• Title/Summary/Keyword: M88

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Hesperetin suppresses LPS/high glucose-induced inflammatory responses via TLR/MyD88/NF-κB signaling pathways in THP-1 cells

  • Lee, Aeri;Gu, HyunJi;Gwon, Min-Hee;Yun, Jung-Mi
    • Nutrition Research and Practice
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    • v.15 no.5
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    • pp.591-603
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    • 2021
  • BACKGROUND/OBJECTIVES: Unregulated inflammatory responses caused by hyperglycemia may induce diabetes complications. Hesperetin, a bioflavonoid, is a glycoside in citrus fruits and is known to have antioxidant and anticarcinogenic properties. However, the effect of inflammation on the diabetic environment has not been reported to date. In this study, we investigated the effect of hesperetin on proinflammatory cytokine secretion and its underlying mechanistic regulation in THP-1 macrophages with co-treatment LPS and hyperglycemic conditions. MATERIALS/METHODS: THP-1 cells differentiated by PMA (1 µM) were cultured for 48 h in the presence or absence of hesperetin under normoglycemic (5.5 mM/L glucose) or hyperglycemic (25 mM/L glucose) conditions and then treated with LPS (100 ng/mL) for 6 h before harvesting. Inflammation-related proteins and mRNA levels were evaluated by enzyme-linked immunosorbent assay, western blot, and quantitative polymerase chain reaction analyses. RESULTS: Hesperetin (0-100 µM, 48 h) treatment did not affect cell viability. The tumor necrosis factor-α and interleukin-6 levels increased in cells co-treated with LPS under hyperglycemic conditions compared to normoglycemic conditions, and these increases were decreased by hesperetin treatment. The TLR2/4 and MyD88 activity levels increased in cells co-treated with LPS under hyperglycemic conditions compared to normoglycemic conditions; however, hesperetin treatment inhibited the TLR2/4 and MyD88 activity increases. In addition, nuclear factor-κB (NF-κB) and Acetyl-NF-κB levels increased in response to treatment with LPS under hyperglycemic conditions compared to normoglycemic conditions, but those levels were decreased when treated with hesperetin. SIRT3 and SIRT6 expressions were increased by hesperetin treatment. CONCLUSIONS: Our results suggest that hesperetin may be a potential agent for suppressing inflammation in diabetes.

Cytogenetic Analysis of Bagrid Catfish, Pseudobagrus fulvidraco(Teleostomi : Siluriformes) (동자개, Pseudobagrus fulvidraco(Teleostomi : Siluriformes)의 세포유전학적 연구)

  • Park, In-Seok;Lee, Chung-Lyul
    • Korean Journal of Ichthyology
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    • v.8 no.2
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    • pp.10-15
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    • 1996
  • The chromosome numbers of bagrid catfish, Pseudobagrus fulvidraco was 52, nine pairs (No. 1 to 9) were metacentrics with the range of relative length 2.89~6.22 and arm ratio 1.09~1.58 ; thirteen pairs (No. 10 to 22) were submetacentrics with the range of relative length 2.88~5.88 and arm ratio 1.80~3.65 ; and all other pairs (No. 23 to 26) were acrocentrics with the range of relative length 2.63~3.30 and arm ratio 9.01~10.67, and fundamental number was 104. Heteromorphic sex chromosomes were not found. There was not exist significant difference in resultant erythrocyte measurements and parameters between female and male (p<0.05). The mean sizes of cell and nucleus, were $11.03{\times}9.67{\mu}m$ and $4.18{\times}3.66{\mu}m$ respectively. The number of erythrocytes of both females and males were $6{\sim}7{\times}10^5/ml$. Gill tissues from diploid individuals had cells with one or two nucleoli.

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Attrition Effect of Beads on Enzymatic Saccharification of Raw Starch (생전분의 효소당화에서 유리구 마찰효과)

  • Choi, Seong-Hyun;Kim, Chan-Jo;Lee, Seuk-Keun
    • Applied Biological Chemistry
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    • v.32 no.4
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    • pp.374-377
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    • 1989
  • To optimize the enzymatic saccharification of raw-starch, reaction conditions by shaking with glass beads were adapted together with ${\alpha}-amylase$ from Streptomyces sp. 4M-2 and amyloglucosidase from commercial source. When raw-starch was degraded by the ${\alpha}-amylase$ in shaking flask with beads (raw-starch : bead in diam. of 3mm=1 : 5 by weight) at the shaker speed of 300rpm, the saccharification rate of corn and potato starch were increased up to 88% and 69% after 30 hrs of reaction, respectively. Application of the amyloglucosidase in combination with the ${\alpha}-amylase$ enhanced the rate of saccharifcation: 88% of saccharification was obtained in 6 hrs for raw-corn starch under the same reaction conditions as above.

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한국의 주요 기타 자연동굴

  • 한국동굴학회
    • Journal of the Speleological Society of Korea
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    • v.18 no.19
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    • pp.52-88
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    • 1989
  • 정선군 정선읍 봉양6리에 소재한 석회암동굴로서 높이 4m, 폭이 3.5m 금장이 100m이고 세대 부락에서 1km떨어진 해발 550m지점에 자리잡고 있다. 입구에서 커다란 광장이 나타났다. 좀 더 들어가면 다른 광장이 나타나는데 광장 끝 부분에 못이 있는데 바닥은 모래로 되어있다.(중략)

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Carnosic acid inhibits TLR4-MyD88 signaling pathway in LPS-stimulated 3T3-L1 adipocytes

  • Park, Mi-Young;Mun, Seong Taek
    • Nutrition Research and Practice
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    • v.8 no.5
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    • pp.516-520
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    • 2014
  • BACKGROUND/OBJECTIVES: Carnosic acid (CA), found in rosemary (Rosemarinus officinalis) leaves, is known to exhibit anti-obesity and anti-inflammatory activities. However, whether its anti-inflammatory potency can contribute to the amelioration of obesity has not been elucidated. The aim of the current study was to investigate the effect of CA on Toll-like receptor 4 (TLR4) pathways in the presence of lipopolysaccharide (LPS) in 3T3-L1 adipocytes. MATERIALS/METHODS: 3T3-L1 adipocytes were treated with CA ($0-20{\mu}M$) for 1 h, followed by treatment with LPS for 30 min; mRNA expression of adipokines and protein expression of TLR4-related molecules were then measured. RESULTS: LPS-stimulated 3T3-L1 adipocytes showed elevated mRNA expression of tumor necrosis factor (TNF)-${\alpha}$, interleukin-6, and monocyte chemoattractant protein-1, and CA significantly inhibited the expression of these adipokine genes. LPS-induced up regulation of TLR4, myeloid differentiation factor 88, TNF receptor-associated factor 6, and nuclear factor-${\kappa}B$, as well as phosphorylated extracellular receptor-activated kinase were also suppressed by pre-treatment of 3T3-L1 adipocytes with CA. CONCLUSIONS: Results of this study suggest that CA directly inhibits TLR4-MyD88-dependent signaling pathways and decreases the inflammatory response in adipocytes.