Cycloartenyl Ferulate downregulates lipopolysaccharide stimulated iNOS mRNA via NF-kB suppression in RAW 264.7 macrophages

Islam, Samia; Ushio, Hideki; Hori, Masaru; Ozaki, Hiroshi

doi:10.3329/ajmbr.v2i4.30992

Cited by 2 publications

(2 citation statements)

References 15 publications

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“…As shown in Fig 1A and 1B, secretion of the inflammatory cytokines IL-6 and TNF-α was significantly suppressed by RBO treatment, while secretion of the anti-inflammatory cytokine IL-10 was reciprocally upregulated (Fig 1F). In this regard, Islam et al also reported that cycloartenyl ferulate extracted from rice bran downregulated the transcription of iNOS mRNA in an NF-kB-dependent manner in LPS-stimulated RAW 264.7 macrophages [30]. In contrast, Sierra et al reported that RBO enhanced the production of Th1-prone cytokines (i.e., IL-2 and TNF-α) and the proliferation of B cells in splenocytes compared to high-oleic sunflower oil [31].…”

Section: Discussionmentioning

confidence: 99%

Rice bran oil ameliorates inflammatory responses by enhancing mitochondrial respiration in murine macrophages

Lee

Park

et al. 2019

PLoS ONE

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Previous studies have revealed the anti-inflammatory properties of rice bran oil (RBO), but the detailed mechanisms are poorly understood. Recent studies on the molecular/cellular anti-inflammatory mechanisms of dietary components have demonstrated that mitochondrial respiration plays a key role in macrophage functioning. Since dietary lipids are major substrates for mitochondrial respiration through β-oxidation, the current study examined whether RBO regulates inflammatory responses by modulating mitochondrial energy metabolism. Palm oil (PO), enriched with palmitic acid which are known to be effectively taken up by cells and used for oxidative phosphorylation, served as a positive control. In the in vitro model of LPS-stimulated RAW 264.7 murine cells, the levels of pro-inflammatory cytokines (IL-6 and TNF-α) in the culture supernatant were significantly reduced by RBO treatment. In contrast, secretion of the anti-inflammatory cytokine IL-10 was upregulated by RBO. Transcription of genes encoding inflammatory mediator molecules (COX-2 and iNOS) and expression of activation markers (CD80, CD86, and MHC-II) in LPS-stimulated RAW 264.7 cells were suppressed by RBO. Mitochondrial respiration (as assessed by an extracellular flux analyzer) increased upon RBO treatment, as the basal respiration, maximal respiration, ATP production, and spare respiratory capacity were upregulated. In an in vivo study, C57BL/6 mice were fed a negative control diet containing corn oil (CO), PO, or RBO for 4 weeks, and bone marrow-derived macrophages (BMDM) were isolated from their tibias and femurs. In pro-inflammatory M1-polarized BMDM (M1-BMDM), the RBO-induced suppression of IL-6 and TNF-α was recapitulated in vivo. Mitochondrial respiration in M1-BMDM also increased following the RBO intervention and the PO control treatment as compared to CO fed negative control. Overall, the current study for the first time demonstrates that RBO regulates inflammatory responses in murine macrophages by upregulating mitochondrial respiration. Further clinical studies are required to validate the animal study.

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Section: Discussionmentioning

confidence: 99%

Rice bran oil ameliorates inflammatory responses by enhancing mitochondrial respiration in murine macrophages

Lee

Park

et al. 2019

PLoS ONE

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“…Studies have shown that LPS, as a toxin that induces oxidative damage, has been widely used to establish animal models of inflammation and bacterial infections. LPS activates the NF-κB signaling pathway through toll-like receptor (TLR-4), and promotes the production of downstream inflammatory cytokines including IL-1β, IL-6, TNF-α [6]. It is reported that cell SOD activity was decreased, the level of oxidative stress was increased and cell activity was reduced in LPS treated pheochromocytoma murine adrenoma cell (PC12).…”

Section: Introductionmentioning

confidence: 99%

Inhibition of USP14 suppresses ferroptosis and inflammation in LPS-induced goat mammary epithelial cells through ubiquitylating the IL-6 protein

Zhu¹,

Sui²,

Shi³

et al. 2022

Hereditas

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Background Ferroptosis, a novel manner of cell death depended on iron ion, contributed to goat mammary epithelial cell dysfunction. Interleukin-6 (IL-6) is a major pro-inflammatory factor during many inflammation-related diseases including mastitis, and a quite recently identified ferroptosis inducer. This study aims to explore the role of IL-6 in the dysfunction of goat mammary epithelial cells (GMECs) and how the level of IL-6 was regulated. Methods Primary GMECs were isolated, cultured and treated with lipopolysaccharide (LPS) alone or together with Ferrostatin-1 (Fer-1), a well-known ferroptosis inhibitor. CCK-8 was used to detect cell viability, ELISA was used to detect TNF-α content, and the levels of ROS, GSH and MDA were analyzed with DCFDA-cell ROS detection kit, GSH assay kit and MDA assay kit, respectively. The iron ion level was measured with an iron assay kit. Results The expression level of IL-6 protein in GMECs was up-regulated in response to LPS treatment, and the secretion of TNF-α, the cell oxidative stress level and the Fe2+ ion content was robustly increased, which could be reversed by Fer-1 treatment. Knockdown of IL-6 decreased cell oxidative stress level and inhibited ferroptosis in LPS-treated GMECs. Further, ubiquitin experiment and co-immunoprecipitation assay showed that USP14 upregulated IL-6 protein expression by reducing the ubiquitination of IL-6, and overexpression of IL-6 reversed the inhibitory effect of USP14 shRNA on LPS-treated GMECs ferroptosis. The NRF2 inhibitor Brusatol reversed the inhibitory effect of IL-6 shRNA on LPS-treated ferroptosis. Conclusion IL-6 protein is deubiquitinated by USP14 and upregulated in LPS-treated GMECs, further promoting ferroptosis and inflammation through the NRF2 signaling pathway.

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Cycloartenyl Ferulate downregulates lipopolysaccharide stimulated iNOS mRNA via NF-kB suppression in RAW 264.7 macrophages

Cited by 2 publications

References 15 publications

Rice bran oil ameliorates inflammatory responses by enhancing mitochondrial respiration in murine macrophages

Rice bran oil ameliorates inflammatory responses by enhancing mitochondrial respiration in murine macrophages

Inhibition of USP14 suppresses ferroptosis and inflammation in LPS-induced goat mammary epithelial cells through ubiquitylating the IL-6 protein

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