• 제목/요약/키워드: p-38

검색결과 9,378건 처리시간 0.045초

p38 MAPK을 이용한 항염증 효능 규명 프로토타입 개발 (Development of Prototype for Screening Anti-Inflammation Effects concerning p38 MAPK Signal Pathway)

  • 김철;예상준;남기엽;김상균;장현철;김진현;김영은;송미영
    • 한국한의학연구원논문집
    • /
    • 제17권3호
    • /
    • pp.77-85
    • /
    • 2011
  • Objectives : The purpose of this study was to develop a simulator which can analyze the anti-inflammatory effects of medical herbs based on e-cell concerning p38 MAPK signal pathway. Methods : We collected data concerning medical herbs with anti-inflammatory effects and the active compounds to provide as a fundamental databse and to validate the newly developed algorithm. At this time, we used the target database as pubmed and gathered the data by data mining tool, pathway studio. Also we have developed the web-based search system for confirming database related to anti-inflammation. We researched the mechanism of actions of proteins in p38 MAPK signal pathway when active compound has been inserted into the network. We reduced total network into TAK-MKK3-p38 and made the two types of mathematical model about active compounds' interaction. Results & Conclusion : We constructed the database which have 69 cases of medical herbs, 71 cases of active compounds, about 8,000 cases of URL(Uniform Resource Locator) related to papers and reports. We designed the ordinary differential equations for response of TAK, MKK3, p38 in e-cell's cytosol and nucleus. We used this formular as measure whether an active compound of medicinal plants which is inputted by an user would have an anti-inflammation effects. We developed the visualization program which could show the change of concentration over time.

경미한 경부 증상이 있는 대상자의 경추 관절 운동 범위 연구 (Cervical Range of Motion Associations with Sub-clinical Neck Pain)

  • 이해정
    • PNF and Movement
    • /
    • 제1권1호
    • /
    • pp.43-57
    • /
    • 2003
  • 목적: 병원치료가 필요하지 않을 만큼의 경부통증/증상과 관절가동범위, 경흉추의 다각적 면에서 관계를 조사하기 위해서이다. 방법: 연령은 19세에서 42세(평균연령 28세로 실험에 참여하기를 원하는 건강한 성인 40명을 대상으로 하였다. 경흉추의 척추 자세, 경추 능동 관절 가동범위, 경부 분절 길이 등의 다각적인 면을 측정하였다. 모든 측정들은 동일시에 각 대상자에게 서로 다른 측정자에 의해 두 번 실시되었다. 경부 근 지구력은 수정된 Biering-Sorensen 검사법에 의해 측정되었다. 마지막으로 대상자들에게 경부 통증/증상의 재발에 대한 질문을 하였다. 결과: 14명의 대상자들은 경미한 재발성 경부 통증/증상을 보고하였다. 경부 근 지구력 시간(F(1,38)=6.75, p=0.01)과 좌측 회전 가동 범위(F(1,38)=4.56, p=0.04)가 경부 통증을 가진 대상자들에서 유의하게 감소하였다. 신전 가동범위가 재 측정에서 특정군 변화 즉, 정상군 증가, 경부 통증/증상군 감소(F(1,38)=4.67, p=0.04)가 보였다. 경부 통증/증상군은 정상군과 비교 시 후인 가동 범위의 증가하였다(F(1,38) =4.56, p=0.04). 통증 유무에 관계없이 모든 대상자들에서 우측 회전보다 좌측 회전에서 가동범위가 더 크게 나타났고(F(1,38) =4.34, p=0.04), 반복 측정에서 좌측 측방굴곡 (F(1,38) =5.10, p=0.03)과 우측 측방 굴곡(F(1,38) = 5.27, p=0.03)의 감소가 나타났다. 결론: 경미한 증상의 경부통증 대상자군과 정상적인 대상자군을 비교할 때 그룹 간 차이는 경부 근 지구력 시간의 감소, 좌측 회전 가동 범위 감소와 특히, 두 번 째 측정에서 신전범위 감소가 나타났으나 후인의 가동범위는 증가로 관찰되었다. 이러한 결과들은 경부 통증의 발생과 관련된 초기 가동범위 변화를 제안한다.

  • PDF

Picropodophyllotoxin Induces G1 Cell Cycle Arrest and Apoptosis in Human Colorectal Cancer Cells via ROS Generation and Activation of p38 MAPK Signaling Pathway

  • Lee, Seung-On;Kwak, Ah-Won;Lee, Mee-Hyun;Seo, Ji-Hye;Cho, Seung-Sik;Yoon, Goo;Chae, Jung-Il;Joo, Sang Hoon;Shim, Jung-Hyun
    • Journal of Microbiology and Biotechnology
    • /
    • 제31권12호
    • /
    • pp.1615-1623
    • /
    • 2021
  • Picropodophyllotoxin (PPT), an epimer of podophyllotoxin, is derived from the roots of Podophyllum hexandrum and exerts various biological effects, including anti-proliferation activity. However, the effect of PPT on colorectal cancer cells and the associated cellular mechanisms have not been studied. In the present study, we explored the anticancer activity of PPT and its underlying mechanisms in HCT116 cells. The 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay was used to monitor cell viability. Flow cytometry was used to evaluate cell cycle distribution, the induction of apoptosis, the level of reactive oxygen species (ROS), assess the mitochondrial membrane potential (Δψm), and multi-caspase activity. Western blot assays were performed to detect the expression of cell cycle regulatory proteins, apoptosis-related proteins, and p38 MAPK (mitogen-activated protein kinase). We found that PPT induced apoptosis, cell cycle arrest at the G1 phase, and ROS in the HCT116 cell line. In addition, PPT enhanced the phosphorylation of p38 MAPK, which regulates apoptosis and PPT-induced apoptosis. The phosphorylation of p38 MAPK was inhibited by an antioxidant agent (N-acetyl-L-cysteine, NAC) and a p38 inhibitor (SB203580). PPT induced depolarization of the mitochondrial inner membrane and caspase-dependent apoptosis, which was attenuated by exposure to Z-VAD-FMK. Overall, these data indicate that PPT induced G1 arrest and apoptosis via ROS generation and activation of the p38 MAPK signaling pathway.

IL-23 Inhibits Trophoblast Proliferation, Migration, and EMT via Activating p38 MAPK Signaling Pathway to Promote Recurrent Spontaneous Abortion

  • He, Shan;Ning, Yan;Ma, Fei;Liu, Dayan;Jiang, Shaoyan;Deng, Shaojie
    • Journal of Microbiology and Biotechnology
    • /
    • 제32권6호
    • /
    • pp.792-799
    • /
    • 2022
  • As a vital problem in reproductive health, recurrent spontaneous abortion (RSA) affects about 1% of women. We performed this study with an aim to explore the molecular mechanism of interleukin-23 (IL-23) and find optimal or effective methods to improve RSA. First, ELISA was applied to evaluate the expressions of IL-23 and its receptor in HTR-8/SVneo cells after IL-23 treatment. CCK-8, TUNEL, wound healing and transwell assays were employed to assess the proliferation, apoptosis, migration and invasion of HTR-8/SVneo cells, respectively. Additionally, the expressions of apoptosis-, migration-, epithelial-mesenchymal transition- (EMT-) and p38 MAPK signaling pathway-related proteins were measured by western blotting. To further investigate the relationship between IL-23 and p38 MAPK signaling pathway, HTR-8/SVneo cells were treated for 1 h with p38 MAPK inhibitor SB239063, followed by a series of cellular experiments on proliferation, apoptosis, migration and invasion, as aforementioned. The results showed that IL-23 and its receptors were greatly elevated in IL-23-treated HTR-8/SVneo cells. Additionally, IL-23 demonstrated suppressive effects on the proliferation, apoptosis, migration, invasion and EMT of IL-23-treated HTR-8/SVneo cells. More importantly, the molecular mechanism of IL-23 was revealed in this study; that is to say, IL-23 inhibited the proliferation, apoptosis, migration, invasion and EMT of IL-23-treated HTR-8/SVneo cells via activating p38 MAPK signaling pathway. In conclusion, IL-23 inhibits trophoblast proliferation, migration, and EMT via activating p38 MAPK signaling pathway, suggesting that IL-23 might be a novel target for the improvement of RSA.

p38-dependent c-Jun degradation contributes to reduced PGE2 production in sodium orthovanadate-treated macrophages

  • Aziz, Nur;Kim, Eunji;Yang, Yanyan;Kim, Han Gyung;Yu, Tao;Cho, Jae Youl
    • BMB Reports
    • /
    • 제55권8호
    • /
    • pp.389-394
    • /
    • 2022
  • In particular, the phenomenon of c-Jun degradation within the inflammatory response has not yet been fully analyzed. In order to verify this, we investigated LPS-stimulated murine macrophages pre-treated with sodium orthovanadate (SO) in order to uncover the regulatory mechanisms of the MAPKs which regulate c-Jun degradation within the inflammatory response. Through our study, we found that SO suppressed the production of prostaglandin E2 (PGE2) and the expression of COX-2 in LPS-stimulated RAW264.7 cells. Additionally, SO decreased total c-Jun levels, without altering the amount of mRNA, although the phospho-levels of p38, ERK, and JNK were strongly enhanced. Through the usage of selective MAPK inhibitors, and knockdown and overexpression strategies, p38 was revealed to be a major MAPK which regulates c-Jun degradation. Further analysis indicates that the phosphorylation of p38 is a determinant for c-Jun degradation, and is sufficient to induce ubiquitination-dependent c-Jun degradation, recovered through MG132 treatment. Therefore, our results suggest that the hyperphosphorylation of p38 by SO contributes to c-Jun degradation, which is linked to the suppression of PGE2 secretion in inflammatory responses; and thus, finding drugs to increase p38 activity could be a novel strategy for the development of anti-inflammatory drugs.

양송이 품종과 수집 균주간의 Inter-simple sequence repeat (ISSR) 마커 분석 (Analysis of Inter-simple sequence repeat (ISSR) markers in cultivars and collected strains of button mushroom (Agaricus bisporus))

  • 남윤걸;공원식;장갑열;신평균;오민지;임지훈;구창덕;오연이
    • 한국버섯학회지
    • /
    • 제15권3호
    • /
    • pp.139-144
    • /
    • 2017
  • 양송이(Agaricus bisporus)는 국내에서 2015년 약 10,757톤이 생산되어 5번째로 많이 생산되는 버섯이다. 본 연구에서는 ISSR 마커를 사용하여 국내 수집균주와 상업품종간의 유전적 다양성을 분석하였다. 이를 위해 우선, 다양한 마커 중 양송이 속 내 비교 분석이 가능다고 알려진 ISSR마커를 선발하였다. 분석한 마커는 ISSR 807, 808, 809, 810, 811, 834, 835, 836, 841, 842, P3, P8, P17, P22, P30, P38 and P39 총 16종이였고 이들 중 육종에서 모본선발을 위한 효율적인 마커를 선발하기 위하여 양송이 수집균주 ASI 1110, 1114, 1115, 1238, 1246, 1365, 1366, 1369 등 8종을 선발하여 수행하였다. 그 결과 ISSR P31, P38, P39 마커에서 종내 구분이 가능한 다양한 밴드가 나타났다. 이를 바탕으로 선발된 3종의 마커를 이용하여 국내 수집균주와 새아, 새연 등의 상업품종이 포함된 39균주를 UPGMA 프로그램을 통하여 유연관계를 분석하였다. 국내 수집균주와 상업품종간의 계통도를 분석한 결과, 국내 수집균주와 상업품종들이 다른 그룹을 형성하는 것을 확인하였다. 이 결과를 근거로 ISSR P31, P38, P39가 상업품종을 구분할 수 있는 마커로 활용될 것이라 기대된다.

Berberine에 의한 HepG2 세포의 사멸과정에서 활성기산소와 p38 MAP kinase의 역할에 관한 연구 (The Role of ROS and p38 MAP kinase in Berberine-Induced Apoptosis on Human Hepatoma HepG2 Cells)

  • 현미선;우원홍;허정무;김동호;문연자
    • Applied Biological Chemistry
    • /
    • 제51권2호
    • /
    • pp.129-135
    • /
    • 2008
  • Berberine은 전통적인 중의약재로 이용되어지는 isoquinoline alkaloid로 황련, 황백과 같은 식물에서 주로 추출되며, 약리효과로는 항암, 항염, 항균과 같은 다양한 효과를 나타내는 것으로 알려져 있다. 그러나 간암세포에서 berberine의 산화적 스트레스에 의한 세포사멸기전에 대해서는 아직 밝혀진 바 없다. 따라서 본 연구는 사람의 간암세포인 HepG2 세포에서 berberien의 세포사멸기전에 reactive oxygen species(ROS)와 MAP kinase의 연관성을 조사하였다. Berberine은 HepG2 세포에서 처리 시간과 농도에 의존적으로 세포독성효과를 보였으며, $LD_{50}$은 berberine(50 ${\mu}M$) 처리 후 48시간에서 관찰 되었고, 세포고사의 특징인 핵의 응축 및 분절, DNA의 분절이 확인되었다. 또한 berberine에 의해 caspase-3, p53, p38 그리고 Bax의 발현이 현저하게 증가된 반면, anti-apoptotic 신호기전인 Bc1-2의 발현은 감소되었다. 이와 더불어 세포 내 nitric oxide(NO)와 ROS의 생성도 증가되었다. 본 연구 결과 HepG2 세포에서 berberine은 산화적 스트레스인 ROS와 NO의 생성을 유발하고 p38 MAP kinase와 p53의 인산화를 유도하였으며 미토콘드리아에서 Bcl-2의 감소와 bax의 증가, caspase-3의 활성을 경유하여 DNA의 손상을 통한 세포고사가 이루어지는 것을 확인 하였다.

비탄력 고정식 벨트가 노인 여성의 균형능력과 낙상예방에 미치는 영향 (The Effect of Application of a Non-Elastic Fixation Belt on the Balance Ability and Fall Prevention in Elderly Women)

  • 이장태;천승철
    • 한국산학기술학회논문지
    • /
    • 제18권2호
    • /
    • pp.398-404
    • /
    • 2017
  • 본 연구의 목적은 노인 여성의 약화된 천장관절 안정화를 위하여 비탄력 고정식 벨트를 적용하여 균형 능력과 낙상예방에 미치는 영향을 알아보고자 하였다. 노인 여성들은 출산과 폐경으로 천장관절의 약화 및 골반 주위근육들의 약화로 인하여 균형능력의 감소와 낙상위험률이 증가된다. 그러나 이와 관련된 연구는 불충분하다. 연구 대상자들은 실험군과 대조군으로 각각 20명씩 무작위로 배정하였으며, 비탄력 고정식 벨트를 실험군에게 적용한 후 균형 측정기를 사용하여 균형능력과 낙상 위험률을 평가하였다. 또한 비탄력 고정식 벨트를 적용한 실험군에서 하복부근육의 근두께를 초음파기기를 사용하여 실험 전후에 측정하였다. 통계방법은 연구대상자의 일반적 특성을 위하여 독립 t-검정, 균형 및 낙상지수를 위하여 $2{\times}2$ 반복 측정 분산분석 및 근두께를 위하여 짝비교 t-검정을 사용하였다. 두 그룹의 교호작용 효과는 안정성 지수(F1,38=47.24, p=0.001), 퓨리에 지수(F1,38=88.83, p=0.001), 체중분포 지수(F1,38=50.21, p=0.001) 및 낙상 지수(F1,38=21.59, p=0.001)에서 모두 통계적으로 유의하게 나타났다. 또한 비탄력 고정식 벨트를 적용한 결과 실험 후 복횡근(p=0.001)과 내복사근(p=0.001)의 근두께는 통계적으로 유의하게 증가하였다. 노인 여성들의 약화된 천장관절의 강화 및 안정화 방법으로 비탄력 고정식 벨트는 균형 및 낙상 예방에 긍정적이며 용이성, 보편성 및 경제적으로 효과적임을 알 수 있었다.

Effect of low intensity pulsed ultrasound in activating the mitogen-activated protein kinase signaling pathway and inhibition inflammation cytokine synthesis in chondrocytes

  • Kim, Eun-Jung;Kim, Gye-Yeop
    • Physical Therapy Rehabilitation Science
    • /
    • 제3권1호
    • /
    • pp.33-37
    • /
    • 2014
  • Objective: Low intensity pulsed ultrasound (LIPUS) has been shown to accelerate cell proliferation and tissue healing in both animal models and clinical trials. However, details of the clinical effects of LIPUS have not been well characterized. The aim of this study was to investigate the effect of LIPUS on mitogen-activated protein kinase (MAPK) activation in rat articular chondrocytes. Design: Cross-sectional study. Methods: Chondrocyte were cultured in six well cell culture plates for 72 hours at $37^{\circ}C$ with 5% $CO_2$, and then exposed to LIPUS at 1.5 MHz frequency and $30-mW/cm^2$ power. Changes in chondrocyte activities were evaluated in response to oxydative stress in dose-dependent (0 and 300 uM) and time-dependent (0-24 hr) manner. The cell viability were analyzed using MTT [3-(4.5-dimethylthiazol-2-yl)-2.5 diphenyltetrazolium bromide]. The expression of p38 MAPK was measured using western blotting. Results: Oxidative stress was induced in rat chondrocytes using hydrogen peroxide ($H_2O_2$). The cell viability was decreased in chondrocytes after the $H_2O_2$ dose and time-dependent treatment. The p38 MAPK phosphorylation occurred at a significantly increased rate after $H_2O_2$ treated (p<0.05). Expression of p38 MAPK was decreased in the p38 inhibitor groups compared with the oxidative stress-induced chondrocyte damage via the p38 MAPK signaling pathways (p<0.05). Conclusions: It could be concluded that LIPUS can inhibit oxidative stress-induced chondrocyte damage via the p38 MAPK signaling pathways.

Melatonin Induces Apoptotic Cell Death via p53 in LNCaP Cells

  • Kim, Chi-Hyun;Yoo, Yeong-Min
    • The Korean Journal of Physiology and Pharmacology
    • /
    • 제14권6호
    • /
    • pp.365-369
    • /
    • 2010
  • In this study, we examined whether melatonin promotes apoptotic cell death via p53 in prostate LNCaP cells. Melatonin treatment significantly curtailed the growth of LNCaP cells in a dose- and time-dependent manner. Melatonin treatment (0 to 3 mM) induced the fragmentation of poly(ADP-ribose) polymerase (PARP) and activation of caspase-3, caspase-8, and caspase-9. Moreover, melatonin markedly activated Bax expression and decreased Bcl-2 expression in dose increments. To investigate p53 and p21 expression, LNCaP cells were treated with 0 to 3 mM melatonin. Melatonin increased the expressions of p53, p21, and p27. Treatment with mitogen-activated protein kinase (MAPK) inhibitors, PD98059 (ERK inhibitor), SP600125 (JNK inhibitor) and SB202190 (p38 inhibitor), confirmed that the melatonin-induced apoptosis was p21-dependent, but ERK-independent. With the co-treatment of PD98059 and melatonin, the expression of p-p53, p21, and MDM2 did not decrease. These effects were opposite to the expression of p-p53, p21, and MDM2 observed with SP600125 and SB202190 treatments. Together, these results suggest that p53-dependent induction of JNK/p38 MAPK directly participates in apoptosis induced by melatonin.