• 제목/요약/키워드: TNF-β

검색결과 425건 처리시간 0.029초

대군자탕이 뇌허혈에 미치는 억제 효과 (The Inhibitive Effects of Yukgunja-tang on the Cerebral Ischemia)

  • 김희성;이상록;정현우
    • 동의생리병리학회지
    • /
    • 제18권2호
    • /
    • pp.419-426
    • /
    • 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.

Analgesic Effect of Poria cocos Extract on a Rat Model of Adjuvant-induced Arthritis

  • Lee, Gil-Hyun;Yoon, Hae-Gyung;Choi, Go-Eun;Hyun, Kyung-Yae
    • 대한의생명과학회지
    • /
    • 제28권2호
    • /
    • pp.137-144
    • /
    • 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.

Analgesic Effect of Syneilesis aconitifolia Maxim. Extract on Animal Pain Model

  • Gil-Hyun Lee
    • 대한의생명과학회지
    • /
    • 제29권3호
    • /
    • pp.152-158
    • /
    • 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.

Evaluation of the Effects of Euglena gracilis on Enhancing Immune Responses in RAW264.7 Cells and a Cyclophosphamide-Induced Mouse Model

  • Kyeong Ah Jo;Kyeong Jin Kim;Soo-yeon Park;Jin-Young Jeon;Ji Eun Hwang;Ji Yeon Kim
    • Journal of Microbiology and Biotechnology
    • /
    • 제33권4호
    • /
    • pp.493-499
    • /
    • 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.

Properties of hydrolyzed α-lactalbumin, β-lactoglobulin and bovine serum albumin by the alcalase and its immune-modulation activity in Raw 264.7 cell

  • Yu, Jae Min;Son, Ji Yoon;Renchinkhand, Gerelyuya;Kim, Kwang-Yeon;Sim, Jae Young;Nam, Myoung Soo
    • 농업과학연구
    • /
    • 제47권3호
    • /
    • pp.459-470
    • /
    • 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.

TNF-α/IL-17A 유도된 HaCaT 세포주에서 Quercetin의 IκBα/STAT3 인산화 조절에 의한 CCL20 발현 억제 (Quercetin suppress CCL20 by reducing IκBα/STAT3 phosphorylation in TNF-α/IL-17A induced HaCaT cells)

  • 김미란;김민영;황형서
    • Journal of Applied Biological Chemistry
    • /
    • 제63권3호
    • /
    • pp.211-219
    • /
    • 2020
  • Quercetin은 항산화 및 항염증 활성이 잘 알려져 있으나, 건선 피부염 조절에 대한 효능 연구는 거의 보고된 것이 없어, in vitro 건선 피부염 시험 모델인 TNF-α/IL-17A 유도 HaCaT 세포주를 이용해 quercetin에 의한 건선 피부염 개선 효과를 규명하였다. 먼저, TNF-α에 의해 활성화된 HaCaT 세포주에 quercetin을 처리한 결과, IL-1α, IL-1β, IL-6 등 염증성 사이토카인 발현이 TNF-α 처리군 대비 각각 49.1±7.14, 42.8±8.16, 34.5±2.52% 억제되었다. Th17세포 및 수지상세포 등 면역세포를 염증 반응 부위로 유인하는 케모카인 IL-8 및 CCL20의 mRNA 발현량 또한 TNF-α 처리군 대비 38.4±5.83, 52.9±4.59% 감소하였다. TNF-α 자극에 의해 건선피부에서 비특이적으로 증가되는 케라틴 단백질 KRT6A 및 KRT16 발현뿐만 아니라, IκBα 및 STAT3 단백질의 인산화 또한 quercetin에 의해 유의적으로 억제되었다. 또 다른 건선 유발 사이토카인으로 알려진 IL-17A로 HaCaT 세포주를 자극한 후 quercetin에 의한 영향을 관찰한 결과, IκBα mRNA 발현은 55.8±5.28% 감소하였고, STAT3 인산화는 36.3±6.81% 하향 조절되었다. 마지막으로 TNF-α/IL-17A를 동시 자극한 HaCaT 세포주에 quercetin을 처리한 결과, IL-1α, IL-1β, IL-6, TNF-α, CCL20 유전자 발현이 모두 억제되는 것을 확인하였다. 이를 통해 quercetin은 기존 항산화, 항염증 활성뿐만 아니라 건선 피부염 개선에 활성을 갖는 소재임을 확인할 수 있었다.

통규탕의 즉각형 알레르기 반응 억제 효과에 관한 실험적 연구 (Experimental Studies on the Inhibitory Effect of Immediate-Type Allergic Reaction of Tongku-tang)

  • 김영복;윤용갑
    • 동의생리병리학회지
    • /
    • 제16권1호
    • /
    • pp.111-116
    • /
    • 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.

Cardamonin Inhibited IL-1β Induced Injury by Inhibition of NLRP3 Inflammasome via Activating Nrf2/NQO-1 Signaling Pathway in Chondrocyte

  • Jiang, Jianqing;Cai, Mingsong
    • Journal of Microbiology and Biotechnology
    • /
    • 제31권6호
    • /
    • pp.794-802
    • /
    • 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.

Analgesic and anti-inflammatory effects of galangin: a potential pathway to inhibit transient receptor potential vanilloid 1 receptor activation

  • Kaiwen Lin;Datian Fu;Zhongtao Wang;Xueer Zhang;Canyang Zhu
    • The Korean Journal of Pain
    • /
    • 제37권2호
    • /
    • pp.151-163
    • /
    • 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.

농약 중독에 의한 혈중 염증성 사이토카인의 영향에 대한 예비 연구 (Inflammatory cytokines in patients with pesticide poisoning: a pilot study)

  • 김현준;김욱준;이동욱;정승현;조남준;박삼엘;이은영;길효욱
    • 대한임상독성학회지
    • /
    • 제20권1호
    • /
    • pp.15-21
    • /
    • 2022
  • Purpose: Acute pesticide poisoning is lethal and can lead to death. A few studies about the effects of acute pesticide poisoning have focused on the immune system. In the current study, we preliminarily investigated the changes in blood inflammatory cytokine levels in acute pesticide poisoning patients. Methods: In this study, we prospectively investigated the inflammatory cytokines in patients with acute pesticide poisoning. This study included patients admitted from February 2021 to November 2021 with a diagnosis of intentional poisoning by pesticide ingestion. The inflammatory cytokines measured were IFN-γ, IL-1β, IL-6, and TNF-α. Results: Totally, 27 patients were enrolled in this study. The types of pesticide ingested were glufosinate (n=6), glyphosate (n=8), organophosphate (n=4), pyrethroid (n=2), and others (n=7). The levels of inflammatory cytokines obtained were as follows: IFN-γ 2.78±8.03 pg/ml, IL-1β 2.62±2.03 pg/ml, IL-6 44.58±80.16 pg/ml, and TNF-α 11.80±15.60 pg/ml. The overall mortality rate was 11.1% (3/27), and levels of IL-1β and TNF-α were significantly higher in the death group compared to the survival group. Conclusion: Increased levels of IL-6 and TNF-α were observed in patients with acute pesticide poisoning. IL-1β and TNF-α were significantly higher in the death group as compared to the survival group. Our results indicate the occurrence of an inflammatory response due to the activation of immune cells by pesticide poisoning. Future large-scale studies need to be conducted to investigate the application of inflammatory cytokines as predictors and therapeutic targets.