Magnolol Inhibits LPS-Induced Inflammatory Response in Uterine Epithelial Cells
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Magnolol Inhibits LPS-Induced Inflammatory Response in Uterine Epithelial Cells Jia Luo,1 Yanwen Xu,2 Minfang Zhang,2 Ling Gao,2 Cong Fang,2 and Canquan Zhou2,3
Abstract—Endometritis is an inflammation of the uterine lining that is commonly initiated at parturition. The uterine epithelial cells play an important role in defending against invading pathogens. Magnolol, a hydroxylated biphenyl compound isolated from Magnolia officinalis, has been shown to have antiinflammatory effects. The aim of this study was to investigate the anti-inflammatory effect of magnolol in modifying lipopolysaccharide (LPS)-induced signal pathways in mouse uterine epithelial cells. We found that magnolol inhibited TNF-α and IL-6 production in LPS-stimulated mouse uterine epithelial cells. We also found that magnolol inhibited LPS-induced NF-κB activation, IκBα degradation, phosphorylation of ERK, JNK, and P38. Furthermore, magnolol could significantly inhibit the expression of TLR4 stimulating by LPS. These results suggest that magnolol exerts an anti-inflammatory property by downregulating the expression of TLR4 upregulated by LPS, thereby attenuating TLR4-mediated NFκB and MAPK signaling and the release of pro-inflammatory cytokines. These findings suggest that magnolol may be a therapeutic agent against endometritis. KEY WORDS: TLR4; cytokine; magnolol; NF-κB; MAPK; LPS.
inflammatory cytokines, chemokines, and prostaglandins are elevated in the peritoneal fluid of women with endometriosis [5]. TLR4 was suggested to play an important role in such inflammatory situations. Bacterial lipopolysaccharide (LPS), the major constituent of the outer membrane of Gram-negative bacteria, has been reported to be an important risk factor of inflammation. LPS signals mainly via TLR4 receptors [6–8]. Activation of TLR4 by LPS induces the activation of NF-κB and MAPK pathways and finally results in the release of pro-inflammatory cytokines [9]. LPS stimulation of endometrial epithelial cells leads to increased TLR4 expression and triggers the pro-inflammatory cytokines which include TNF-α, IL-1β, and IL-6. These pro-inflammatory cytokines lead to inflammation and various other clinical manifestations. Therefore, treatments aimed at modulating TLR4 signaling may have potential therapeutic advantages for endometriosis. Magnolol (Fig. 1), a compound purified from Magnolia officinalis, is responsible for the plant’s pharmacological activities. Magnolol has been reported to have antibacterial, anti-tumor, and anti-inflammatory effects [10–12]. Magnolol was found to inhibit inflammatory cytokines production in LPS-activated macrophages and to attenuate LPS-induced acute lung injury
INTRODUCTION The uterus is a complex and special organ. It is easily contaminated by bacteria during parturition. Uterine bacterial infection after parturition can lead to disease, infertility, and even death [1]. The endometrium is the first line of defense against invading microbial pathogens. It recognizes pathogen-associated molecular patterns (PAMPs) shared by pathogens via innate immune receptors.
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