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Oxidative Medicine and Cellular Longevity
Volume 2018, Article ID 7616852, 13 pages
Research Article

Ingredients from Litsea garrettii as Potential Preventive Agents against Oxidative Insult and Inflammatory Response

1Key Lab of Chemical Biology (MOE), School of Pharmaceutical Sciences, Shandong University, 44 Wenhua Xi Road, Jinan 250012, China
2Department of Pharmacy, Jinan Maternity and Child Care Hospital, Jianguo Xiaojingsan Road, Jinan 250000, China

Correspondence should be addressed to Tao Shen; nc.ude.uds@oatnehs

Received 21 September 2017; Revised 19 December 2017; Accepted 9 January 2018; Published 20 March 2018

Academic Editor: Roberto Mattioli

Copyright © 2018 Yan-Ru Li et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Oxidative stress and inflammation undoubtedly contribute to the pathogenesis of many human diseases. The nuclear transcription factor erythroid 2-related factor (Nrf2) and the nuclear factor κB (NF-κB) play central roles in regulation of oxidative stress and inflammation and thus are targets for developing agents against oxidative stress- and inflammation-related diseases. Our previous study indicated that the EtOH extract of Litsea garrettii protected human bronchial epithelial cells against oxidative insult via the activation of Nrf2. In the present study, a systemic phytochemical investigation of L. garrettii led to the isolation of twenty-one chemical ingredients, which were further evaluated for their inhibitions on oxidative stress and inflammation using NAD(P)H:quinone reductase (QR) assay and nitric oxide (NO) production assay. Of these ingredients, 3-methoxy-5-pentyl-phenol (MPP, 5) was identified as an Nrf2 activator and an NF-κB inhibitor. Further studies demonstrated the following: (i) MPP upregulated the protein levels of Nrf2, NAD(P)H:quinone oxidoreductase 1 (NQO1), and glutamate-cysteine ligase regulatory subunit (GCLM); enhanced the nuclear translocation and stabilization of Nrf2; and inhibited arsenic [As(III)]-induced oxidative insult in normal human lung epithelial Beas-2B cells. And (ii) MPP suppressed the nuclear translocation of NF-κB p65 subunit; inhibited the lipopolysaccharide- (LPS-) stimulated increases of NF-κB p65 subunit, COX-2, iNOS, TNF-α, and IL-1β; and blocked the LPS-induced biodegrade of IκB-α in RAW 264.7 murine macrophages. Taken together, MPP displayed potential preventive effects against inflammation- and oxidative stress-related diseases.