Dihydrofisetin exerts its anti-inflammatory effects associated with suppressing ERK/p38 MAPK and Heme Oxygenase-1 activation in lipopolysaccharide-stimulated RAW 264.7 macrophages and carrageenan-induced mice paw edema

Li, Kai Kai; Shen, Shuiwen; Deng, Xin; Shiu, Hoi Ting; Siu, Wing Sum; Leung, Ping Chung; Ko, Chun‐Hay; Cheng, Bao

doi:10.1016/j.intimp.2017.11.034

Cited by 35 publications

(22 citation statements)

References 51 publications

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“…Activated macrophages play a pivotal role in the regulation of inflammatory processes [23] and causes mass production of inflammatory mediators such as NO and PGE 2 , as well as pro-inflammatory cytokines such as TNF-α, IL-1β, and IL-6, leading to the progression of various inflammatory disorders [24]. In the present study, LPS-induced NO and PGE 2 were strongly suppressed by CRVS without having cytotoxic effects.…”

Section: Discussionsupporting

confidence: 46%

Cerevisterol Alleviates Inflammation via Suppression of MAPK/NF-κB/AP-1 and Activation of the Nrf2/HO-1 Signaling Cascade

et al. 2020

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As part of our continuous effort to find potential anti-inflammatory agents from endophytic fungi, a Fusarium solani strain, isolated from the plant Aponogeton undulatus Roxb., was investigated. Cerevisterol (CRVS) was identified from endophytic fungi, a Fusarium solani strain, and moreover exhibited anti-inflammatory activity. However, the underlying mode of action remains poorly understood. The aim of this study is to reveal the potential mechanisms of CRVS against inflammation on a molecular level in LPS-activated RAW 264.7 peritoneal macrophage cells. CRVS was isolated from F. solani and characterized based on spectral data analysis. The MTT assay was performed to measure cell viability in CRVS-treated macrophages. Anti-inflammatory activity was assessed by measurement of nitric oxide (NO) and prostaglandin E2 (PGE2) levels, as well as the production of various cytokines, such as tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), and -6 (IL-6) in LPS-stimulated macrophages. RT-PCR and immunoblotting analyses were done to examine the expression of various inflammatory response genes. A reporter gene assay was conducted to measure the level of nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) and activator protein-1 (AP-1) transactivation. CRVS suppresses the LPS-induced production of NO and PGE2, which is a plausible mechanism for this effect is by reducing the expression of iNOS and COX-2. CRVS also decreases the expression of pro-inflammatory cytokines, such as TNF-α, IL-6, and IL-1β. CRVS halted the nuclear translocation of NF-κB by blocking the phosphorylation of inhibitory protein κBα (IκBα) and suppressing NF-κB transactivation. The mitogen-activated protein kinases (MAPK) signaling pathways are also suppressed. CRVS treatment also inhibited the transactivation of AP-1 and the phosphorylation of c-Fos. Furthermore, CRVS could induce the nuclear translocation of nuclear factor erythroid 2-related factor 2 (Nrf2) by down-regulating Kelch-like ECH-associated protein 1 (Keap-1) and up-regulating hemeoxygenases-1 (HO-1) expression. The results suggest that CRVS acts as a natural agent for treating inflammatory diseases by targeting an MAPK, NF-κB, AP-1, and Nrf2-mediated HO-1 signaling cascade.

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Section: Discussionsupporting

confidence: 46%

Cerevisterol Alleviates Inflammation via Suppression of MAPK/NF-κB/AP-1 and Activation of the Nrf2/HO-1 Signaling Cascade

et al. 2020

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“…LPS is a well-known immune stimulant used to activate macrophage and production of cytokine is a major response. Based on the previous studies, the inhibition of pro-inflammatory cytokines (TNF-α, IL-1β, and IL-6) provide solid insights to develop functional products against inflammatory responses (Li et al 2018). According to the results we noted, the treatment of SJB-SHE has a potential to inhibit LPS-activated inflammation in RAW 264.7 macrophages by suppressing Results are expressed as the mean ± SD of three separate experiments.…”

Section: Discussionmentioning

confidence: 72%

“…According to the previous studies, MAPKs such as ERK1/2 and JNK are activated by LPS stimulation (Akira 2001). Taken together, the inhibition of MAPKs phosphorylation is a feasible approach to treat inflammatory diseases (Li et al 2018). In order to identify the effect of SJB-SHE on MAPK inhibition, the phosphorylation levels of ERK1/2 and JNK were evaluated using Western blot analysis.…”

Section: Discussionmentioning

confidence: 99%

Ethanol extract separated from Sargassum horneri (Turner) abate LPS-induced inflammation in RAW 264.7 macrophages

et al. 2019

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Background: This study is aimed at identifying the anti-inflammatory properties of 70% ethanol extract produced from an edible brown seaweed Sargassum horneri (SJB-SHE) with industrial-scale production by Seojin Biotech Co. Ltd. S. horneri is a rich source of nutrient and abundantly growing along the shores of Jeju, South Korea. Methods: Here, we investigated the effect of SJB-SHE on LPS-activated RAW 264.7 macrophages. The cytotoxicity and NO production of SJB-SHE were evaluated using MTT and Griess assays, respectively. Additionally, protein expression and gene expression levels were quantified using ELISA, Western blots, and RT-qPCR. Results: Our results indicated that pre-treatment of RAW 264.7 macrophages with SJB-SHE significantly inhibited LPS-induced NO and PGE 2 production. SJB-SHE downregulated the proteins and genes expression of LPS-induced iNOS and COX2. Additionally, SJB-SHE downregulated LPS-induced production of pro-inflammatory cytokines (tumor necrosis factor-α, interleukin (IL)-6, and IL-1β). Furthermore, SJB-SHE inhibited nuclear factor kappa-B (NF-κB) activation and translocation to the nucleus. SJB-SHE also suppressed the phosphorylation of mitogen-activated protein kinases (ERK1/2 and JNK). Conclusions: Collectively, our results demonstrated that SJB-SHE has a potential anti-inflammatory property to use as a functional food ingredient in the future.

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“…Based on current evidence, the HO-1 pathway plays an important role in the control of inflammation. Overexpression of HO-1 modulates proinflammatory processes in a number of cells including macrophages and endothelial cells [39,40]. Moreover, the anti-inflammatory role of HO-1 has been addressed in models dealing with human diseases, such as lupus erythematosus and rheumatoid arthritis [41][42][43][44], which are typically associated with bone loss.…”

Section: Discussionmentioning

confidence: 99%

Carbon Monoxide Releasing Molecule 3 Inhibits Osteoclastogenic Differentiation of RAW264.7 Cells by Heme Oxygenase-1

Pan

Song

Zong

et al. 2018

Cell Physiol Biochem

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Background/Aims: Increased osteoclastogenic differentiation may disrupt the balance of bone resorption and formation, giving rise to bone defective disease. The study aimed to investigate the influence of carbon monoxide releasing molecule 3 on osteoclastogenic differentiation of RAW264.7 cells, and explore the possible mechanism underlying the regulatory effect. Methods: Influence of CORM-3 on the proliferation of RAW264.7 cells was determined by CCK-8 assay. RAW264.7 cells were divided into four groups: Control group; Osteoclastogenic differentiation group, in which cells were induced osteoclastogenic differentiation in medium supplemented with 100μg/L RANKL and 50μg/L M-CSF; Degassed CORM-3-osteoclastogenic differentiation group, in which cells were pretreated with 200μmol/L degassed CORM-3 for 6hrs, and then induced osteoclastogenic differentiation; CORM-3-osteoclastogenic differentiation group, in which cells were pretreated with 200μmol/L CORM-3, and then induced osteoclastogenic differentiation. The mRNA and protein expression of RANK, TRAP, MMP-9, Cts-K and HO-1 of the cells during the osteoclastogenic differentiation was checked by RT-qPCR and Western blot. The induced osteoclasts were identified by TRAP staining. The HO-1 expression of the RAW264.7 cells was silenced by lentivirus transfection, and the expression of RANK, TRAP, MMP-9 and Cts-K was examined by RT-qPCR and Western blot. Results: CORM-3 promoted the proliferation of RAW264.7 cells at the concentration of 200μmol/L. Pretreatment with CORM-3, but not degassed CORM-3, significantly decreased the mRNA and protein expression of osteoclast-specific marker TRAP, RANK, MMP-9 and Cts-K induced by RANKL and M-CSF on day 5, 7 and 9 during the osteoclastogenic differentiation (P< 0.05). After HO-1 was silenced by lentivirus transfection, the mRNA and protein expression of TRAP, RANK, MMP-9 and Cts-K in group with CORM-3 pretreatment maintained the same level as in osteoclastogenic differentiation group. Conclusion: CORM-3 inhibits osteoclastogenic differentiation of RAW264.7 cells via releasing CO. The inhibitory effect is mediated partially by HO-1 pathway. The results suggest the potential application of CORM-3 on some bone defective diseases.

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Dihydrofisetin exerts its anti-inflammatory effects associated with suppressing ERK/p38 MAPK and Heme Oxygenase-1 activation in lipopolysaccharide-stimulated RAW 264.7 macrophages and carrageenan-induced mice paw edema

Cited by 35 publications

References 51 publications

Cerevisterol Alleviates Inflammation via Suppression of MAPK/NF-κB/AP-1 and Activation of the Nrf2/HO-1 Signaling Cascade

Cerevisterol Alleviates Inflammation via Suppression of MAPK/NF-κB/AP-1 and Activation of the Nrf2/HO-1 Signaling Cascade

Ethanol extract separated from Sargassum horneri (Turner) abate LPS-induced inflammation in RAW 264.7 macrophages

Carbon Monoxide Releasing Molecule 3 Inhibits Osteoclastogenic Differentiation of RAW264.7 Cells by Heme Oxygenase-1

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