• Title/Summary/Keyword: Release effect

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Sinapic Acid Attenuates the Neuroinflammatory Response by Targeting AKT and MAPK in LPS-Activated Microglial Models

  • Tianqi Huang;Dong Zhao;Sangbin Lee;Gyochang Keum;Hyun Ok Yang
    • Biomolecules & Therapeutics
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    • v.31 no.3
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    • pp.276-284
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    • 2023
  • Sinapic acid (SA) is a phenolic acid that is widely distributed in fruits and vegetables, which has various bioactivities, such as antidiabetic, anticancer and anti-inflammatory functions. Over-activated microglial is involved in the development progress of neurodegenerative diseases, such as Parkinson's disease and Alzheimer's disease. The objective of this study was to investigate the effect of SA in microglia neuroinflammation models. Our results demonstrated that SA inhibited secretion of the nitric oxide (NO) and interleukin (IL)-6, reduced the expression of inducible nitric oxide synthase (iNOS) and enhanced the release of IL-10 in a dose-dependent manner. Besides, our further investigation revealed that SA attenuated the phosphorylation of AKT and MAPK cascades in LPS-induced microglia. Consistently, oral administration of SA in mouse regulated the production of inflammation-related cytokines and also suppressed the phosphorylation of MAPK cascades and AKT in the mouse cerebral cortex. These results suggested that SA may be a possible therapy candidate for anti-inflammatory activity by targeting the AKT/MAPK signaling pathway.

Dry Needling and Electro-Dry Needling Improved the Trigger Thumb in a Patient Based on Anatomical Structure Without A1 Pulley Release: A Case Report (방아쇠 무지 환자를 A1 활차 박리없이 근골격계에 기반하여 침과 전침으로 호전시킨 1례: 증례보고)

  • Myung Hyun Yoon
    • The Journal of Churna Manual Medicine for Spine and Nerves
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    • v.17 no.2
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    • pp.101-108
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    • 2022
  • Objectives Most of the acupuncture or dry needling points for trigger finger were limited around the metacarpophalangeal joint, A1 pulley, and flexor muscle tendon. Thus, this study aimed to report a case of a patient with trigger thumb which improved using dry needling on additional muscle points. Methods The author has investigated why additional points are needed including what its accompanying effects are. Dry needling and electro-dry needling have been conducted based on anatomical structure. Moreover, a follow-up observation was performed twice to evaluate if the effects of this treatment have been maintained. Treatment progress was evaluated using a numeric rating scale (NRS) and Quinnell's classification of trigger finger. Results After 28 days of treatment, NRS and Quinnell's trigger grade decreased significantly without adverse effects. The treatment effect has been maintained until follow-up observation. Conclusions Additional points are recommended for the radical treatment of trigger finger.

Anti-inflammatory Effects of Herbal Formula KCNS-001 for Mitigating Atopic Dermatitis (한약조성물 KCNS-001이 자유라디칼과 염증매개인자에 미치는 영향)

  • Lee, Jeong-Bok;Choi, Jae-Hwan;Bang, Ok-Sun;Yu, Young-Beob
    • The Korea Journal of Herbology
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    • v.24 no.3
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    • pp.97-102
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    • 2009
  • Objectives : We determined the anti-inflammatory activity of KCNS-001 that is a herbal formula including 6 medicinal plants and that are used to mitigate atopic dermatitis in oriental medicine. Methods : To evaluate anti-inflammatory effect of KCNS-001, we measured the production of reactive oxygen species (ROS), nitric oxide (NO) and cyclooxygenase-2 (COX-2) in LPS-activated Raw 264.7 cells. Cell viability was determined by MTT assay. The concentrations of ROS and relative level of NO were measured with DPPH assay and Griess reagent, respectively. COX-2 and TNF-$\alpha$ were detected by enzyme immuno assay (EIA) and enzyme-linked immunosorbent assay (ELISA). Results : ROS and NO production were reduced by KCNS-001 in a dose-dependent manner. KCNS-001 significantly inhibited activity of COX-2 and suppressed the release of tumor necrosis factor-alpha (TNF-$\alpha$). Conclusions : These results indicate that the KCNS-001 may have an anti-inflammatory agent for the treatment of various inflammatory disease.

Absolute calibration of near-infrared Period-Luminosity-Metallicity relations for RR Lyrae variables using Gaia EDR3

  • Bhardwaj, Anupam;Rejkuba, Marina;Yang, Soung-Chul
    • The Bulletin of The Korean Astronomical Society
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    • v.46 no.1
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    • pp.35.1-35.1
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    • 2021
  • RR Lyrae stars are sensitive probe for the precision stellar astrophysics and also for the cosmic distance scale thanks to their well-defined near-infrared Period-Luminosity relations (PLRs). These horizontal branch variables can be used for primary calibration of the first-rung of population II distance ladder providing an evaluation of the ongoing tension between Cepheid-Supernovae based Hubble constant and the Planck results. Therefore, absolute calibration of RR Lyrae PLRs is now crucial to complement or test the tip of the red giant branch based distances, and in turn, population II star based Hubble constant measurements. While the pulsation models of RR Lyrae can reproduce most observables, they predict a significant metallicity effect on their JHKs-band PLRs that is inconsistent with so-far limited observational studies. We remedy this inconsistency of metallicity dependence in RR Lyrae PLRs by combining their near-infrared observations in the globular clusters of different mean-metallicities with the new parallaxes from the Gaia early data release 3 (EDR3). Our empirical results on Period-Luminosity-Metallicity (PLZ)relations are consistent with theoretical predictions but the precision of absolute calibrations is still affected by the parallax uncertainties and the systematic zero-point offset present in the Gaia EDR3.

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Efficacy of Muscle Energy Technique for Temporomandibular Disorders: A Systematic Review and Meta-analysis (턱관절 장애에 대한 근에너지 기법의 효과: 체계적 문헌 고찰 및 메타분석)

  • HongRyoul Yoon;JungWon Byun;SoonJoong Kim
    • The Journal of Churna Manual Medicine for Spine and Nerves
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    • v.18 no.2
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    • pp.31-42
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    • 2023
  • Objectives This study aimed to conduct a systematic review evaluating the effectiveness of muscle energy technique(MET) in temporomandibular joint disorders (TMD). Methods Searches were conducted in 11 electronic databases until October 2023. Randomized controlled trials(RCT) comparing the effect of MET for TMD were included. All studies were evaluated using the Cochrane Risk of Bias tool. Results Nine documents that fulfilled all the criteria were obtained for analysis. All studies showed some concerns in high risk of bias, but showed a significant improvement in pain and maximum mouth opening compared to baseline of MET or control group. MET was not better than extracorporeal shock wave therapy or myofascial release in some outcomes. Conclusions MET seems to be an effective treatment for TMD in some regards, however, can be considered as an adjunct therapy which has weak evidence. Further studies are required due to the inconclusive data and poor homogeneity found in this review.

Inflammasome-Dependent Peroxiredoxin 2 Secretion Induces the Classical Complement Pathway Activation

  • Cheol Ho Park;Hyun Sook Lee;Man Sup Kwak;Jeon-Soo Shin
    • IMMUNE NETWORK
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    • v.21 no.5
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    • pp.36.1-36.16
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    • 2021
  • Peroxiredoxins (Prxs) are ubiquitously expressed peroxidases that reduce hydrogen peroxide or alkyl peroxide production in cells. Prxs are released from cells in response to various stress conditions, and they function as damage-associated molecular pattern molecules. However, the secretory mechanism of Prxs and their roles have not been elucidated. Thus, we aimed to determine whether inflammasome activation is a secretory mechanism of Prxs and subsequently identify the effect of the secreted Prxs on activation of the classical complement pathway. Using J774A.1, a murine macrophage cell line, we demonstrated that NLRP3 inflammasome activation induces Prx1, Prx2, Prx5, and Prx6 secretion in a caspase-1 dependent manner. Using HEK293T cells with a transfection system, we revealed that the release of Prx1 and Prx2 relies on gasdermin-D (GSDMD)-mediated secretion. Next, we confirmed the binding of both Prx1 and Prx2 to C1q; however, only Prx2 could induce the C1q-mediated classical complement pathway activation. Collectively, our results suggest that inflammasome activation is a secretory mechanism of Prxs and that GSDMD is a mediator of their secretion. Moreover, secreted Prx1 and Prx2 bind with C1q, but only Prx2 mediates the classical complement pathway activation.

Quinic Acid Alleviates Behavior Impairment by Reducing Neuroinflammation and MAPK Activation in LPS-Treated Mice

  • Yongun Park;Yunn Me Me Paing;Namki Cho;Changyoun Kim;Jiho Yoo;Ji Woong Choi;Sung Hoon Lee
    • Biomolecules & Therapeutics
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    • v.32 no.3
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    • pp.309-318
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    • 2024
  • Compared to other organs, the brain has limited antioxidant defenses. In particular, the hippocampus is the central region for learning and memory and is highly susceptible to oxidative stress. Glial cells are the most abundant cells in the brain, and sustained glial cell activation is critical to the neuroinflammation that aggravates neuropathology and neurotoxicity. Therefore, regulating glial cell activation is a promising neurotherapeutic treatment. Quinic acid (QA) and its derivatives possess anti-oxidant and anti-inflammatory properties. Although previous studies have evidenced QA's benefit on the brain, in vivo and in vitro analyses of its anti-oxidant and anti-inflammatory properties in glial cells have yet to be established. This study investigated QA's rescue effect in lipopolysaccharide (LPS)-induced behavior impairment. Orally administering QA restored social impairment and LPS-induced spatial and fear memory. In addition, QA inhibited proinflammatory mediator, oxidative stress marker, and mitogen-activated protein kinase (MAPK) activation in the LPS-injected hippocampus. QA inhibited nitrite release and extracellular signal-regulated kinase (ERK) phosphorylation in LPS-stimulated astrocytes. Collectively, QA restored impaired neuroinflammation-induced behavior by regulating proinflammatory mediator and ERK activation in astrocytes, demonstrating its potential as a therapeutic agent for neuroinflammation-induced brain disease treatments.

Application of shrinkage prediction models to restraint crack formation in unbonded post-tensioned slabs

  • Gabriela R. Martínez Lara;Myoungsu Shin;Yong-Hoon Byun;Goangseup Zi;Thomas H.-K. Kang
    • Computers and Concrete
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    • v.33 no.4
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    • pp.349-359
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    • 2024
  • This study aims to investigate the effect of restraint configuration on crack formation due to shrinkage-and-creep-induced volumetric change in unbonded post-tensioned slabs. The first part of this study focuses on the comparison of existing shrinkage and creep calculation models that are used to predict the volume-changing behavior of concrete. The second part of this study presents the finite element analysis of a series of architectural configuration prototypes subjected to shrinkage and creep, which comprise unbonded post-tensioned slabs with various restraint configurations. The shrinkage and creep effects were simulated in the analysis by imposing strains obtained from one selected calculation model. The results suggest that a slab up to 300 ft. (90 m) in length does not require a closure strip if it is unrestrained by perimeter walls, and that the most effective restraint crack mitigation strategy for a slab restrained by perimeter walls is a partial wall release.

Fisetin-Mediated Perturbations of Membrane Permeability and Intracellular pH in Candida albicans

  • Younhee Kim
    • Journal of Microbiology and Biotechnology
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    • v.34 no.4
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    • pp.783-794
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    • 2024
  • The antifungal activity of fisetin against Candida albicans is explored, elucidating a mechanism centered on membrane permeabilization and ensuing disruption of pH homeostasis. The Minimum Inhibitory Concentration (MIC) of fisetin, indicative of its interaction with the fungal membrane, increases in the presence of ergosterol. Hoechst 33342 and propidium-iodide staining reveal substantial propidium-iodide accumulation in fisetin-treated C. albicans cells at their MIC, with crystal violet uptake assays confirming fisetin-induced membrane permeabilization. Leakage analysis demonstrates a significant release of DNA and proteins in fisetin-treated cells compared to controls, underscoring the antifungal effect through membrane disruption. Green fluorescence, evident in both the cytoplasm and vacuoles of fisetin-treated cells under BCECF, AM staining, stands in contrast to controls where only acidic vacuoles exhibit staining. Ratiometric pH measurements using BCECF, AM reveal a noteworthy reduction in intracellular pH in fisetin-treated cells, emphasizing its impact on pH homeostasis. DiBAC4(3) uptake assays demonstrate membrane hyperpolarization in fisetintreated cells, suggesting potential disruptions in ion flux and cellular homeostasis. These results provide comprehensive insights into the antifungal mechanisms of fisetin, positioning it as a promising therapeutic agent against Candida infections.

The Effect of Nitric Oxide Donor or Nitric Oxide Synthase Inhibitor on Oxidant Injury to Cultured Rat Lung Microvascular Endothelial Cells (산화질소 공여물과 산화질소 합성효소 길항제가 백서 폐미세혈관 내피세포 산화제 손상에 미치는 영향)

  • Chang, Joon;Michael, John R.;Kim, Se-Kyu;Kim, Sung-Kyu;Lee, Won-Young;Kang, Kyung-Ho;Yoo, Se-Hwa;Chae, Yang-Seok
    • Tuberculosis and Respiratory Diseases
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    • v.45 no.6
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    • pp.1265-1276
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    • 1998
  • Background : Nitric oxide(NO) is an endogenously produced free radical that plays an important role in regulating vascular tone, inhibition of platelet aggregation and white blood cell adhesion to endothelial cells, and host defense against infection. The highly reactive nature of NO with oxygen radicals suggests that it may either promote or reduce oxidant-induced cell injury in several biological pathways. Oxidant injury and interactions between pulmonary vascular endothelium and leukocytes are important in the pathogenesis of acute lung injury, including acute respiratory distress syndrome(ARDS). In ARDS, therapeutic administration of NO is a clinical condition providing exogenous NO in oxidant-induced endothelial injury. The role of exogenous NO from NO donor or the suppression of endogenous NO production was evaluated in oxidant-induced endothelial injury. Method : The oxidant injury in cultured rat lung microvascular endothelial cells(RLMVC) was induced by hydrogen peroxide generated from glucose oxidase(GO). Cell injury was evaluated by $^{51}$chromium($^{51}Cr$) release technique. NO donor, such as S-nitroso-N-acetylpenicillamine(SNAP) or sodium nitroprusside(SNP), was added to the endothelial cells as a source of exogenous NO. Endogenous production of NO was suppressed with N-monomethyl-L-arginine(L-NMMA) which is an NO synthase inhibitor. L-NMMA was also used in increased endogenous NO production induced by combined stimulation with interferon-$\gamma$(INF-$\gamma$), tumor necrosis factor-$\alpha$(TNF-$\alpha$), and lipopolysaccharide(LPS). NO generation from NO donor or from the endothelial cells was evaluated by measuring nitrite concentration. Result : $^{51}Cr$ release was $8.7{\pm}0.5%$ in GO 5 mU/ml, $14.4{\pm}2.9%$ in GO 10 mU/ml, $32.3{\pm}2.9%$ in GO 15 mU/ml, $55.5{\pm}0.3%$ in GO 20 mU/ml and $67.8{\pm}0.9%$ in GO 30 mU/ml ; it was significantly increased in GO 15 mU/ml or higher concentrations when compared with $9.6{\pm}0.7%$ in control(p < 0.05; n=6). L-NMMA(0.5 mM) did not affect the $^{51}Cr$ release by GO. Nitrite concentration was increased to $3.9{\pm}0.3\;{\mu}M$ in culture media of RLMVC treated with INF-$\gamma$ (500 U/ml), TNF-$\alpha$(150 U/ml) and LPS($1\;{\mu}g/ml$) for 24 hours ; it was significantly suppressed by the addition of L-NMMA. The presence of L-NMMA did not affect $^{51}Cr$ release induced by GO in RLMVC pretreated with INF-$\gamma$, TNF-$\alpha$ and LPS. The increase of $^{51}Cr$ release with GO(20 mU/ml) was prevented completely by adding 100 ${\mu}M$ SNAP. But the add of SNP, potassium ferrocyanate or potassium ferricyanate did not protect the oxidant injury. Nitrite accumulation was $23{\pm}1.0\;{\mu}M$ from 100 ${\mu}M$ SNAP at 4 hours in phenol red free Hanks' balanced salt solution. But nitrite was not detectable from SNP upto 1 mM The presence of SNAP did not affect the time dependent generation of hydrogen peroxide by GO in phenol red free Hanks' balanced salt solution. Conclusion : Hydrogen peroxide generated by GO causes oxidant injury in RLMVC. Exogenous NO from NO donor prevents oxidant injury, and the protective effect may be related to the ability to release NO. These results suggest that the exogenous NO may be protective on oxidant injury to the endothelium.

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