide dismutase (SOD) and catalase (CAT) depletions. EOs significantly attenuated APAP-induced liver damages. Further study confirmed that eucalyptol is an inhibitor of Keap1, the affinity K D of eucalyptol and Keap1 was 1.42 × 10 −5 , which increased the Nrf2 translocation from the cytoplasm into the mitochondria. The activated Nrf2 increased the mRNA expression of uridine diphosphate glucuronosyltransferases (UGTs) and sulfotransferases (SULTs), also inhibiting CYP2E1 activities. Thus, the activated Nrf2 suppressed toxic intermediate formation, promoting APAP hepatic non-toxicity, whereby APAP was metabolized into APAP-gluc and APAP-sulf. Collectively, APAP non-toxic metabolism was accelerated by eucalyptol in protecting the liver against APAP-induced injury, indicating eucalyptol or EOs from AV potentials as a natural source of hepatoprotective agent.

The present study aimed to determine the expression of vascular endothelial growth factor A (VEGFA) and microRNA (miRNA/miR)-27a in hippocampal tissues, and serum from a depression model of rats. In addition, the present study aimed to understand the mechanism of regulation of miR-27a in depression. A total of 40 male rats were selected, and divided into the control and depression model groups. The rats in the model group were subjected to 14 types of stimulations to model depression. By determining the body weight, syrup consumption rate and open field test score, the extent of depression in the rats was evaluated. Quantitative-polymerase chain reaction was used to determine the expression of VEGFA mRNA and miR-27a in hippocampal tissues, and serum. ELISA was used to measure the content of VEGFA protein in serum, while western blotting was employed to determine the expression of VEGFA protein in hippocampal tissues. A dual luciferase assay was carried out to identify the interactions between VEGFA mRNA and miR-27a. The rats in the depression model group showed depression symptoms and the depression model was successfully constructed. Rats with depression had lower VEGFA mRNA and protein expression in the hippocampus, and peripheral blood compared with the control group. Rats in the depression model group had reduced levels of miR-27a in the hippocampus and peripheral blood, which may be associated with the levels of VEGFA. miR-27a was able to bind with the 3′-untranslated region of VEGFA mRNA to regulate its expression. The present study demonstrated that miR-27a expression in hippocampal tissues and blood from rats with depression is upregulated, while the expression of VEGFA mRNA and protein is downregulated. miR-27a may participate in the pathological process of depression in rats by regulating VEGFA.

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