An ethanol extract of &lt;i&gt;Aster yomena&lt;/i&gt; (Kitam.) Honda inhibits lipopolysaccharide-induced inflammatory responses in murine RAW 264.7 macrophages

Kang, Hye-Joo; Jeong, Ji-Suk; Park, No-Jin; Go, Geun-Bae; Kim, Sung Ok; Park, Cheol; Kim, Byung Woo; Hong, Su‐Hyun; Choi, Yung Hyun

doi:10.5582/bst.2016.01217

Cited by 15 publications

(13 citation statements)

References 43 publications

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“…We confirmed that H 2 O 2 suppressed cell viability of SH-SY5Y cells based on MTT assay. According to previous study, ethanol extract from AY (EEAY) showed no cytotoxicity at concentration up to 500 μg/mL [32]. EEAY decreased adipocyte differentiation in the 3T3-L1 cells by suppressing adipogenic transcriptional factors without cytotoxicity at the concentration of 200 μg/mL [13].…”

Section: Discussionmentioning

confidence: 94%

Neuroprotective effect ofAster yomena(Kitam.) Honda against hydrogen peroxide-induced oxidative stress in SH-SY5Y cells

Kim

Lee

et al. 2020

JABC

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Oxidative stress is one of the contributors of neurodegenerative disorders including Alzheimer's disease. According to previous studies, Aster yomena (Kitam.) Honda (AY) possesses variable pharmacological activities including anti-coagulant and anti-obesity effect. In this study, we aimed to determine the neuroprotective effect of ethyl acetate fraction from Aster yomena (Kitam.) Honda (EFAY) against oxidative stress. Therefore, we carried out 3-(4,5-dimethylthiazol-2-yl)-2,3-diphenyl tetrazolium bromide, lactate dehydrogenase (LDH), and 2',7'-dichlorofluorescin diacetate assays in SH-SY5Y neuronal cells treated with hydrogen peroxide (H 2 O 2). H 2 O 2-treated control cells exhibited reduced viability of cells, and increased LDH release and reactive oxygen species (ROS) production compared to normal cells. However, treatment with EFAY restored the cell viability and inhibited LDH release and ROS production. To investigate the underlying mechanisms by which EFAY attenuated neuronal oxidative damage, we measured protein expressions using Western blot analysis. Consequently, it was observed that EFAY downregulated cyclooxygenase-2 and interleukin-1β protein expressions in H 2 O 2-treated SH-SY5Y cells that mediated inflammatory reaction. In addition, apoptosis-related proteins including B-cell lymphoma-2-associated X protein/B-cell lymphoma-2 ratio, cleaved caspase-9, and cleaved-poly (ADP-ribose) polymerase protein expressions were suppressed when H 2 O 2-treated cells were exposed to EFAY. Our results indicate that EFAY ameliorated H 2 O 2-induced neuronal damage by regulating inflammation and apoptosis. Altogether, AY could be potential therapeutic agent for neurodegenerative diseases.

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Section: Discussionmentioning

confidence: 94%

Neuroprotective effect ofAster yomena(Kitam.) Honda against hydrogen peroxide-induced oxidative stress in SH-SY5Y cells

Kim

Lee

et al. 2020

JABC

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“…The transcription factor, NF-B is translocated to the nucleus by inflammatory stimuli such as LPS, and regulates DNA transcription and production of various pro-inflammatory genes such as inducible NO synthase (iNOS), cyclooxygenase-2 (COX-2), IL-1, TNF- 27,28) .…”

Section: Discussionmentioning

confidence: 99%

“…iNOS and COX-2 are responsible for the production of NO and PGE2, respectively. Bone cells stimulated by LPS increase iNOS gene expression and induce the release of overproduced NO 27) . NO not only inhibits osteoblast growth and increases apoptosis, but also regulates osteoclast activity and recruitment 27) .…”

Section: Discussionmentioning

confidence: 99%

Anti-Oral Microbial Activity and Anti-Inflammatory Effects of Rosmarinic Acid in Lipopolysaccharide-Stimulated MC3T3-E1 Osteoblastic Cells on a Titanium Surface

Heo

2020

J Dent Hyg Sci

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“…Although three enzymes, endothelial NOS, neuronal NOS, and iNOS, are involved in the synthesis of NO, iNOS expression is increased by inflammatory stimuli such as inflammatory and bacterial endotoxins and contributes to excessive NO production. 16 – 19 Among COXs, which is involved in the production of PGE 2 , COX-1 is expressed in most tissues and serves to maintain normal physiological functions, whereas COX-2 is transiently induced in response to growth factors or inflammatory stimuli. 20 – 22 Various types of inflammatory responses are directly associated with the production of abnormally high levels of NO and PGE 2 by upregulation of iNOS and COX-2.…”

Section: Discussionmentioning

confidence: 99%

Diallyl Trisulfide Suppresses the Production of Lipopolysaccharide-induced Inflammatory Mediators in BV2 Microglia by Decreasing the NF-κB Pathway Activity Associated With Toll-like Receptor 4 and CXCL12/CXCR4 Pathway Blockade

et al. 2018

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BackgroundDiallyl trisulfide (DATS), a garlic-derived organosulfuric compound, has been documented for potential anti-inflammatory effects. However, the mechanism in microglia remains unknown. In this study, we investigated the anti-inflammatory effects of DATS in lipopolysaccharide (LPS)-stimulated BV2 microglial cells.MethodsThe effects of DATS on LPS-induced pro-inflammatory mediators such as nitric oxide (NO) and prostaglandin E2 (PGE2) were assessed under conditions not in the cytotoxicity of DATS. The protein expression of inflammation regulatory genes was measured by Western blot analysis.ResultsDATS significantly inhibited the LPS-induced secretion of NO and PGE2, which was associated with the suppression of their regulatory genes, inducible NO synthase and COX-2. DATS had been shown to inhibit nuclear translocation of NF-κB by destroying the degradation and phosphorylation of IκB-α inhibitors in the cytoplasm. In addition, DATS effectively inhibited the expression of LPS-induced toll-like receptor 4 (TLR4) and myeloid differentiation factor 88. Furthermore, DATS markedly reduced the LPS-induced expression of chemokine (CXC motif) ligand (CXCL) 12 and CXC receptor (CXCR) 4, demonstrating its capacity to block chemo-attractive activity.ConclusionsThese results indicate that DATS inhibits the activation of the CXCL12/CXCR4 axis associated with antagonizing effect on TLR4 and blocks NF-κB signaling, thus demonstrating anti-inflammatory effects against LPS stimulation.

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An ethanol extract of <i>Aster yomena</i> (Kitam.) Honda inhibits lipopolysaccharide-induced inflammatory responses in murine RAW 264.7 macrophages

Cited by 15 publications

References 43 publications

Neuroprotective effect ofAster yomena(Kitam.) Honda against hydrogen peroxide-induced oxidative stress in SH-SY5Y cells

Neuroprotective effect ofAster yomena(Kitam.) Honda against hydrogen peroxide-induced oxidative stress in SH-SY5Y cells

Anti-Oral Microbial Activity and Anti-Inflammatory Effects of Rosmarinic Acid in Lipopolysaccharide-Stimulated MC3T3-E1 Osteoblastic Cells on a Titanium Surface

Diallyl Trisulfide Suppresses the Production of Lipopolysaccharide-induced Inflammatory Mediators in BV2 Microglia by Decreasing the NF-κB Pathway Activity Associated With Toll-like Receptor 4 and CXCL12/CXCR4 Pathway Blockade

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