• Korean Journal of Acupuncture
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• 제24권3호
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• pp.139-148
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• 2007

목 적 : 약침으로서 씀바귀의 염증 효과를 알아보기 위해 RAW 264.7 대식세포에서 Tnf 생성을 확인하였다. 방 법: 씀바귀를 RAW 264.7 대식세포에 미리 처치한 후 LPS로 염증 반응을 유도하였다. ELISA, Western blotting, RT-PCR, 그리고 EMSA을 통해 Tnf의 생성과 발현에 대한 효과를 평가하였다. 결 과 : LPS 유도된 세포에서 씀바귀 1, 5, 10, 50 ${\mu}g/ml$의 농도는 각각 23.7, 37.8, 66.4, 86.1% Tnf 생성을 억제한 것을 ELISA 통해 확인되었다. LPS로 유도된 대식세포에서 Tnf 생성은 농도에 따라 감소하였고, Western blotting, RT-PCR 분석에서는 씀바귀 5과 50 ${\mu}g/ml$가 LPS로 유도된 대식세포에서 Tnf의 mRNA와 단백질 발현을 저해 하는 것으로 관찰되었다. 또한 EMSA에서도 씀바귀 5과 50 ${\mu}g/ml$가 LPS로 유도된 Nf-kB를 감소시키는 것을 확인하였다. 고 찰 : 이런 결과는 씀바귀가 $Nf-{\kappa}B$를 저해하면서 LPS로 유발된 Tnf 생성을 감소시킨다는 것을 보여주었고, 이는 더 나아가 염증 질환에서 씀바귀가 약침으로써의 치료적 효과를 나타낼 수 있을 것으로 사료된다. 고 찰 : 이런 결과는 씀바귀가 $Nf-_{k}B$를 저해하면서 LPS로 유발된 Tnf 생성을 감소시킨다는 것을 보여주었고, 이는 더 나아가 염증 질환에서 씀바귀가 약침으로써의 치료적 효과를 나타낼 수 있을 것으로 사료된다.

• Asian Pacific Journal of Cancer Prevention
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• 제16권18호
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• pp.8533-8539
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• 2016

Background: B-cell chronic lymphocytic leukemia B (B-CLL), the most common type of leukemia, may be caused by apoptosis deficiency in the body. Adipose tissue-derived mesenchymal stem cells (AD-MSCs) as providers of pro-apoptotic molecules such as tumor necrosis factor-related apoptosis-inducing ligand (TRAIL), can be considered as an effective anti-cancer therapy candidate. Therefore, in this study we assessed the role of tumor necrosis factor-producing mesenchymal stem cells oin apoptosis of B-CLL cells resistant to fludarabine-based chemotherapy. Materials and Methods: In this study, after isolation and culture of AD-MSCs, a lentiviral LeGO-iG2-TRAIL-GFP vector containing a gene producing the ligand pro-apoptotic with plasmid PsPAX2 and PMDG2 virus were transfected into cell-lines to generate T293HEK. Then, T293HEK cell supernatant containing the virus produced after 48 and 72 hours was collected, and these viruses were transduced to reprogram AD-MSCs. Apoptosis rates were separately studied in four groups: group 1, AD-MSCs-TRAIL; group 2, AD-MSCs-GFP; group 3, AD-MSCs; and group 4, CLL. Results: Observed apoptosis rates were: group 1, $42{\pm}1.04%$; group 2, $21{\pm}0.57%$; group 3, $19{\pm}2.6%$; and group 4, % $0.01{\pm}0.01$. The highest rate of apoptosis thus occurred ingroup 1 (transduced TRAIL encoding vector). In this group, the average medium-soluble TRAIL was 72.7pg/m and flow cytometry analysis showed a pro-apoptosis rate of $63{\pm}1.6%$, which was again higher than in other groups. Conclusions: In this study we have shown that tumor necrosis factor (TNF) secreted by AD-MSCs may play an effective role in inducing B-CLL cell apoptosis.

• Natural Product Sciences
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• 제5권2호
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• pp.70-74
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• 1999

In the course of a search for tumor necrosis factor $(TNF)-{\alpha}$ inhibitory compounds from medicinal plants, we identified neolignans, honokiol and magnolol, from the alcoholic extract of Magnolia offcinalis as active inhibitory principles. These compounds dose-dependently inhibited $TNF-{\alpha}$ production without displaying cytotoxicity and their inhibitory activities measured by $IC_{50}$ values were 53.7 and $61.4\;{\mu}M$, respectively.

• Journal of Evidence-Based Herbal Medicine
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• 제1권1호
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• pp.7-11
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• 2008

The purpose of this study was to investigate the anti-inflammatory effects of extract from Hwang lyun tang (HLT) on the THP-1 cell and HMC-1 cell. To evaluate of anti-inflammatory of HLT, we examined cytokines production in lipopolysacchride (LPS)-induced THP-1 cell and A23187, PMA-induced HMC-1 cell. Extract of HLT inhibit LPS-induced interleukin (IL)-8 production in human monocyte THP-1 cells. Extract of HLT inhibit A23187, PMA-induced IL-8, tumor necrosis factor-$\alpha$ (INF-$\alpha$) production in HMC-1 cells. HLT down-regulated LPS-induced IL-8 production and A23187, PMA-induced IL-8, TNF-$\alpha$ production, which may be provide a clinical basis for anti-inflammatory properities of HLT.

• Journal of Evidence-Based Herbal Medicine
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• 제1권1호
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• pp.1-5
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• 2008

Objectives : The purpose of this study was to investigate the anti-inflammatory effects of extract from Jak-Yak Tang (JYT) on the THP-1 cell and HMC-1 cell. Method : To evaluate of anti-inflammatory of JYT, we examined cytokines production in lipopolysacchride (LPS)-induced THP-1 cell and A23187, PMA-induced HMC-1 cell. Result : Extract of JYT inhibit LPS-induced interleukin (IL)-8 production in human monocyte THP-1 cells. Extract of JYT inhibit A23187, PMA-induced IL-8, tumor necrosis factor-$\alpha$ (INF-$\alpha$) production in HMC-1 cells. Conclusion : NT down-regulated LPS-induced IL-8 production and A23187, PMA-induced IL-8, TNF-$\alpha$ production, which may be provide a clinical basis for anti-inflammatory properities of JYT.

• 동의생리병리학회지
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• 제16권5호
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• pp.1020-1024
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• 2002

The purpose of this research was to investigate the effects of Kamidaebo-tang water extract (KDT) on murine peritoneal macrophages. KDT (50 or 250 mg/kg) was administerd p.o. once a day for 7 days to mice. KDT increased the production of tumor necrosis factor-α and nitric oxide from murine peritoneal macrophages, but decreased the production of interleukin-1β. Also, KDT enhanced the production of lucigenin chemiluminescence from peritoneal macrophages. These results suggest that KDT enhances the non-specific immune response via increase of tumor necrosis factor-α and nitric oxide and phagocytic activity from peritoneal macrophages.

• Advances in Traditional Medicine
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• 제10권1호
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• pp.37-43
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• 2010

Palmitic acid (PA) is one of free fatty acids, which is found from Gaultheria itoana Hayata and Sarcopyramis nepalensis. Although PA has a variety of pharmacological effects including mediates hypothalamic insulin resistance, induces IP-10 expression, and promote apoptotic activities, the anti-inflammatory mechanism of PA in mouse peritoneal macrophages remains unclear. In this study, we showed that PA exerted an anti-inflammatory action through suppression the production of tumor necrosis factor-$\alpha$, interleukin-6, cyclooxygenases-2 and nitric oxide in lipopolysaccaride-stimulated mouse peritoneal macrophages. Our study suggests an important molecular mechanism of PA, which might explain its beneficial effect in the regulation of inflammatory reactions.

• Natural Product Sciences
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• 제15권3호
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• pp.139-143
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• 2009

The anaphylactic allergic reaction is involved in many allergic diseases such as asthma and allergic rhinitis. In this report, I investigated the effect of ripe fruits of Rubus coreanus Miq. (Rosaceae) (RFRC) on the anaphylactic allergic reaction and studied its possible mechanisms of action. RFRC inhibited compound 48/80-induced systemic anaphylactic reaction in mice. RFRC dose-dependently decreased the IgE-mediated passive cutaneous anaphylaxis. In addition, RFRC decreased the gene expression and production of tumor necrosis factor-$\alpha$ (TNF-$\alpha$) and interleukin (IL)-6 in phorbol 12-myristate 13-acetate (PMA) plus calcium ionophore A23187 (A23187)-stimulated human mast cells. These findings provide evidence that RFRC could be a candidate as an anti-allergic agent.

• Advances in Traditional Medicine
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• 제2권2호
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• pp.106-112
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• 2002

The effect of aqueous extract of Magnoliae Cortex (Magnoliaceae) (MCAE) on the immediate-type allergic reaction was investigated. MCAE inhibited compound 48/80 induced systemic anaphylactic reaction in rats. MCAE (0.1 and 1 g/kg) also significantly inhibited local immunoglobulin E (lgE)-mediated passive cutaneous anaphylactic (PCA) reaction. MCAE (0.001 to 1 mg/ml) dose-dependently inhibited the histamine release from rat peritoneal mast cells (RPMC) activated by compound 48/80 or anti-dinitrophenyl (DNP) 1gE. Moreover, MCAE (0.01 to 1 mg/ml) had a significant inhibitory effect on anti-DNP IgE-mediated tumor necrosis $factor-{\alpha}$ $(TNF-{\alpha})$ production. These results indicate that MCAE inhibits immediate-type allergic reaction in vivo and in vitro.

• Advances in Traditional Medicine
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• 제1권1호
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• pp.89-96
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• 2000

A human hepatoma cell line, Hep G2 cells are a reliable for the study of alcohol-induced hepatotoxicity. In this study, the author investigated the effect of an aqueous extract of Asparagus $cochinchinensis_{MERRIL}$ (Liliaceae) roots (ACAE) on ethanol (EtOH)-induced cytotoxicity in Hep G2 cells. ACAE dose-dependently inhibited the EtOH-induced tumor necrosis $factor-{\alpha}\;(TNF-{\alpha})$ secretion. ACAE also inhibited the EtOH and $TNF-{\alpha}-induced$ cytotoxicity. Furthermore, the author found that ACAE inhibited the $TNF-{\alpha}-induced$ apoptosis of Hep G2 cells. These results suggest that ACAE may prevent the EtOH-induced cytotoxicity through inhibition of the apoptosis of Hep G2 cells.