Epimagnolin A inhibits IL‐6 production by inhibiting p38/NF‐κB and AP‐1 signaling pathways in PMA‐stimulated THP‐1 cells

Chun, Hyun-Woo; Kim, Soojin; Pham, Thu-Huyen; Bak, Yesol; Oh, Jae-Wook; Ryu, Hyung Won; Oh, Sei‐Ryang; Jiang, Hong; Yoon, Do‐Young

doi:10.1002/tox.22746

Cited by 16 publications

(19 citation statements)

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“…Fargesin is one of the main components of Magnolia fargesii and has traditionally been used to treat sinusitis and inflammation. Moreover, fargesin's anti-inflammatory effects can inhibit NF-ĸB signaling and reduce nitric oxide in a variety of cell types [25][26][27]. A recent study has shown that fargesin can inhibit murine malignancy by regulating the P38/MAPK signaling pathway [28].…”

Section: Introductionmentioning

confidence: 99%

Fargesin ameliorates osteoarthritis via macrophage reprogramming by downregulating MAPK and NF-κB pathways

Zhang

Pan

et al. 2021

Arthritis Res Ther

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Background To investigate the role and regulatory mechanisms of fargesin, one of the main components of Magnolia fargesii, in macrophage reprogramming and crosstalk across cartilage and synovium during osteoarthritis (OA) development. Methods Ten-week-old male C57BL/6 mice were randomized and assigned to vehicle, collagenase-induced OA (CIOA), or CIOA with intra-articular fargesin treatment groups. Articular cartilage degeneration was evaluated using the Osteoarthritis Research Society International (OARSI) score. Immunostaining and western blot analyses were conducted to detect relative protein. Raw264.7 cells were treated with LPS or IL-4 to investigate the role of polarized macrophages. ADTC5 cells were treated with IL-1β and conditioned medium was collected to investigate the crosstalk between chondrocytes and macrophages. Results Fargesin attenuated articular cartilage degeneration and synovitis, resulting in substantially lower Osteoarthritis Research Society International (OARSI) and synovitis scores. In particular, significantly increased M2 polarization and decreased M1 polarization in synovial macrophages were found in fargesin-treated CIOA mice compared to controls. This was accompanied by downregulation of IL-6 and IL-1β and upregulation of IL-10 in serum. Conditioned medium (CM) from M1 macrophages treated with fargesin reduced the expression of matrix metalloproteinase-13, RUNX2, and type X collagen and increased Col2a1 and SOX9 in OA chondrocytes, but fargesin alone did not affect chondrocyte catabolic processes. Moreover, fargesin exerted protective effects by suppressing p38/ERK MAPK and p65/NF-κB signaling. Conclusions This study showed that fargesin switched the polarized phenotypes of macrophages from M1 to M2 subtypes and prevented cartilage degeneration partially by downregulating p38/ERK MAPK and p65/NF-κB signaling. Targeting macrophage reprogramming or blocking the crosstalk between macrophages and chondrocytes in early OA may be an effective preventive strategy.

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Section: Introductionmentioning

confidence: 99%

Fargesin ameliorates osteoarthritis via macrophage reprogramming by downregulating MAPK and NF-κB pathways

Zhang

Pan

et al. 2021

Arthritis Res Ther

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“…The liver function has been improved by inhibiting NF-κB induced-activation of proinflammatory factors such as tumor necrosis factor-alpha (TNFα), interleukin-6 (IL-6), and PGE2, and iNOS, COX-2, and matrix metallopeptidase-9 in LPSstimulated RAW 264.7 macrophages as well as in acute liver fibrosis mouse model [38,40,41]. Lignan can inhibit binding affinity between NF-κB and AP-1 transcription factors to interleukins (IL-6 promoter and IL-6) production through p38/NF-κB and AP-1 signaling pathways in cancer [42]. It has been reported that LBDE repressed the activation of COX-2 and iNOS genes by blocking the activation of NF-κB [12,15,23].…”

Section: Discussionmentioning

confidence: 99%

Lirioresinol B dimethyl ether inhibits NF-κB and COX-2 and activates IκBα expression in CCl4-induced hepatic fibrosis

Shehzad

Rehmat

Ul-Islam

et al. 2020

BMC Complement Med Ther

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Background: Inflammation is one of the key components in the initiation and progression of hepatic diseases. If not treated, inflammation may cause cell dysplasia, and ultimately cancer. In the current study, we investigated the anti-inflammatory and anti-cancer activities of plant isolated compound Lirioresinol B Dimethyl Ether (LBDE) extracted from the seeds of Magnolia fargesii CHENG (Magnoliaceae) against HepG2 cells as well as in BALB/C male mice. Methods: We assessed the antioxidant and anti-proliferative effects of plant compounds using DPPH assay and HepG2 cell lines. Carbon tetrachloride (CCl 4 ) and Diethylnitrosamine (DEN) were used to induce liver cell dysplasia followed by hepatocellular carcinoma (HCC) in BALB/C male mice for 12 weeks. We investigated the underlying mechanism by using histopathology and immunoblot experiments.Results: Intraperitoneal injection of LBDE (50 mg/kg body weight/day) inhibited CCl 4 -induced HCC. Free radical scavenging assay shows the strong anti-oxidant activity of LBDE. Western blot results show that LBDE downregulated nuclear factor kappa B (NFκB) and cyclooxygenase (COX-2) by preventing the phosphorylation of I kappa B alpha (IκBα) in CCl 4 treated group. LBDE also improved liver function by decreasing Alkaline Phosphatase (ALP), aspartate aminotransferase (AST) and Alanine Aminotransferase (ALT) levels. Histopathology results revealed that LBDE decreased granulomas and express normal morphology of hepatocytes.Conclusions: These preliminary results show that LBDE has the potential to inhibit CCl 4 -induced liver cell dysplasia and prevents cancer development by regulating NFκB/COX-2 activation.

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“…After 2 h of PSO pretreatment, JME/CF15 cells were stimulated with 10 ng/ml IL-13 for 24 h at 37˚C to generate a cell-based AR model. In this paper, cells were pretreated with 10 nM PMA for 24 h and 15 µl SP600125 for 24 h at 37˚C, as outlined in previous studies (22,23) Database. According to the GEO (https://www.ncbi.nlm.nih.…”

Section: Methodsmentioning

confidence: 99%

Psoralen inhibits the inflammatory response and mucus production in allergic rhinitis by inhibiting the activator protein 1 pathway and the downstream expression of cystatin‑SN

et al. 2021

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Psoralen (PSO) exerts anti-inf lammatory pharmacological effects and plays an important role in a variety of inflammatory diseases. However, the effects of PSO with allergic rhinitis (AR) are yet to be reported. In the present study, an in vitro AR model was generated by inducing JME/CF15 human nasal epithelial cells with IL-13, after which MTT was used to assess the cytotoxicity of PSO. The expression levels of inflammatory cytokines (granulocyte-macrophage colony-stimulating factor and Eotaxin) were determined by ELISA. Furthermore, the expression of inflammatory IL-6 and -8, as well as mucin 5AC, was assessed by reverse transcription-quantitative PCR and western blotting, and cellular reactive oxygen species were detected using a 2',7'-dichlorodihydrofluorescein diacetate fluorescent probe. Western blotting was also used to detect the expression and phosphorylation of c-Fos and c-Jun in the activator protein 1 (AP-1) pathway, as well as the expression of cystatin-SN (CST1). PSO inhibited the inflammatory response and mucus production in IL-13-induced JME/CF15 cells. Furthermore, the levels of c-Fos and c-Jun phosphorylation in the AP-1 pathway were decreased in IL-13-induced JME/CF15 cells following PSO treatment. The expression of pathway proteins was activated by the addition of PMA, an AP-1 pathway activator, which concurrently reversed the inhibitory effects of PSO on the inflammatory response and mucus formation. The addition of an AP-1 inhibitor (SP600125) further inhibited pathway activity, and IL-13-induced inflammation and mucus formation was restored. In conclusion, PSO regulates the expression of CST1 by inhibiting the AP-1 pathway, thus suppressing the IL-13-induced inflammatory response and mucus production in nasal mucosal epithelial cells.

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Epimagnolin A inhibits IL‐6 production by inhibiting p38/NF‐κB and AP‐1 signaling pathways in PMA‐stimulated THP‐1 cells

Cited by 16 publications

References 50 publications

Fargesin ameliorates osteoarthritis via macrophage reprogramming by downregulating MAPK and NF-κB pathways

Fargesin ameliorates osteoarthritis via macrophage reprogramming by downregulating MAPK and NF-κB pathways

Lirioresinol B dimethyl ether inhibits NF-κB and COX-2 and activates IκBα expression in CCl4-induced hepatic fibrosis

Psoralen inhibits the inflammatory response and mucus production in allergic rhinitis by inhibiting the activator protein 1 pathway and the downstream expression of cystatin‑SN

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