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Inhibitory Effects of <i>Ehretia tinifolia</i> Extract on the Excessive Oxidative and Inflammatory Responses in Lipopolysaccharide-Stimulated Mouse Kupffer Cells

<i>Ehretia tinifolia</i> (<i>E. tinifolia</i>) L., an evergreen tree with substantial biological activity, including antioxidant and anti-inflammatory effects, has been used in many herbal and traditional medicines. To elucidate its antioxidant and anti-inflammatory activity...

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Main Authors: Jae Sung Lim (Author), Sung Ho Lee (Author), Hyosuk Yun (Author), Da Young Lee (Author), Namki Cho (Author), Guijae Yoo (Author), Jeong Uk Choi (Author), Kwang Youl Lee (Author), Tran The Bach (Author), Su-Jin Park (Author), Young-Chang Cho (Author)
Format: Book
Published: MDPI AG, 2023-09-01T00:00:00Z.
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Summary:<i>Ehretia tinifolia</i> (<i>E. tinifolia</i>) L., an evergreen tree with substantial biological activity, including antioxidant and anti-inflammatory effects, has been used in many herbal and traditional medicines. To elucidate its antioxidant and anti-inflammatory activity and the underlying mechanisms, we applied a methanol extract of <i>E. tinifolia</i> (ETME) to lipopolysaccharide (LPS)-stimulated mouse immortalized Kupffer cells. ETME suppressed the LPS-induced increase in nitric oxide, a mediator for oxidative stress and inflammation, and restored LPS-mediated depletion of total glutathione level by stabilizing antioxidative nuclear factor erythroid 2-related factor 2 (Nrf2) and the subsequent increase in heme oxygenase-1 levels. Furthermore, ETME inhibited the LPS-induced production of pro-inflammatory cytokines, including tumor necrosis factor-α, interleukin (IL)-1β, and IL-6. The inhibitory effects of ETME on pro-inflammatory responses were regulated by ETME-mediated dephosphorylation of mitogen-activated protein kinases (MAPKs: p38, p44/p42, and stress-associated protein kinase/c-Jun N-terminal kinase) and inhibition of nuclear localization of nuclear factor kappa B (NF-κB). These results suggest that ETME is a possible candidate for protecting Kupffer cells from LPS-mediated oxidative stress and excessive inflammatory responses by activating antioxidant Nrf2/HO-1 and inhibiting pro-inflammatory NF-κB and MAPKs, respectively.
Item Description:10.3390/antiox12101792
2076-3921

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