• 대한본초학회지
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• 제29권6호
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• pp.21-26
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• 2014

Objectives : Taraxacum coreanum (TC) have been used as a traditional medicine to treat inflammatory diseases and anti-oxidant effect in Korea. However, the anti-inflammatory effect of TC water extract on lipopolysaccharide (LPS)-induced inflammation is not well-known. Therefore, this study was performed to identify the anti-inflammatory effect of TC on LPS induced inflammatory. Methods : RAW 264.7 cells were treated with 500 ng/mL of LPS. Water extracts of TC (0.1, 0.25, 0.5 mg/ml) was treated 1 h prior to LPS. Cell viability was measured by MTT assay. Levels of nitric oxide (NO) were measured with Griess reagent and pro-inflammatory cytokines were measured by enzyme-linked immunosorbent assay (ELISA) and real-time polymerase chain reaction (real-time PCR). We also examined molecular mechanisms such as mitogen-activated protein kinases (MAPKs) and nuclear factor-B ($NF-{\kappa}B$) activation by western blot. Results : Water Extract from TC itself did not have any cytotoxic effect in RAW 264.7 cells. TC treatment inhibited the production of NO production, and pro-inflamamtory cytokines such as interleukin (IL)-6 and $IL-1{\beta}$ on protein and mRNA levels. In addition, TC treatment inhibited the LPS-induced activation of MAPKs such as extracellular signal-regulated kinase1/2 (ERK1/2), p38 kinases (p38), c-Jun $NH_2$-terminal kinase (JNK) and $NF-{\kappa}B$. Conclusions : In summary, our result suggest that treatment of TC could reduce the LPS-induced inflammation. Thereby, TC could be used as a protective agent against inflammation. Also, this study could give a clinical basis that TC could be a drug or agent to prevent inflammation.

• 대한한의학회지
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• 제44권2호
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• pp.119-131
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• 2023

Objectives: Betula Platyphylla(BP) has been used as a analgesic, anti-microbial, anti-oxidant drug in Eastern Asia. However, it is still unknown whether BP ethanol extract could exhibit the inhibitory activities against ultraviolet B(UVB)-induced skin injury on human keratinocytes, HaCaT cells. This study was aimed to investigate the protective activity of BP ethanol extract on UVB-irradiated skin injury in HaCaT cells. Methods: The skin injury model of HaCaT cells was established under UVB stimulation. HaCaT keratinocyte cells were pre-treated with BP ethanol extract for 1 h, and then stimulated with UVB. Then, the cells were harvested to measure the cell viability, production of reactive oxygen species(ROS), pro-inflammatory cytokines such as interleukin(IL) 1-beta, IL-6, and tumor necrosis factor(TNF)-𝛼, hyaluronidase, type 1 collagen, matrix metalloproteinase(MMP)s. In addition, we examined the mitogen activated protein kinases(MAPKs) and inhibitory kappa B alpha(I𝜅;-B𝛼) as inhibitory mechanisms of BP ethanol extract. Results: The treatment of BP ethanol extract inhibited the UVBinduced cell death and ROS production in HaCaT cells. BP ethanol extract treatment inhibited the UVB-induced increase of IL-1beta, IL-6, and TNF-𝛼. BP ethanol extract treatment inhibited the increase of hyaluronidase, MMP and decrease of collagen. BP ethanol extract treatment inhibited the activation of MAPKs and the degradation of I𝜅-B𝛼. Conclusions: Our result suggest that treatment of BP ethanol extract could inhibit the UVB-induced skin injury via deactivation of MAPKs and nuclear factor kappa B(NF-𝜅B) in HaCaT cells. This study could suggest that BP ethanol extract could be a beneficial agent to prevent skin damage or inflammation.

• 동의생리병리학회지
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• 제23권6호
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• pp.1392-1398
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• 2009

The purpose of this study was to investigate the anti-inflammatory effects of aqueous extract from Sophora Japonica (SJ) on the RAW 264.7 cells. To evaluate the anti-inflammatory effects of SJ, we examined the cytokine productions including nitric oxide (NO), interleukin (IL)-1b, IL-6 and tumor necrosis factor-a (TNF-a) in lipopolysaccharide (LPS)-induced RAW 264.7 cells and also inhibitory mechanisms such as mitogen-activated protein kinases (MAPKs) and nuclear factor kappa b (NF-kB) using Western blot. SJ inhibited LPS-induced production of NO, TNF-a but not of IL-1b and IL-6 in RAW 264.7 cells. SJ inhibited the activation of MAPKs such as extracelluar signal-regulated kinase (ERK 1/2), c-Jun NH2-terminal kinase (JNK) and p38 but not of NF-kB in the LPS-stimulated RAW 264.7 cells. In conclusion, SJ down-regulated LPS-induced NO and TNF-a productions via MAPKs, which could be a clinical basis for inflammatory diseases and autoimmune diseases.

• Korean Journal of Acupuncture
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• 제39권2호
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• pp.43-53
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• 2022

Objectives : Paeonia lactiflora Pallas (PLP) have been reported to have pharmacological effects such as anti-inflammatory and analgesic. However, it is not yet known whether PLP extract has anti-inflammatory effect on HaCaT cells, human keratinocyte. Methods : To confirm the anti-inflammatory effect of PLP on keratinocyte, TNF-𝛼/IFN-𝛾-stimulated HaCaT cells were used. HaCaT cells were pre-treated with PLP for 1h before stimulation with TNF-𝛼/IFN-𝛾. Then HaCaT cells were stimulated with TNF-𝛼/IFN-𝛾 for 24 h, the cells and media were harvested to measure the inflammatory cytokines levels. Granulocyte-macrophage colony stimulating factor (GM-CSF), monocyte chemoattractant protein-1 (MCP-1), interleukin 1 beta (IL-1𝛽), and TNF-𝛼 were analyzed by enzyme-linked immunosorbent assay (ELISA), and the mRNA expression of thymus and activation-regulated chemokines (TARC), IL-6, and IL-8 were measured by reverse transcription-polymerase chain reaction (RT-PCR). We also investigated the inhibitory mechanism of the mitogen-activated protein kinase (MAPKs) including ERK, JNK, and p38 and nuclear factor-kappaB (NF-𝜅B) by PLP using western blot. Results : PLP did not show cytotoxicity in HaCaT cells. In TNF-𝛼/IFN-𝛾-stimulated HaCaT cells, PLP significantly inhibited the expression of GM-CSF, MCP-1 IL-1𝛽, TNF-𝛼, TARC and IL-6. PLP inhibited the phosphorylation of ERK and translocation of NF-𝜅B into the nucleus. Conclusions : These results indicate that PLP could ameliorate the TNF-𝛼/IFN-𝛾-stimulated inflammatory response through inhibition of MAPK and NF-kB signal pathway. This suggests that PLP could be used beneficial agent to improve skin inflammation.

• 한국가금학회지
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• 제46권1호
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• pp.31-37
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• 2019

닭의 clathrin-associated adaptor protein $3-{\delta}$ subunit 2(AP3S2)는 clathrin-coated vesicle를 가진 표적 세포막으로 암 배양 단백질 수송에 관여한다. AP3S2는 C형 간염 바이러스 감염으로 간 섬유화를 매개하고, 2형 당뇨병과 관련이 있는 것으로 알려져 있다. 또한, AP3S2는 clathrin-dependent endocytosis를 통해 숙주 세포로의 바이러스 유입에 관련된 역할을 하는 것으로 알려져 있다. 본 연구는 기존 연구에서 닭 신장조직에서 차별 발현 유전자로 발굴된 닭 AP3S2 유전자의 분자유전학적 특성을 구명하고, 닭의 조직에서의 유전자 발현 양상을 조사하며, 톨-유사수용체 3 (Toll-like receptor 3; TLR3) 자극에 의한 전사 조절을 연구하였다. 닭 AP3S2 유전자가 코딩하는 단백질의 구조는 다른 종과 매우 보존적이고 진화적으로 제브라 피쉬와 가장 가깝고, 포유류와 가장 먼 것으로 추정되었다. 닭의 다양한 조직에서 닭 AP3S2 유전자의 전사 수준을 조사한 결과, 폐에서 가장 높게 발현되었으며, 그 다음은 비장 순이었다. 닭의 배아 섬유아세포 주인 DF-1세포에서 조사한 결과, AP3S2 유전자의 발현은 TLR3 신호자극에 의해 감소하였다. 전사조절인자인 $NF{\kappa}B$나 AP-1의 억제제를 이용하여 조사한 결과, $NF{\kappa}B$나 AP-1의 억제에 의해 유전자 발현이 영향을 받지 않았다. 이 결과는 DF-1 세포에서 닭 AP3S2 유전자의 발현은 적어도 이 두 전사조절인자와는 독립적인 경로에 의해 조절됨을 시사한다. 본 연구의 결과는 닭 AP3S2가 바이러스 감염에 역할을 하고, TLR3 신호에 관여함을 제시한다. 추가연구를 통해 닭 AP3S2의 전사 조절과 바이러스 침입 메커니즘을 구명할 필요가 있다고 사료된다.

• Journal of Microbiology and Biotechnology
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• 제30권11호
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• pp.1614-1625
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• 2020

A number of species of the genus Trichilia (Meliaceae) exhibit anti-inflammatory effects. However, the effect of Trichilia martiana C. DC. (TM) on lipopolysaccharide (LPS)-induced inflammation has not, to the best of our knowledge, yet been determined. Therefore, in the present study, the antiinflammatory effect of TM on LPS-stimulated RAW264.7 macrophages was evaluated. The ethanol extract of TM (TMEE) significantly inhibited LPS-induced nitric oxide (NO), prostaglandin 2 (PGE₂), inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2). TMEE also reduced the levels of inflammatory cytokines, including tumor necrosis factor-alpha (TNF-α), interleukin (IL)-1β and IL-6. The upregulation of mitogen-activated protein kinases (MAPKs) and NF-κB activation was revealed to be downregulated following TMEE pretreatment. Furthermore, TMEE was indicated to lead to the nucleus translocation of nuclear factor erythroid-derived 2-related factor 2 (Nrf2) and the expression of heme oxygenase-1 (HO-1). In H292 airway epithelial cells, the pretreatment of TMEE significantly downregulated the production of LPS-stimulated IL-1β, and TMEE was indicated to increase the expression of HO-1. In animal models exhibiting LPS-induced acute lung injury (ALI), treatment with TMEE reduced the levels of macrophages influx and TNF-α production in the bronchoalveolar lavage fluid (BALF) of ALI mice. Additionally, TMEE significantly downregulated the activation of ERK, JNK and IκB, and upregulated the expression of HO-1 in the lungs of ALI mice. In conclusion, the results of the current study demonstrated that TMEE could exert a regulatory role in the prevention or treatment of the endotoxin-mediated inflammatory response.

• 대한본초학회지
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• 제37권3호
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• pp.9-19
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• 2022

Objectives : Angelicae Gigantis Radix (AG) is a plant of the Ranunculus family. AG have been reported to have various pharmacological effects on human health which include uterine growth promotion, anti-inflammatory, analgesic, and immune enhancement. However, research on dermatitis disease is insufficient. Therefore, we investigated the effects of AG on tumor necrosis factor-α (TNF-α)/interferon-γ (IFN-γ) stimulated HaCaT cell. Methods : To investigate the effect of AG on HaCaT cell, HaCaT cells were pre-treated with AG for 1 hour and then stimulated with TNF-α/IFN-γ. After 24 hours, media and cells were harvested to analyze the inflammatory mediators. Concentration of human interleukin-1beta (IL-1β), monocyte chemoattractant protein-1 (MCP-1), granulocyte-macrophage colony-stimulating factor (GM-CSF), and TNF-α in the media were assessed by ELISA. mRNA expression of human thymus and activation-regulated chemokine (TARC), IL-6, and IL-8 were analyzed by RT-PCR. Additionally, the mechanisms of mitogen-activated protein kinases (MAPKs) and nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) signaling pathway were investigated by Western blot. Results : The treatment of AG inhibited gene expression levels of IL-6, IL-8, and TARC and protein expression levels of IL-1β, MCP-1, and GM-CSF. Also, AG significantly reduced extracellular signal-regulated kinase (ERK) phosphorylation and NF-κB translocation in TNF-α/IFN-γ stimulated HaCaT cell. Conclusions : Taken together, these results demonstrate that AG can alleviate inflammatory diseases such as atopic dermatitis by regulating the expression of inflammatory cytokines. Also, it suggest that AG may a promising candidate drug for the treatment of inflammatory disease such as atopic dermatitis.

• Asian Pacific Journal of Cancer Prevention
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• 제15권3호
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• pp.1219-1225
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• 2014

Epigallocatechin-3-gallate (EGCG) is the most abundant polyphenol molecule from green tea and is known to exhibit antioxidative as well as tumor suppressing activity. In order to examine EGCG tumor invasion and suppressing activity against adult T-cell leukemia (ATL), two HTLV-1 positive leukemia cells (HuT-102 and C91-PL) were treated with non-cytotoxic concentrations of EGCG for 2 and 4 days. Proliferation was significantly inhibited by 100 ${\mu}M$ at 4 days, with low cell lysis or cytotoxicity. HTLV-1 oncoprotein (Tax) expression in HuT-102 and C91-PL cells was inhibited by 25 ${\mu}M$ and 125 ${\mu}M$ respectively. The same concentrations of EGCG inhibited NF-kB nuclearization and stimulation of matrix metalloproteinase-9 (MMP-9) expression in both cell lines. These results indicate that EGCG can inhibit proliferation and reduce the invasive potential of HTLV-1-positive leukemia cells. It apparently exerted its effects by suppressing Tax expression, manifested by inhibiting the activation of NF-kB pathway and induction of MMP-9 transcription in HTLV-1 positive cells.

• Nutrition Research and Practice
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• 제15권6호
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• pp.798-806
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• 2021

BACKGROUND/OBJECTIVES: Obesity is associated with chronic inflammation. The spleen is the largest organ of the lymphatic system and has an important role in immunity. Obesity-induced inflammatory responses are triggered by Toll-like receptor (TLR)-myeloid differentiation primary response 88 (MyD88) pathway signaling. Phenethyl isothiocyanate (PEITC) and 3,3'-diindolylmethane (DIM), major dietary glucosinolates present in cruciferous vegetables, have been reported to produce anti-inflammatory effects on various diseases. However, the effects of PEITC and DIM on the obesity-induced inflammatory response in the spleen are unclear. The purpose of this study was to examine the anti-inflammatory effects of PEITC and DIM on the spleen and their mechanism in high fat/cholesterol diet (HFCD)-fed C57BL/6 mice. MATERIALS/METHODS: We established an animal model of HFCD-induced obesity using C57BL/6 mice. The mice were divided into six groups: normal diet with AIN-93G diet (CON), high fat diet (60% calories from fat) with 1% cholesterol (HFCD), HFCD with PEITC 30 mg/kg/day or 75 mg/kg/day (HFCD+P30, HFCD+P75), and HFCD with DIM 1.5 mg/kg/day or 7.5 mg/kg/day (HFCD+D1.5, HFCD+D7.5). Enzyme-linked immunosorbent assay was used to evaluate pro-inflammatory cytokine secretion. Western blot and quantitative polymerase chain reaction were used to analyze protein and mRNA levels of nuclear factor kappa B (NF-κB) p65, interleukin 6 (IL-6), cyclooxygenase 2 (COX-2), TLR2, TLR4, and MyD88 in spleen tissue. RESULTS: Serum IL-6 levels were significantly higher in the HFCD group than in groups fed a HFCD with PEITC or DIM. Levels of NF-κB p65 protein and TLR2/4, MyD88, NF-κB p65, IL-6, and COX-2 mRNA were significantly higher in the HFCD group than in the CON group and were reduced by the PEITC and DIM supplements. CONCLUSIONS: PEITC- and DIM-supplemented diets improved splenic inflammation by modulating the TLR2/4-MyD88 pathway in HFCD-fed mice. We suggest that dietary glucosinolates may at least partially improve obesity-induced inflammation of the spleen.

• Journal of Ginseng Research
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• 제46권1호
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• pp.62-70
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• 2022

Background: Maternal Toxoplasma gondii (T. gondii) infection during pregnancy has been associated with various mental illnesses in the offspring. Ginsenoside Rh2 (GRh2) is a major bioactive compound obtained from ginseng that has an anti-T. gondii effect and attenuates microglial activation through toll-like receptor 4 (TLR4)/nuclear factor-kappa B (NF-κB) signaling pathway. GRh2 also alleviated tumor-associated or lipopolysaccharide-induced depression. However, the effects and potential mechanisms of GRh2 on depression-like behavior in mouse offspring caused by maternal T. gondii infection during pregnancy have not been investigated. Methods: We examined GRh2 effects on the depression-like behavior in mouse offspring, caused by maternal T. gondii infection during pregnancy, by measuring depression-like behaviors and assaying parameters at the neuronal and molecular level. Results: We showed that GRh2 significantly improved behavioral measures: sucrose consumption, forced swim time and tail suspended immobility time of their offspring. These corresponded with increased tissue concentrations of 5-hydroxytryptamine and dopamine, and attenuated indoleamine 2,3-dioxygenase or enhanced tyrosine hydroxylase expression in the prefrontal cortex. GRh2 ameliorated neuronal damage in the prefrontal cortex. Molecular docking results revealed that GRh2 binds strongly to both TLR4 and high mobility group box 1 (HMGB1). Conclusion: This study demonstrated that GRh2 ameliorated the depression-like behavior in mouse offspring of maternal T. gondii infection during pregnancy by attenuating the excessive activation of microglia and neuroinflammation through the HMGB1/TLR4/NF-κB signaling pathway. It suggests that GRh2 could be considered a potential therapy in preventing and treating psychiatric disorders in the offspring mice of mothers with prenatal exposure to T. gondii infection.