• Journal of Dental Anesthesia and Pain Medicine
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• v.22 no.4
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• pp.277-287
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• 2022

Background: Inflammatory dental diseases that occur during pregnancy can cause preterm labor and/or intrauterine growth restriction. Therefore, proactive treatment of dental diseases is necessary during pregnancy. Dexmedetomidine (DEX) is a widely used sedative in the dental field, but research on the effect of DEX on pregnancy is currently insufficient. In this study, we investigated the effects of co-treatment with DEX and lipopolysaccharide (LPS) on inflammatory responses in human amnion-derived WISH cells. Methods: Human amnion-derived WISH cells were treated with 0.001, 0.01, 0.1, and 1 ㎍/mL DEX with 1 ㎍/mL LPS for 24 h. Cytotoxicity of WISH cells was evaluated by 3-(4,5-dimethylthiazol)-2,5-diphenyltetrazolium bromide (MTT) assay. The protein expression of cyclooxygenase-2 (COX-2), prostaglandin E₂ (PGE₂), p38, and nuclear factor kappa B (NF-𝜅B) was examined by western blot analysis. The mRNA expression of pro-inflammatory cytokines such as interleukin (IL)-1𝛽 and tumor necrosis factor (TNF)-𝛼 was analyzed by real-time quantitative polymerase chain reaction. Results: Co-treatment with DEX and LPS showed no cytotoxicity in the WISH cells. The mRNA expression of IL-1𝛽 and TNF-𝛼 decreased after co-treatment with DEX and LPS. DEX and LPS co-treatment decreased the protein expression of COX-2, PGE₂, phospho-p38, and phospho-NF-𝛋B in WISH cells. Conclusion: Co-treatment with DEX and LPS suppressed the expression of COX-2 and PGE₂, as well as pro-inflammatory cytokines such as IL-1𝛽 and TNF-𝛼 in WISH cells. In addition, the anti-inflammatory effect of DEX and LPS co-treatment was mediated by the inhibition of p38/NF-𝜅B activation.

• Herbal Formula Science
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• v.30 no.2
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• pp.45-57
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• 2022

Objectives : Yukil-san (YIS, 六一散; Liu yi san) is composed of Talcum and Glycyrrhizae Radix, the name is said to be derived from the proportion of the two herbal components of the formula. The YIS originated from 'Formulas from the discussion illuminating the Yellow Emperor's Basic Question'(黃帝素問宣明論方; Huang di su wen xuan ming lun fang) written by Liu Wan-Su (劉完素). YIS could clear summerheat, resolve dampness, and augment the qi. This formula may be used to treat the common cold, influenza, acute gastroenteritis, cystitis, urethritis and bacillary dysentery. But, there is insufficient of study about the effects of YIS on the anti-inflammatory activities. The present study evaluated the anti-inflammatory effects of YIS on lipopolysaccharide (LPS)-activated RAW 264.7 cells. Methods : Cell viability was assessed by MTT assay and nitric oxide (NO) was evaluated by measuring the nitrite content in culture medium. Pro-inflammatory cytokines such as tumor necrosis factor-α, interleukin-1β and IL-6 were quantified by ELISA kit. The expression of proteins related with nuclear factor-κB (NF-κB) pathway and inducible NO synthase (iNOS) were assessed by western blot analysis. Results : YIS significantly inhibited the expression of iNOS increased by LPS, and thus significantly inhibited the production of NO. In addition, YIS significantly inhibited pro-inflammatory cytokines. In the regulation of inflammation, NF-κB pathway plays a crucial role. YIS inhibited the expression of p-IκBα and thus inhibited the translocation of NF-κB to the nucleus. Conclusions : These results suggest that YIS ameliorates inflammatory response in LPS-activated RAW 264.7 cells through the inhibition of inflammatory mediators, via suppression of the NF-κB pathway. Therefore, this study provides objective evidence for the anti-inflammatory effect of YIS including the underlying mechanisms.

• Journal of Sasang Constitutional Medicine
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• v.21 no.1
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• pp.139-149
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• 2009

1. Objectives The roots of Sophora flavescens Aiton (SFA) are widely used as a herbal remedy for allergic inflammation. In this study, we invested the effect of SFA on passive cutaneous anaphylaxis reaction and histamin releas and we demonstrated that SFA suppressed the production of pro-inflammatory cytokines, such as tumor necrosis factor-${\alpha}$ (TNF-${\alpha}$), interleukin- 6 (IL-6), and interleukin -8 (IL-8), through inhibition of the $NF{\kappa}B$, JNK and p38 pathway in the human mast cell line, HMC-1. 2. Methods To accomplish this, we invested passive cutaneous anaphylaxis reaction and histamin release at an animal experiment. In addition, we investigated the effect of SFA on the production of inflammation-related cytokines in HMC-1 cells that were co-treated with PMA and A23187, which can induce production of pro-inflammatory cytokines. 3. Results and Conclusions SFA induced passive cutaneous anaphylaxis reaction and histamin releas and supressed the expression of TNF-${\alpha}$, IL-6, and IL-8. In addition, the protein levels of TNF-${\alpha}$ were also decreased by SFA treatment. Furthermore, SFA inhibited the nuclear translocation of nuclear factor $NF{\kappa}B$ through inhibition of the phosphorylation and degradation of $I{\kappa}B-{\alpha}$, which is an inhibitor of $NF{\kappa}B$. Moreover, SFA also inhibited induction of MAPKs (JNK, p38) and $NF{\kappa}B$ promoter-mediated luciferase activity. Taken together, these results suggest that SFA could be used as a treatment for mast cell-derived allergic inflammatory diseases.

• Food Science and Biotechnology
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• v.18 no.3
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• pp.813-817
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• 2009

The effect of 4 seaweed extracts (Desmarestia viridis, Dictyopteris divaricata, Scytosiphon lomentaria, and Ishige okamurae) on pro-inflammatory mediators as well as nuclear factor $(NF)-{\kappa}B$ in the stimulated Raw 264.7 cells was investigated. They reduced iNOS and interlukin $(IL)-1{\beta}$ expressions at transcription level. Of those, 3 extracts (D. divaricata, I. okamurae, and S. lomentaria) inhibited the COX-2 expression at translation level. $I{\kappa}B-{\alpha}$ degradation was inhibited by D. divaricata and S. lomentaria extracts. Therefore, we concluded that the extracts from D. divaricata and S. lomentaria could inhibit the activation of murine macrophage through the blocking of $NF-{\kappa}B$ activation.

• Korean Journal of Pharmacognosy
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• v.39 no.2
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• pp.110-117
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• 2008

In this study, we investigated the anti-inflammatory effects of salidroside (SAL) isolated from the MeOH extract of Acer tegmentosum Maxim heartwood in RAW 264.7 macrophage cells. SAL pretreatment significantly inhibited nitric oxide (NO) and prostaglandin $E_2$ ($PGE_2$) productions in the lipopolysaccharide (LPS)-induced RAW 264.7 cells. Western blot and RT-PCR analyses revealed that SAL inhibited the LPS-induced expressions of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) at the protein and mRNA levels in a concentration-dependent manner. In addition, SAL reduced the release and the mRNA expressions of tumor necrosis $factor-{\alpha}$ ($TNF-{\alpha}$) and interleukin-6 (IL-6). Furthermore, nuclear factorkappa B ($NF{-\kappa}B$) luciferase reporter assay was performed to know the involvement of SAL in the production of pro-inflammatory cytokines, we confirmed that LPS-induced transcription activity of $NF{-\kappa}B$ was inhibited by SAL. Taken together, our data indicate that anti-inflammatory property of salidroside might be the result from the inhibition of iNOS, COX-2, $TNF-{\alpha}$ and IL-6 expressions via the down-regulation of $NF{-\kappa}B$ activity.

• Asian Pacific Journal of Cancer Prevention
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• v.15 no.16
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• pp.6627-6632
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• 2014

Purpose: The present study concerns molecular mechanisms involved in induction of apoptosis by a fungal taxol extracted from the fungus Cladosporium oxysporum in T47D human breast cancer cells. Materials and Methods: Apoptosis-induced by the fungal taxol was assessed by MTT assay, nuclear staining, DNA fragmentation, flow cytometry and pro- as well as anti-apoptotic protein expression by Western blotting. Results: Our results showed inhibition of T47D cell proliferation with an $IC_{50}$ value of $2.5{\mu}M/ml$ after 24 h incubation. It was suggested that the extract may exert its anti-proliferative effect on human breast cancer cell line by suppressing growth, arresting through the cell cycle, increase in DNA fragmentation as well as down-regulation of the expression of NF-${\kappa}B$, Bcl-2 and Bcl-XL and up-regulation of pro-apoptotic proteins like Bax, cyt-C and caspase-3. Conclusions: We propose that the fungal taxol contributes to growth inhibition in the human breast cancer cell through apoptosis induction via a mitochondrial mediated pathway, with possible potential as an anticancer therapeutic agent.

• Journal of Life Science
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• v.31 no.2
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• pp.183-191
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• 2021

Euglena gracilis is a microalga of great biotechnological interest that can create high levels of bioactive compounds, such as tocopherol, paramylon, and folic acid. The objective of this study was to investigate the biological activities of extracts from E. gracilis, especially those focused on immunological activity. E. gracilis biomass was extracted with hot water (HWE) and the remaining pellet was continuously extracted with methanol (HWME). First, we examined the effect of two extracts from E. gracilis on the production of nitric oxide (NO) and the expression of pro-inflammation cytokines, including IL-1β, IL-6, and TNF-α in murine macrophage RAW 264.7 cells. HWE treatment dose-dependently increased the production of IL-1β and TNF-α. On the other hand, treatment with HWME significantly decreased the generation of NO and pro-inflammatory cytokines (IL-6 and TNF-α) in lipopolysaccharide (LPS)-stimulated macrophage cells. In addition, other biological activities of the extracts were further analyzed: α-glucosidase inhibition, protein tyrosine phosphatase (PTP1B) inhibition, tyrosinase inhibition, xanthine oxidase (XO) inhibition, and angiotensin-converting enzyme (ACE) inhibition. Analysis of these biological activities showed that HWE has more inhibitory effects than HWME against α-glucosidase, tyrosinase, and XO agents. However, the inhibition of PTP1B and ACE with HWME were higher than with HWE. Taken together, the results suggested that E. gracilis possesses various biological activities―especially immunological capabilities―through regulation of cytokine production. Therefore, E. gracilis extract may be potentially useful for food material with immune-regulating effects.

• Journal of Acupuncture Research
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• v.31 no.2
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• pp.75-85
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• 2014

Objectives : We investigated whether bee venom(BV) inhibit cell growth through enhancement of death receptor expressions in the human cervix cancer C33A cells. Methods : BV($1{\sim}5{\mu}g/ml$) inhibited the growth of cervix cancer C33A cells by the induction of apoptotic cell death in a dose dependent manner. Results : Consistent with apoptotic cell death, expression of Fas, death receptor(DR) 3, 4, 5 and 6 was increased concentration dependently in the cells. Moreover, Fas, DR3 and DR6 revealed more sensitivity to BV. Thus, We reconfirmed whether they actually play a critical role in anti-proliferation of cervix cancer C33A cells. Consecutively, expression of DR downstream pro-apoptotic proteins including caspase-8, -3, -9 was upregulated and Bax was concomitantly overwhelmed the expression of Bcl-2. NF-${\kappa}B$ were also inhibited by treatment with BV in C33A cells. Conclusions : These results suggest that BV could exert anti-tumor effect through induction of apoptotic cell death in human cervix cancer C33A cells via enhancement of death receptor expression, and that BV could be a promising agent for preventing and treating cervix cancer.

• Korean Journal of Clinical Laboratory Science
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• v.52 no.4
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• pp.389-397
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• 2020

Microglial cells function as major immune cells in the brain, playing an important role in the protection and damage of neurons. BV2 microglia, activated by drug stimulation, secrete inflammatory cytokines by activating the nuclear factor kappa-light-chain-enhancer of the activated B cells pathway and are involved in neuroinflammatory and immune responses. The overactivation of microglia by stimuli can cause neuronal damage, leading to brain disease. Noni, a natural product, reduces the activity of microglia to prevent neuronal damage and is a potential natural medicine because it exerts excellent regeneration and anti-inflammatory effects on damaged cells. In this study, when noni was used to treat BV2 cells stimulated by the anti-cancer drug doxorubicin, it reduced the release of pro-inflammatory cytokines from BV2. On the other hand, neuronal damage is a side effect of doxorubicin. Therefore, the cytokines released from doxorubicin-stimulated BV2 cells treated with noni had a positive effect on the neuronal viability compared to those released from doxorubicin-stimulated BV2 cells not treated with Noni. Thus, Noni increases neuronal viability. These results suggest that noni inhibits the release of cytokines by regulating the nuclear factor kappa-light-chain-enhancer of the activated B cells pathway of BV2, thereby inhibiting neuronal damage.

• Journal of Mushroom
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• v.14 no.4
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• pp.220-224
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• 2016

Chronic inflammation, which results from continuous exposure to antigens, is one of major reasons for tissue damage and diseases such as rheumatoid arthritis and type 2 diabetes. In this study, we investigated the anti-inflammatory effects of extracts (hexane, $CHCl_3$, MeOH, $MeOH/H_2O$, and $H_2O$) from GW10-45, which is our new cultivar of an edible mushroom Pleurotus ferulae (ASI 2803 and ASI 2778), in RAW264.7 murine macrophages. None of the extracts showed cytotoxicity in RAW264.7 cells and the hexane, CHCl and H extracts reduced nitric oxide (NO) production, an important inflammatory marker, in lipopolysaccharide (LPS)-stimulated RAW264.7 cells. Particularly, the extract (CG45) inhibited NO production more than the other extracts did. To elucidate the effects of CG45 on molecular targets involved in pro-inflammatory responses, we performed western blot analysis. Expression of inducible nitric oxide (iNOS) significantly decreased in LPS and CG45 co-incubated cells compared to that in LPS only-treated cells. Additionally, another protein thatplays a critical role in inflammation, was down-regulated in cells treated with both LPS and CG45. In the nuclear factor $(NF)-{\kappa}B$ pathway, phosphorylation of $I{\kappa}B{\alpha}$ decreased in RAW264.7 cells treated with both LPS and CG45. Furthermore, CG45 inhibited the phosphorylation of $NF-{\kappa}B$ in LPS-stimulated RAW264.7 cells. Conclusively, CG45 could suppress pro-inflammatory responses in LPS-stimulated RAW264.7 cells by down-regulating not only the phosphorylation of $NF-{\kappa}B$ and $I{\kappa}B{\alpha}$ but also the expression of iNOS and COX-2 without any cytotoxicity.