• Biomedical Science Letters
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• v.28 no.2
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• pp.137-144
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• 2022

Poria cocos is a natural substance known to have anticancer, antioxidant and anti-inflammatory effects. The aim of this study is to investigate the analgesic effects of Poria cocos extract (PCE). We evaluated the analgesic effects of PCE using adjuvant induced arthritis rat model. Male SD rats were administered intra-orally with PCE according to prescribed dosage, during 6 days. After 6 days later, serum TNF-α, IL-1β, and IL-6 levels were measured by ELISA. In our experiment, administration of PCE decreased TNF-α, IL-1β, IL-6 and PGE2 level in serum. Furthermore, it was confirmed that allodynia was relieved in evaluation of pain behavior. It was confirmed that administration of PCE reduces nociceptive pain by reducing nociceptive stimuli by acting as an anti-inflammatory drug.

• Biomedical Science Letters
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• v.29 no.3
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• pp.152-158
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• 2023

The aim of this study is to investigate the analgesic effects of Syneilesis aconitifolia Maxim. extract (SAM). We evaluated analgesic effects of SAM on animal pain model. Male SD rats were administered intra-orally with SAM according to prescribed dosage. During 7 days. After 7 days later, serum TNF-α, IL-1β, and IL-6 levels were measured by ELISA. In our experiment, administration of SAM decreased IL-1β, IL-6, TNF-α and PGE2 level in serum. Furthermore, it was confirmed that allodynia was relieved in evaluation of pain behavior. It was confirmed that administration of SAM reduces nociceptive pain by reducing nociceptive stimuli by acting as an anti-inflammatory drug.

• Journal of Physiology & Pathology in Korean Medicine
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• v.18 no.2
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• pp.419-426
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• 2004

This experimental study was designed to investigate the effects of Yukgunja-tang(YGJT) on the inhibition of cerebral ischemia in rats. And We measured regional cerebral blood f1ow(rCBF) and pial arterial diameter(PAD) in cerebral ischemic rats, and cytokines production in serum Of cerebral ischemic rats. The results were as follows; Both rCBF and PAD were significantly and stably increased by YGJT(10 mg/kg, i.p.) during the period of cerebral reperfusion, which contrasted with the findings of rapid and marked increase in control group. In cytokine production of serum by drawing from femoral arterial blood after middle cerebral arterial occlusion(MCAO) 1 hr, IL-1β and TGF-β production of sample group were similar to that of control group, but sample group was decreased TNF-α production compared with control group, and was significantly increased IL-10 production in compared with control group. In cytokine production of serum by drawing from femoral arterial blood after reperfusion 1 hr, sample group was significantly decreased IL-1β and TNF-α production compared with control group, but TGF-β production of sample group was similar to that of control group, and sample group was significantly increased IL-10 production compared with control group. In cytokine production of serum by drawing from femoral arterial blood after reperfusion 4 hrs, sample group was significantly decreased IL-1β production compared with control group, and sample group was decreased TNF-α production in compared with control group, but TGF-β production of sample group was similar to that of control group, and sample group was increased IL-10 production compared with control group. This results were suggested that YGJT has inhibitive effect on the brain damage by inhibited IL-1β production and TNF-α production, but accelerated IL-10 production. We thought that YGJT should have an anti-ischemic effect through the improvement of cerebral hemodynamics and inhibitive effect on the brain damage.

• Journal of Microbiology and Biotechnology
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• v.33 no.4
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• pp.493-499
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• 2023

In this study we evaluated the immune-enhancing effects of β-glucan, the main component of Euglena gracilis (Euglena), and Euglena on inflammatory factor expression in RAW264.7 macrophages and ICR mice with cyclophosphamide-induced immunosuppression. Macrophages were treated with β-glucan or Euglena for 48 h. The β-glucan and Euglena groups exhibited higher levels of inducible nitric oxide synthase, nitric oxide, and tumor necrosis factor (TNF)-α than the control (vehicle alone) group. Animals were fed saline and β-glucan (400 mg/kg body weight (B.W.)) or Euglena (400 or 800 mg/kg B.W.) for 19 days, and on days 17-19, cyclophosphamide (CCP, 80 mg/kg B.W.) was administered to induce immunosuppression in the ICR mouse model. CCP reduced the body weight, spleen index, and cytokine expression of the mice. To measure cytokine and receptor expression, splenocytes were treated with concanavalin A (ConA) or lipopolysaccharide (LPS) as a mitogen for 24 h. In vivo, ConA stimulation significantly upregulated the expression of interferon (IFN)-γ, interleukin (IL)-10, IL-12 receptor β1, IL-1β, and IL-2 in splenocytes from the β-glucan- or Euglena-treated groups compared with those in the splenocytes from the CCP-treated group; LPS stimulation increased the levels of the cytokines TNF-α, IL-1β, and IL-6 in splenocytes from the β-glucan- or Euglena- treated groups compared with those from the CCP-treated group, but most of these differences were not significant. These results demonstrate the effect of Euglena in ameliorating macrophages and immunosuppression in CCP-treated mice. Thus, Euglena has the potential to enhance macrophage- and splenocyte- mediated immune-stimulating responses.

• Korean Journal of Agricultural Science
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• v.47 no.3
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• pp.459-470
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• 2020

This study investigated the effects of the proteolytic hydrolysates of α-lactalbumin (LA), β-lactoglobulin (LG) and bovine serum albumin (BSA) by alcalase on inflammatory cytokines. The proteolytic hydrolysates were separated into two fraction of peptides, ≤ 10,000 Da and > 10,000 Da, respectively, because various low molecular weight peptides were generated during the hydrolysis reaction time. Among the hydrolysate peptides, BSA (all types), β-LG (> 10,000 Da), and α-LA (> 10,000 Da) showed an inhibitory activity against thymic stromal lymphopoietin (TSLP) mRNA expression in lipopolysaccharide-induced RAW264.7 murine macrophages. α-LA (> 10,000 Da), β-LG (hydrolysates), and BSA (> 10,000 Da) showed an inhibitory activity against tumor necrosis factor (TNF)-α expression. α-LA (all types), β-LG (hydrolysates, > 10,000 Da), and BSA (> 10,000 Da) showed an inhibitory activity against interleukin-6 (IL-6) expression. α-LA (> 10,000 Da), β-LG (> 10,000 Da), and BSA (all types) showed an inhibitory activity against inducible nitric oxide synthase (iNOS) expression. α-LA (> 10,000 Da), β-LG (> 10,000 Da), and BSA (all types) showed an inhibitory activity against cyclooxygenase (COX)-2 expression. The lowest level of TNF-α production was measured with α-LA (> 10,000 Da) and β-LG (> 10,000 Da) for all types, and a similar low level was measured for all types of BSA. The highest level of IL- 6 production was measured with α-LA (≤ 10,000 Da) among α-LA, β-LG, and IL-6. The low level of NO production was similar with α-LA, β-LG, and BSA but not with α-LA (≤ 10,000 Da). These potential peptides from whey protein hydrolysates could be used for food, medicinal, and industrial applications.

• Journal of Applied Biological Chemistry
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• v.63 no.3
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• pp.211-219
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• 2020

Quercetin is a polyphenol compound with excellent antioxidant and anti-inflammatory activity. However, little has been reported about the efficacy of quercetin to control psoriasis. Thus, we aimed to investigate the effect of quercetin to regulate psoriatic dermatitis with HaCaT cell lines activated by TNF-α and IL-17A, which are in vitro psoriasis skin models. When quercetin was treated with TNF-α-activated HaCaT cell line, inflammatory cytokine expressions such as IL-1α, IL-1β and IL-6 were reduced by 49.1±7.14, 42.8±8.16, and 34.5±2.52%, respectively. In addition, mRNA expression levels of IL-8 and CCL20 the chemokines that attract immune cells such as Th17 cells and dendritic cells to the inflammatory reaction site, were also reduced by 38.4±5.83 and 52.9±4.59% compared to the TNF-α treatment group. The expression of proteins KRT6A and KRT16, which was nonspecifically increased in psoriatic skin was also significantly suppressed. Moreover, phosphorylation of IκBα and STAT3 proteins activated by TNF-α was also significantly inhibited. After stimulating the HaCaT with IL-17A, known as another psoriasis-inducing cytokine, it was observed that IκBα mRNA expression decreased by 55.8±5.28%, and STAT3 phosphorylation was downregulated by 36.3±6.81%. Finally, after co-activation by TNF-α/IL-17A, quercetin inhibited all of IL-1α, IL-1β, IL-6, TNF-α and CCL20 gene expression. The above results strongly suggest that quercetin is a material that has not only anti-oxidant and anti-inflammatory activities, but also has an activity in improving psoriasis.

• Journal of Physiology & Pathology in Korean Medicine
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• v.16 no.1
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• pp.111-116
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• 2002

This report describes an inhibitory effect of Tongku-tang(TKT) on mast cell-mediated immediate-type allergic reactions. TKT is an Oriental herbal prescription, which has been successfully applied for the treatment of allergic disorders, mainly skin anaphylactic diseases in eastern medicine. TKT has concentration-dependently inhibited the ear swelling response induced by intradermal injection of non-specific mast cell degranulator compound 48/80 in mice. TKT also inhibited mast cell-dependent passive cutaneous anaphylaxis activated by dinitrophenyl (DNP)-IgE antibody in rats. I studied the effect of TKT on the histamine and β-hexosaminase release from the rat peritoneal mast cells by compound 48/80. TKT did not inhibit significantly the histamine and β-hexosaminase release from the rat peritoneal mast cells by compound 48/80. However, TKT inhibited both TNF-α and IL-1β secretion induced by phorbol 12-myristate 13-acetate and A23187 respectively. These results provide evidence that TKT may be beneficial in the treatment of immediate-type allergic reaction.

• Journal of Microbiology and Biotechnology
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• v.31 no.6
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• pp.794-802
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• 2021

In this study we investigated the role and mechanism of cardamonin on IL-1β induced injury in OA. CHON-001 cells were treated with cardamonin and IL-1β and transfected with silencing nuclear factor erythroid 2-related factor 2 (siNrf2). Cell viability was detected by Cell Counting Kit-8 assay and flow cytometer assay was utilized for cell apoptosis assessment. IL-6, IL-8, TNF-α and Nrf2 mRNA expression was tested by qRT-PCR. Western blot was employed to evaluate MMP-3, MMP-13, Collagen II, Nrf2, NQO-1, NLRP3, Caspase 1 and apoptosis-associated speck-like protein containing a caspase-1 recruitment domain (ASC) protein levels. In CHON-001 cells, IL-1β suppressed cell viability and Collagen II level while promoting cell apoptosis and expression of pro-inflammatory cytokines (IL-6, IL-8, TNF-α), MMPs (MMP-3, MMP-13), NQO-1, and NLRP3 inflammasome (NLRP3, Caspase 1 and ASC), with no significant influence on Nrf2. Cardamonin reversed the effect of IL-1β on cell viability, cell apoptosis, pro-inflammatory cytokines, MMPs, Collagen II, and NLRP3 inflammasome levels. In addition, cardamonin advanced Nrf2 and NQO-1 expression of CHON-001 cells. SiNrf2 reversed the function of cardamonin on IL-1β-induced cell apoptosis and expression of pro-inflammatory cytokines, Nrf2, NQO-1, and NLRP3 inflammasome in chondrocytes. Taken together Cardamonin inhibited IL-1β induced injury by inhibition of NLRP3 inflammasome via activating Nrf2/NQO1 signaling pathway in chondrocyte.

• The Korean Journal of Pain
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• v.37 no.2
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• pp.151-163
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• 2024

Background: Galangin, commonly employed in traditional Chinese medicine for its diverse medicinal properties, exhibits potential in treating inflammatory pain. Nevertheless, its mechanism of action remains unclear. Methods: Mice were randomly divided into 4 groups for 7 days: a normal control group, a galangin-treated (25 and 50 mg/kg), and a positive control celecoxib (20 mg/kg). Analgesic and anti-inflammatory effects were evaluated using a hot plate test, acetic acid-induced writhing test, acetic acid-induced vascular permeability test, formalin-induced paw licking test, and carrageenan-induced paw swelling test. The interplay between galangin, transient receptor potential vanilloid 1 (TRPV1), NF-κB, COX-2, and TNF-α proteins was evaluated via molecular docking. COX-2, PGE2, IL-1β, IL-6, and TNF-α levels in serum were measured using ELISA after capsaicin administration (200 nmol/L). TRPV1 expression in the dorsal root ganglion was analyzed by Western blot. The quantities of substance P (SP) and calcitonin gene-related peptide (CGRP) were assessed using qPCR. Results: Galangin reduced hot plate-induced licking latency, acetic acid-induced contortions, carrageenan-triggered foot inflammation, and capillary permeability in mice. It exhibited favorable affinity towards TRPV1, NF-κB, COX-2, and TNF-α, resulting in decreased levels of COX-2, PGE2, IL-1β, IL-6, and TNF-α in serum following capsaicin stimulation. Galangin effectively suppressed the upregulation of TRPV1 protein and associated receptor neuropeptides CGRP and SP mRNA, while concurrently inhibiting the expression of NF-κB, TNF-α, COX-2, and PGE2 mRNA. Conclusions: Galangin exerts its anti-inflammatory pain effects by inhibiting TRPV1 activation and regulating COX-2, NF-κB/TNF-α expression, providing evidence for the use of galangin in the management of inflammatory pain.

• Journal of Life Science
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• v.30 no.1
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• pp.106-112
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• 2020

Aminoacyl tRNA synthetase complex interacting multifunctional protein 2 (AIMP2) is a scaffolding protein required for the assembly of multi-tRNA synthetase, and it can exert pro-apoptotic activity in response to DNA damage. In the presence of DNA damage, AIMP2 binds to mouse double minute 2 homolog (MDM2) to protect p53 from MDM2 attack. TGF-β signaling results in the nuclear translocation of AIMP2, whereby AIMP2 interacts with FUSE-binding protein, and, thus, suppresses c-myc. TNF receptor-associated factor 2 (TRAF2) is an important mediator between TNF-receptors 1 and 2 which are involved in the signaling of c-Jun N-terminal kinase (JNK), nuclear factor κB (NF-κB), and p38 mitogen-activated protein kinases (MAPKs). TRAF2 is required for the activations of JNK and NF-κB via TNF-α and the mediation of anti-apoptosis signaling. AIMP2 can also enhance pro-apoptosis in the TNF-α signaling. During this signaling, AIMP2 assists the association of E3 ubiquitin ligase, the cellular inhibitor of apoptosis protein 1 (c-IAP1) which is well known and responsible for the degradation of TRAF2. The formation of a complex among AIMP2, TRAF2, and c-IAP1 results in proteasome-mediated TRAF2 degradation. AIMP2 can induce apoptosis via downregulation of TRAF2 to interact directly in TNF-α signaling. This review provides new insight into the molecular mechanism responsible for AIMP2 and TRAF2 complex formation and treatments for TNFα-associated diseases.