• Journal of Physiology & Pathology in Korean Medicine
• /
• v.18 no.3
• /
• pp.887-892
• /
• 2004

Cheonggeumganghwa-tang(CGT) has been used for the purpose of prevention and treatment of bronchial asthma and allergic asthma in Korea. To investigate the biological effect of CGT, the author examined cytotoxicity and inflammatory cytokines secretion with human mast cell line, HMC-1. HMC-1 was stimulated with phorbol 12-myristate 13-acetate (PMA) and calcium ionophore A23187. CGT by itself had no effect on viability of HMC-1. The effects of CGT on the secretion of tumor necrosis factor-alpha (TNF-α) and interleukin (IL)-6 from HMC-1 were evaluated with enzyme-linked immunosorbent assay (ELISA). CGT (1 ㎎/㎖) inhibited PMA plus A23187 -induced TNF-α and IL-6 secretion, by 93.86 ± 2.05%, 68.69 ± 2.86%, respectively. CGT also inhibited the NF-κB (p50) expression. Taken together, these results suggest that CGT inhibit the production of inflammatory cytokines in HMC-1 cells through blockade of NF-κB activation.

• BMB Reports
• /
• v.42 no.6
• /
• pp.380-386
• /
• 2009

In neurodegenerative diseases, such as Alzheimer' and Parkinson', microglial cell activation is thought to contribute to CNS injury by producing neurotoxic compounds. Prothrombin and kringle-2 increase levels of NO and the mRNA expression of iNOS, IL-1$\beta$, and TNF-$\alpha$ in microglial cells. In contrast, the human prothrombin kringle-2 derived peptide NSA9 inhibits NO release and the production of pro-inflammatory cytokines such as IL-1$\beta$, TNF-$\alpha$, and IL-6 in LPS-activated EOC2 microglia. In this study, we investigated the anti-inflammatory effects of NSA9 in human prothrombin- and kringle-2-stimulated EOC2 microglia. Treatment with 20-100 ${\mu}M$ of NSA9 attenuated both prothrombin- and kringle-2-induced microglial activation. NO production induced by MAPKs and NF-$\kappa$B was similarly reduced by inhibitors of ERK (PD98059), p38 (SB203580), NF-$\kappa$B (N-acetylcysteine), and NSA9. These results suggest that NSA9 acts independently as an inhibitor of microglial activation and that its effects in EOC2 microglia are not influenced by the presence of kringle-2.

• Journal of Pharmacopuncture
• /
• v.18 no.1
• /
• pp.19-26
• /
• 2015

Objectives: Quercetin, a flavonoid compound, has been reported to induce apoptosis in cancer cells, but its anti-inflammatory effects, which are also closely linked with apoptosis, if any, on non-small-cell lung cancer (NSCLC) have not so far been critically examined. In this study, we tried to determine if quercetin had any demonstrable anti-inflammatory potential, which also could significantly contribute to inducing apoptosis in a NSCLC cell line, A549. Methods: In this context, several assays, including cytotoxicity, flow cytometry and fluorimetry, were done. Gene expression was analyzed by using a western blot analysis. Results: Results revealed that quercetin could induce apoptosis in A549 cells through mitochondrial depolarization by causing an imbalance in B-cell lymphoma 2/Bcl2 Antagonist X (Bcl2/Bax) ratio and by down-regulating the interleukine-6/signal transducer and activator of transcription 3 (IL-6/STAT3) signaling pathway. An analysis of the data revealed that quercetin could block nuclear factor kappa-light-chain-enhancer of activated B cells (NF-${\kappa}B$) activity at early hours, which might cause a down-regulation of the IL-6 titer, and the IL-6 expression, in turn, could inhibit p-STAT3 expression. Down-regulation of both the STAT3 and the NF-${\kappa}B$ expressions might, therefore, cause down-regulation of Bcl2 activity because both are major upstream effectors of Bcl2. Alteration in Bcl2 responses might result in an imbalance in the Bcl2/Bax ratio, which could ultimately bring about mitochondria mediated apoptosis in A549 cells. Conclusion: Overall, the finding of this study indicates that a quercetin induced anti-inflammatory pathway in A549 cells appeared to make a significant contribution towards induction of apoptosis in NSCLC and, thus, may have a therapeutic use such as a strong apoptosis inducer in cancer cells.

• Biomolecules & Therapeutics
• /
• v.21 no.5
• /
• pp.398-404
• /
• 2013

During a screening program to search the anticolitic herbal medicines, 80% ethanol extract of the rhizome of Anemarrhena asphodeloides (AA) was found to potently inhibit the expression of proinflammatory cytokines TNF-${\alpha}$ and IL-1${\beta}$, as well as the activation of NF-${\kappa}B$ in LPS-stimulated colonic macrophages, followed by that of the rhizome of C. chinensis (CC). AA also potently inhibited TNBS-induced colitic markers, shortening of the colon and increase of macroscopic score, myeloperoxidase activity, TNF-${\alpha}$, IL-1${\beta}$, and IL-6, in mice. The synergistic effect of CC against the anticolitic effect of AA was investigated. CC synergistically inhibited the anticolitic effect of AA. AC-mix (AA+CC, 1:1) potently inhibited them. AC-mix also inhibited the activation of NF-${\kappa}B$, as well as the expression of TNF-${\alpha}$, IL-1${\beta}$, IL-6, iNOS and COX-2. The effects of AC-mix against oxazolone-induced colitis were investigated in mice. AC-mix also potently inhibited oxazolone-induced inflammatory markers, colon shortening, macroscopic score, myeloperoxidase activity, NF-${\kappa}B$ activation and proinflammatory cytokines. Overall, the anti-colitic effect of AC-mix was superior to that of mesalazine. Based on these findings, AC-mix may improve colitis by inhibiting NF-${\kappa}B$ activation.

• Journal of Life Science
• /
• v.27 no.11
• /
• pp.1315-1323
• /
• 2017

Turmeric is a rhizomatous herbaceous perennial plant (Curcuma longa (CL)) of the ginger family, Zingiberaceae. A yellow-pigmented fraction isolated from the rhizomes of CL contains curcuminoids belonging to the dicinnamoyl methane group. Curcumin is an important active ingredient responsible for the biological activity of CL. However, CL is not usually used as a food source due to its bitter taste. The present study was designed to determine the effect of the CL fermented by Rhizopus oryzae (FCL) on pro-inflammatory factors such as nuclear factor ${\kappa}B$ ($NF-{\kappa}B$), tumor necrosis factor alpha ($TNF-{\alpha}$), interleukin-6 (IL-6), nitric oxide (NO), prostaglandin $E_2$ ($PGE_2$), inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) in lipopolysaccharide (LPS)-induced RAW 264.7 cell line. The cell viability was determined by MTT assay. To evaluate the anti-inflammatory effect of FCL 80% EtOH extracts, IL-6 and $TNF-{\alpha}$ were measured by ELISA kit. Also, the amount of $NO/PGE_2/NF-{\kappa}B$ was measured using the $NO/PGE_2/NF-{\kappa}B$ detection kit and the iNOS/COX-2 expression was measured by Western blotting. The results showed that the FCL reduced NO, $PGE_2$, iNOS, COX-2, $NF-{\kappa}B$, IL-6 and $TNF-{\alpha}$ production without cytotoxicity. These results suggest that FCL extracts may be a developed the functional food related to anti-inflammation due to the significant effects on inflammatory factors.

• The Journal of Internal Korean Medicine
• /
• v.29 no.2
• /
• pp.385-400
• /
• 2008

Objectives : This study was carried out to investigate the effects of Soyumjungjang-tang(SJT) on the experimental ulcerative colitis induced by dextran sulfate sodium(DSS) in mice. Methods : Ulcerative colitis was induced through supplying 4% DSS solution as the drinking water for 7 days in 6-week-old male ICR mice. The colitic mice were divided into three groups: the sample groups were orally administered SJT in doses of 25mg/kg(S25 group) or 100mg/kg(S100 group) once a day for 10 days, from 3 days before starting drinking the DSS solution, and the control(C) group was administered normal saline instead of SJT. The DSS solution or SJT was not administered to the normal(N) group. The length of colon, histologic finding, the activities of myeloperoxidase(MPO) and alkaline phosphatase(AP), and the expressions of $IL-1{\beta}$, IL-6, COX-2, $NF-{\kappa}B$, and $I{\kappa}B$ in colonic mucosa was checked using immunoblot, ELISA, etc. The activities of chondroitinase, tryptophanase, ${\beta}-glucuronidase$ and ${\beta}-glucosidase$ in stool were also measured. Results : The length of colon shortened, histologic finding deteriorated, the activities of MPO, AP, chondroitinase, tryptophanase, ${\beta}-glucuronidase$ and ${\beta}-glucosidase$, and the expressions of $IL-1{\beta}$, IL-6, COX-2, $NF-{\kappa}B$ increased, and the expression of $I{\kappa}B$ decreased in the C group. All measures, except $NF-{\kappa}B$, were restored in S25 group, but some measures deteriorated more in the S100 group than in the C group. Conclusions : According to the above results, it is supposed that SJT has a potential therapeutic effect on ulcerative colitis.

• Journal of Microbiology and Biotechnology
• /
• v.30 no.6
• /
• pp.822-829
• /
• 2020

Nutraceutical treatments can reduce inflammation and prevent the development of inflammatory diseases. In this study, the anti-inflammatory effects of Smilax guianensis Vitman extract (SGE) were examined. SGE suppressed lipopolysaccharide (LPS)-mediated nitrite production in RAW 264.7 cells. SGE also prevented the LPS-induced expression of inducible nitric oxide synthase (iNOS) but not cyclooxygenase (COX)-2. Western blot analysis showed that SGE attenuated LPS-induced phosphorylation of IκB kinase (IKK), inhibitor of kappa B (IκB), and p65. Additionally, SGE inhibited LPS-induced IκB degradation in RAW 264.7 cells. Western blot analysis of the cytosolic and nuclear fractions, as well as immunofluorescence assay results, revealed that SGE suppressed LPS-induced p65 nuclear translocation in RAW 264.7 cells. Moreover, SGE reduced LPS-induced interleukin (IL)-1β, IL-6, and tumor necrosis factor-α (TNF-α) mRNA expression and IL-1β and IL-6 protein expression in RAW 264.7 cells. Collectively, these results indicate that SGE suppresses the NF-κB signaling pathway and thereby inhibits the production of NO, IL-1β, and IL-6.

• Nutrition Research and Practice
• /
• v.11 no.2
• /
• pp.90-96
• /
• 2017

BACKGROUND/OBJECTIVES: Although the antioxidative effects of lycopene are generally known, the molecular mechanisms underlying the anti-inflammatory properties of lycopene are not fully elucidated. This study aimed to examine the role and mechanism of lycopene as an inhibitor of inflammation. METHODS/MATERIALS: Lipopolysaccharide (LPS)-stimulated SW 480 human colorectal cancer cells were treated with 0, 10, 20, and $30{\mu}M$ lycopene. The MTT assay was performed to determine the effects of lycopene on cell proliferation. Western blotting was performed to observe the expression of inflammation-related proteins, including nuclear factor-kappa B ($NF-{\kappa}B$), inhibitor kappa B ($I{\kappa}B$), mitogen-activated protein kinase (MAPK), extracellular signal-related kinase (ERK), c-jun NH2-terminal kinase (JNK), and p38 (p38 MAP kinase). Real-time polymerase chain reaction was performed to investigate the mRNA expression of tumor necrosis factor ${\alpha}$ ($TNF-{\alpha}$), interleukin-1 beta ($IL-1{\beta}$), interleukin-6 (IL-6), inducible nitric oxide synthase (iNOS), and cyclooxygenase-2 (COX-2). Concentrations of nitric oxide (NO) and prostaglandin $E_2$ ($PGE_2$) were determined via enzyme-linked immunosorbent assays. RESULTS: In cells treated with lycopene and LPS, the mRNA expression of $TNF-{\alpha}$, $IL-1{\beta}$, IL-6, iNOS, and COX-2 were decreased significantly in a dose-dependent manner (P < 0.05). The concentrations of $PGE_2$ and NO decreased according to the lycopene concentration (P < 0.05). The protein expressions of $NF-{\kappa}B$ and JNK were decreased significantly according to lycopene concertation (P < 0.05). CONCLUSIONS: Lycopene restrains $NF-{\kappa}B$ and JNK activation, which causes inflammation, and suppresses the expression of $TNF-{\alpha}$, $IL-1{\beta}$, IL-6, COX-2, and iNOS in SW480 human colorectal cancer cells.

• Journal of Korean Medicine Rehabilitation
• /
• v.15 no.2
• /
• pp.31-43
• /
• 2005

목적 : 방풍은 임상적으로 관절염을 포함한 다양한 염증성 질환 치료제로 사용되어 왔다. 본 연구에서는 인간 비만세포를 이용하여 세포 독성에 영향을 주지 않는 농도에서 방풍의 항염 효과 및 그 기전을 검토했다. 방법 : 인간의 HMC-1세포를 IMDM에서 페니실린, 스트렙토마이신, 모노티오글리세린을 첨가하여 배양하고 방품추출액을 투여하였다. 그 다음 MTT, CLISA, RT-PCR, 세포내 칼슘측정, 핵단백분석을 이용하여 TNF-${\alpha}$, IL-6, IL-8 각각의 형성과 mRNA발현, 세포내 칼슘 수준, NF-${\kappa}B$ 발현에 대한 방풍추출액의 반응을 측정하고 통계처리 하였다. 결과 : 방풍은 PMA와 calcium ionophore A23187로 활성화된 비민세포에서 세포내 칼슘 수준과 NF-${\kappa}B$, TNF-${\alpha}$와 IL-6의 발현을 억제시켰고 RT-PCR을 이용한 mRNA 발현에서 TNF-${\alpha}$와 IL-6의 발현을 억제하였다. 결론 : 방풍은 비만세포내 칼슘 수준 및 NF-${\kappa}B$의 활성을 억제하고 염증성 세포 활성 물질인 TNF-${\alpha}$와 IL-6의 분비도 억제하여 항염효과를 나타냄을 암시하고 있다.

• Biomolecules & Therapeutics
• /
• v.22 no.4
• /
• pp.288-294
• /
• 2014

Mangostenone F (MF) is a natural xanthone isolated from Garcinia mangostana. However, little is known about the biological activities of MF. This study was designed to investigate the anti-inflammatory effect and underlying molecular mechanisms of MF in lipopolysaccharide (LPS)-stimulated RAW264.7 macrophages. MF dose-dependently inhibited the production of NO, iNOS, and pro-inflammatory cytokines (TNF-${\alpha}$, IL-6, and IL-$1{\beta}$) in LPS-stimulated RAW264.7 macrophages. Moreover, MF decreased the NF-${\kappa}B$ luciferase activity and NF-${\kappa}B$ DNA binding capacity in LPS-stimulated RAW264.7 macrophages. Furthermore, MF suppressed the NF-${\kappa}B$ activation by inhibiting the degradation of $I{\kappa}B{\alpha}$ and nuclear translocation of p65 subunit of NF-${\kappa}B$. In addition, MF attenuated the AP-1 luciferase activity and phosphorylation of ERK, JNK, and p38 MAP kinases. Taken together, these results suggest that the anti-inflammatory effect of MF is associated with the suppression of NO production and iNOS expression through the down-regulation of NF-${\kappa}B$ activation and MAPK signaling pathway in LPS-stimulated RAW264.7 macrophages.