• Nutrition Research and Practice
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• v.13 no.3
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• pp.189-195
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• 2019

BACKGROUND/OBJECTIVES: Although aged black garlic has various biological activities such as anti-allergy, anti-inflammation and neuroprotection, effect of aged black garlic on chemically contact dermatitis is unclarified. MATERIALS/METHODS: To evaluate anti-dermatitic activity of aged black garlic extract, we investigated effects of a fraction of aged black garlic extract (BG10) on both in vivo and in vitro. RESULTS: BG10 almost inhibited formation of nitric monoxide and interleukin-6 (IL-6; $IC_{50}$, $7.07{\mu}g/mL$) at $25{\mu}g/mL$, and dose-dependently reduced production of tumor necrosis $factor-{\alpha}$ ($TNF-{\alpha}$; $IC_{50}$, $52.07{\mu}g/mL$) and prostaglandin $E_2$ ($IC_{50}$, $38.46{\mu}g/mL$) in lipopolysaccharide-stimulated RAW264.7 cells. In addition, BG10 significantly inhibited the expression of inducible nitric oxide synthase, cyclooxygenase-2 and nuclear $NF-{\kappa}B$, and improved that of cytosolic levels of $NF-{\kappa}B$ and $I{\kappa}B{\alpha}$ in the cells. Consistent with in vitro studies, BG10 (0.5 mg/mL) not only reduced ear edema but also suppressed the formation of IL-6 and $TNF-{\alpha}$ induced by 12-O-tetradecanoylphorbol-13-acetate in ear tissues of mice. CONCLUSIONS: These findings suggest BG10 has anti-dermatitic activity through inhibiting activation of macrophages. Therefore, such effects of BG10 may provide information for the application of aged black garlic for prevention and therapy of contact dermatitis.

• Fisheries and Aquatic Sciences
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• v.22 no.2
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• pp.6.1-6.10
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• 2019

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-${\alpha}$, interleukin (IL)-6, and IL-$1{\beta}$). Furthermore, SJB-SHE inhibited nuclear factor kappa-B (NF-${\kappa}B$) 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.

• Korean Journal of Pharmacognosy
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• v.52 no.3
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• pp.192-201
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• 2021

Dangguisu-san (DGSS) is widely known traditional herbal medicinal formula in Korea for treatment of traumatic injury by traffic accident, ecchymosis, abdominal distension and anti-thrombosis of blood. This study was conducted to develop the simultaneous analyze method using high performance liquid chromatography (HPLC) and examine the effect of anti-inflammatory activity of DGSS-dry extract (DGSS-DE) and DGSS-mix extract powder (DGSS-MEP). Physicochemical characteristics of DGSS-DE and DGSS-MEP showed that there is no significant difference in pH, titratable acidity, total soluble solid content and browning degree except for color value (L, a, b). 15 functional constituents of DGSS were identified and the correlation coefficient values of DGSS-DE and DGSS-MEP were conformed 0.950. Also, DGSS-DE and DGSS-MEP significantly decreased the secretion of nitric oxide (NO), prostaglandin E₂ (PGE₂), interleukin-1β (IL-1β), interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) through inhibited expression of inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2), IL-1β, IL-6, and TNF-α. From these result, DGSS-MEP showed similar chemical composition and anti-inflammatory effect to DGSS-DE. Therefore, DGSS-DE and DGSS-MEP may be useful as potential source of drug to prevent inflammation.

• Journal of Microbiology and Biotechnology
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• v.31 no.8
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• pp.1069-1078
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• 2021

Sevoflurane postconditioning (SPostC) has been proved effective in cardioprotection against myocardial ischemia/reperfusion injury. It was also reported that heat shock protein 70 (HSP70) could be induced by sevoflurane, which played a crucial role in hypoxic/reoxygenation (HR) injury of cardiomyocytes. However, the mechanism by which sevoflurane protects cardiomyocytes via HSP70 is still not understood. Here, we aimed to investigate the related mechanisms of SPostC inducing HSP70 expression to reduce the HR injury of cardiomyocytes. After the HR cardiomyocytes model was established, the cells transfected with siRNA for HSP70 (siHSP70) or not were treated with sevoflurane during reoxygenation. The lactate dehydrogenase (LDH) level was detected by colorimetry while cell viability and apoptosis were detected by MTT and flow cytometry. Reverse transcription-quantitative polymerase chain reaction (RT-qPCR) and Western blotting were used to detect HSP70, apoptosis-, cell cycle-associated factors, iNOS, and Cox-2 expressions. Enzyme-linked immuno sorbent assay (ELISA) was used to measure malondialdehyde (MDA) and superoxide dismutase (SOD). SPostC decreased apoptosis, cell injury, oxidative stress and inflammation and increased viability of HR-induced cardiomyocytes. In addition, SPostC downregulated Bax and cleaved caspase-3 levels, while SPostC upregulated Bcl-2, CDK-4, Cyclin D1, and HSP70 levels. SiHSP70 had the opposite effect that SPostC had on HR-induced cardiomyocytes. Moreover, siHSP70 further reversed the effect of SPostC on apoptosis, cell injury, oxidative stress, inflammation, viability and the expressions of HSP70, apoptosis-, and cell cycle-associated factors in HR-induced cardiomyocytes. In conclusion, this study demonstrates that SPostC can reduce the HR injury of cardiomyocytes by inducing HSP70 expression.

• Biomolecules & Therapeutics
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• v.29 no.2
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• pp.127-134
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• 2021

Neuroinflammation―a common pathological feature of neurodegenerative disorders such as Alzheimer's disease―is mediated by microglial activation. Thus, inhibiting microglial activation is vital for treating various neurological disorders. 7,3',4'-Trihydroxyisoflavone (THIF)―a secondary metabolite of the soybean compound daidzein―possesses antioxidant and anticancer properties. However, the effects of 7,3',4'-THIF on microglial activation have not been explored. In this study, antineuroinflammatory effects of 7,3',4'-THIF in lipopolysaccharide (LPS)-stimulated BV2 microglial cells were examined. 7,3',4'-THIF significantly suppressed the production of the proinflammatory mediators nitric oxide (NO), inducible nitric oxide synthase (iNOS), and cyclooxygenase-2 (COX-2) as well as of the proinflammatory cytokine interleukin-6 (IL-6) in LPS-stimulated BV2 microglial cells. Moreover, 7,3',4'-THIF markedly inhibited reactive oxygen species (ROS) generation. Western blotting revealed that 7,3',4'-THIF diminished LPS-induced phosphorylation of extracellular signal-regulated kinase (ERK), c-Jun N-terminal kinase (JNK), glycogen synthase kinase-3β (GSK-3β), and nuclear factor kappa B (NF-κB). Overall, 7,3',4'-THIF exerts antineuroinflammatory effects against LPS-induced microglial activation by suppressing mitogen-activated protein kinase (MAPK) and NF-κB signaling, ultimately reducing proinflammatory responses. Therefore, these antineuroinflammatory effects of 7,3',4'-THIF suggest its potential as a therapeutic agent for neurodegenerative disorders.

• Biomolecules & Therapeutics
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• v.29 no.2
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• pp.144-153
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• 2021

Astrocytes play various important roles such as maintaining brain homeostasis, supporting neurons, and secreting inflammatory mediators to protect the brain cells. In aged subjects, astrocytes show diversely changed phenotypes and dysfunctions. But, the study of aged astrocytes or astrocytes from aged subjects is not yet sufficient to provide a comprehensive understanding of their important processes in the regulation of brain function. In this study, we induced an in vitro aged astrocyte model through late passage cultivation of rat primary cultured astrocytes. Astrocytes were cultured until passage 7 (P7) as late passage astrocytes and compared with passage 1 (P1) astrocytes as early passage astrocytes to confirm the differences in phenotypes and the effects of serial passage. In this study, we confirmed the morphological, molecular, and functional changes of late passage astrocytes showing aging phenotypes through SA-β-gal staining and measurement of nuclear size. We also observed a reduced expression of inflammatory mediators including IL-1β, IL-6, TNFα, iNOS, and COX2, as well as dysregulation of wound-healing, phagocytosis, and mitochondrial functions such as mitochondrial membrane potential and mitochondrial oxygen consumption rate. Culture-conditioned media obtained from P1 astrocytes promoted neurite outgrowth in immature primary cultures of rat cortices, which is significantly reduced when we treated the immature neurons with the culture media obtained from P7 astrocytes. These results suggest that late passage astrocytes show senescent astrocyte phenotypes with functional defects, which makes it a suitable model for the study of the role of astrocyte senescence on the modulation of normal and pathological brain aging.

• Journal of Microbiology and Biotechnology
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• v.32 no.1
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• pp.15-26
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• 2022

Luteolin is a common dietary flavone possessing potent anti-inflammatory activities. However, when administrated in vivo, luteolin becomes methylated by catechol-O-methyltransferases (COMT) owing to the catechol ring in the chemical structure, which largely diminishes its anti-inflammatory effect. In this study, we made a modification on luteolin, named LUA, which was generated by the chemical reaction between luteolin and 2,2'-azobis(2-amidinopropane) dihydrochloride (AAPH). Without a catechol ring in the chemical structure, this new flavone could escape from the COMT-catalyzed methylation, thus affording the potential to exert its functions in the original form when administrated in the organism. Moreover, an LPS-stimulated RAW cell model was applied to detect the anti-inflammatory properties. LUA showed much more superior inhibitory effect on LPS-induced production of NO than diosmetin (a major methylated form of luteolin) and significantly suppressed upregulation of iNOS and COX-2 in macrophages. LUA treatment dramatically reduced LPS-stimulated reactive oxygen species (ROS) and mRNA levels of pro-inflammatory mediators such as IL-1β, IL-6, IL-8 and IFN-β. Furthermore, LUA significantly reduced the phosphorylation of JNK and p38 without affecting that of ERK. LUA also inhibited the activation of NF-κB through suppression of p65 phosphorylation and nuclear translocation.

• Microbiology and Biotechnology Letters
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• v.50 no.1
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• pp.22-30
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• 2022

Haliotis discus hannai called abalone, is the valuable marine mollusks and the by-products of abalone processing are viscera. Brownish abalone male viscera (AMV), which have not been reported as having anti-inflammatory effects, was extracted with acetone and fractionated by different six acetone/hexane ratios (0, 10, 20, 30, 40, and 100%) using a silica column via in vitro ABTS and DPPH radical and nitric oxide (NO) production assay-guided fractionation. Among the fractions, the acetone/hexane ratio 40%, A40 exhibited the most potent radical scavenging activities and inhibition of lipopolysaccharide (LPS)-induced NO production without cytotoxicity. A40 inhibited LPS-induced intracellular reactive oxygen species (ROS) production in a dose-dependent manner. Western blot analysis revealed that A40 down-regulated the activation of NF-κB, MAPK (ERK 1/2, p-38, and JNK), and inflammatory enzymes, inducible nitric oxide synthase (iNOS) and cyclooxygenase (COX)-2. Moreover, this fraction inhibited the generation of pro-inflammatory cytokines such as interleukin (IL)-1β, IL-6, and tumor necrosis factor (TNF)-α. These results suggested that AMV containing A40 with anti-inflammatory and anti-oxidantive effects, is the effective therapeutic and functional material for treating inflammatory disorders.

• Microbiology and Biotechnology Letters
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• v.50 no.2
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• pp.310-318
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• 2022

The fruits of Paulownia tomentosa (Thunb.) (PT) Steud. have been reported to exert a variety of biological activities. A previous study confirmed that compounds isolated from PT fruits (PTF) exerted anti-inflammatory effects on TNF-α-stimulated airway epithelial cells. However, there is no report on the protective effects of PTF on acute lung injury (ALI). Here, we examined the ameliorative effects of PTF in an experimental animal model of lipopolysaccharide (LPS)-induced ALI. In ALI mice, increased levels of inflammatory cell influx were confirmed in the lungs of mice, and an increase of microphage numbers, TNF-α, IL-6 and MCP-1 production and protein content were detected in mouse bronchoalveolar lavage fluid. However, these increases were significantly reversed with PTF pretreatment. In addition, PTF inhibited the increased expression of iNOS and COX-2 in the lungs of ALI mice. Furthermore, the upregulation of MAPK and NF-κB activation was decreased in the lungs of ALI mice by PTF. In the in vitro experiment, PTF pretreatment exerted an anti-inflammatory effect by inhibiting the secretion of nitric oxide, TNF-α and IL-6 in LPS-stimulated RAW264.7 macrophages. Collectively, these results indicated that PTF has ameliorative effects on airway inflammation in an experimental animal model of ALI.

• Korean Journal of Clinical Laboratory Science
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• v.54 no.3
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• pp.201-208
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• 2022

Neuroinflammation is defined as a neurological inflammation within the brain and the spinal cord. In neuroinflammation, microglia are the tissue-resident macrophages of the central nervous system, which act as the first line of defense against harmful pathogens. Dexmedetomidine (Dex) has an anti-inflammatory effect in many neurological conditions. Additionally, the microRNA-30a-5p (miR-30a-5p) mimic has been proven to be effective in macrophages in inflammatory conditions. This study aimed to investigate the synergistic anti-inflammatory effects of both miR-30a-5p and Dex in lipopolysaccharide (LPS)-induced BV2 cells. This study showed that miR-30a-5p and Dex decreased nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) translocation in LPS-induced BV2 cells. MiR-30a-5p and Dex alleviated tumor necrosis factor-alpha (TNF-α) and interleukin-6 (IL-6), LPS-induced phosphorylation c-Jun N-terminal kinases (JNK), extracellular signal-regulated kinase (ERK) and p38. Also, the expression of the NOD-like receptor pyrin domain containing 3 inflammasome (NLRP3), cleaved caspase-1, and ASC was inhibited. Furthermore, LPS-stimulated nitric oxide (NO) production, inducible nitric oxide synthase (iNOS), and cyclooxygenase-2 (COX-2) expression were attenuated by Dex and miR-30a-5p. Our results indicate that a combination of Dex and miR-30a-5p, attenuates NF-κB activation, the mitogen-activated protein kinase (MAPK) signaling pathway, and inflammatory mediators involved in LPS-induced inflammation and inhibits the activation of the NLRP3 inflammasome in LPS-activated BV2 cells.