Schisandrae Fructus ethanol extract attenuates particulate matter 2.5-induced inflammatory and oxidative responses by blocking the activation of the ROS-dependent NF-κB signaling pathway

Hyesook Lee; Cheol Park; Da Hye Kwon; Hyun Hwangbo; So Young Kim; Min Yeong Kim; Seon Yeong Ji; Da Hye Kim; Jin-Woo Jeong; Gi-Young Kim; Hye-Jin Hwang; Yung Hyun Choi

doi:10.4162/nrp.2021.15.6.686

Schisandrae Fructus ethanol extract attenuates particulate matter 2.5-induced inflammatory and oxidative responses by blocking the activation of the ROS-dependent NF-κB signaling pathway

Nutr Res Pract. 2021 Dec;15(6):686-702. doi: 10.4162/nrp.2021.15.6.686. Epub 2021 May 7.

Authors

Hyesook Lee^{1

2}, Cheol Park³, Da Hye Kwon^{1

2}, Hyun Hwangbo^{1

2}, So Young Kim^{1

2}, Min Yeong Kim^{1

2}, Seon Yeong Ji^{1

2}, Da Hye Kim^{1

2}, Jin-Woo Jeong⁴, Gi-Young Kim⁵, Hye-Jin Hwang⁶, Yung Hyun Choi^{1

2}

Affiliations

¹ Anti-Aging Research Center, Dong-Eui University, Busan 47340, Korea.
² Department of Biochemistry, Dong-Eui University College of Korean Medicine, Busan 47227, Korea.
³ Division of Basic Sciences, College of Liberal Studies, Dong-Eui University, Busan 47340, Korea.
⁴ Nakdonggang National Institute of Biological Resources, Sangju 37242, Korea.
⁵ Department of Marine Life Sciences, Jeju National University, Jeju 63243, Korea.
⁶ Department of Food and Nutrition, Dong-Eui University, Busan 47340, Korea.

Abstract

Background/objectives: Schisandrae Fructus, the fruit of Schisandra chinensis Baill., has traditionally been used as a medicinal herb for the treatment of various diseases, and has proven its various pharmacological effects, including anti-inflammatory and antioxidant activities. In this study, we investigated the inhibitory effect of Schisandrae Fructus ethanol extract (SF) on inflammatory and oxidative stress in particulate matter 2.5 (PM2.5)-treated RAW 264.7 macrophages.

Materials/methods: To investigate the anti-inflammatory and antioxidant effects of SF in PM2.5-stimulated RAW 264.7 cells, the levels of pro-inflammatory mediator such as nitric oxide (NO) and prostaglandin E₂ (PGE₂), cytokines including interleukin (IL)-6 and IL-1β, and reactive oxygen species (ROS) were measured. To elucidate the mechanism underlying the effect of SF, the expression of genes involved in the generation of inflammatory factors was also investigated. We further evaluated the anti-inflammatory and antioxidant efficacy of SF against PM2.5 in the zebrafish model.

Results: The results indicated that SF treatment significantly inhibited the PM2.5-induced release of NO and PGE₂, which was associated with decreased inducible NO synthase and cyclooxygenase-2 expression. SF also attenuated the PM2.5-induced expression of IL-6 and IL-1β, reducing their extracellular secretion. Moreover, SF suppressed the PM2.5-mediated translocation of nuclear factor-kappa B (NF-κB) from the cytosol into nuclei and the degradation of inhibitor IκB-α, indicating that SF exhibited anti-inflammatory effects by inhibiting the NF-κB signaling pathway. In addition, SF abolished PM2.5-induced generation of ROS, similar to the pretreatment of a ROS scavenger, but not by an inhibitor of NF-κB activity. Furthermore, SF showed strong protective effects against NO and ROS production in PM2.5-treated zebrafish larvae.

Conclusions: Our findings suggest that SF exerts anti-inflammatory and antioxidant effects against PM2.5 through ROS-dependent down-regulating the NF-κB signaling pathway, and that SF can be a potential functional substance to prevent PM2.5-mediated inflammatory and oxidative damage.

Keywords: NF-kappa B; Particulate matter; inflammation; oxidative stress; reactive oxygen species.