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

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

  • Oxid Med Cell Longev. 2018 Mar 20;2018:7616852. doi: 10.1155/2018/7616852.
Yan-Ru Li 1 Guo-Hui Li 2 Lin Sun 1 Lin Li 1 Yue Liu 1 De-Gang Kong 1 Shu-Qi Wang 1 Dong-Mei Ren 1 Xiao-Ning Wang 1 Hong-Xiang Lou 1 Tao Shen 1
Affiliations

Affiliations

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

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.

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