INHIBITION OF THE MYD88 PATHWAY BY CURCUMIN, THE ACTIVE CONSTITUENT OF TURMERIC(CURCUMA LONGA L.), CAUSES APOPTOSIS IN HEPATIC STELLATE CELLS(HSCS)

被引:0
|
作者
Shu J
Kuchta K
He Y
Deng Y
Lin Y
Ye G
Lv X
Liu X
Kobayashi Y
机构
[1] Department of Gastroenterology, Guangzhou Red Cross Hospital, Jinan University
[2] National Institute of Health Sciences, Division of Pharmacognosy
[3] Medical Corporation Soujikai
[4] Faculty of Medicine, Shimane University
关键词
siRNA;
D O I
暂无
中图分类号
R285 [中药药理学];
学科分类号
1008 ;
摘要
HSCs were divided into four groups,namely control group(A),MyD88 siRNA group(B),curcumin group(C),and curcumin+MyD88 siRNA group(D).Groups B and D were subjected to transient transfection with siRNA for 48h.Groups C and D were incubated with curcumin(25μmol/L)for 24h.MyD88 protein expression was observed by Western Blot,apoptosis was detected by flow cytometry,
引用
收藏
页码:93 / 94
页数:2
相关论文
共 12 条
  • [1] Curcumin induces apoptosis in hepatic stellate cells via inhibition of the MyD88 pathway
    Shu, J. C.
    Kuchta, K.
    He, Y. J.
    Deng, Y. M.
    Lin, Y.
    Ye, G. R.
    Lv, X.
    Liu, X. Y.
    Kobayashi, Y.
    PLANTA MEDICA, 2015, 81 (16) : 1511 - 1511
  • [2] Curcumin, the main active constituent of turmeric (Curcuma longa L.), induces apoptosis in hepatic stellate cells by modulating the abundance of apoptosis-related growth factors
    He, Ya-Jun
    Kuchta, Kenny
    Lv, Xia
    Lin, Yu
    Ye, Guo-Rong
    Liu, Xu-You
    Song, Hui-Dong
    Wang, Le-Xin
    Kobayashi, Yuta
    Shu, Jian-Chang
    ZEITSCHRIFT FUR NATURFORSCHUNG SECTION C-A JOURNAL OF BIOSCIENCES, 2015, 70 (11-12): : 281 - 285
  • [3] Curcumin Promotes Apoptosis of Activated Hepatic Stellate Cells by Inhibiting Protein Expression of the MyD88 Pathway
    He, Ya-Jun
    Kuchta, Kenny
    Deng, Yan-Mei
    Cameron, Silke
    Lin, Yu
    Liu, Xu-You
    Ye, Guo-Ron
    Lv, Xia
    Kobayashi, Yuta
    Shu, Jian-Chang
    PLANTA MEDICA, 2017, 83 (18) : 1392 - 1396
  • [4] Molecular Engineering of Curcumin, an Active Constituent of Curcuma longa L. (Turmeric) of the Family Zingiberaceae with Improved Antiproliferative Activity
    Ali, Amena
    Ali, Abuzer
    Tahir, Abu
    Bakht, Md. Afroz
    Salahuddin
    Ahsan, Mohamed Jawed
    PLANTS-BASEL, 2021, 10 (08):
  • [5] MyD88 in hepatic stellate cells promotes the development of alcoholic fatty liver via the AKT pathway
    Li, Yukun
    Wei, Miaomiao
    Yuan, Qi
    Liu, Yu
    Tian, Tian
    Hou, Lingling
    Zhang, Jinhua
    JOURNAL OF MOLECULAR MEDICINE-JMM, 2022, 100 (07): : 1071 - 1085
  • [6] MyD88 in hepatic stellate cells promotes the development of alcoholic fatty liver via the AKT pathway
    Yukun Li
    Miaomiao Wei
    Qi Yuan
    Yu Liu
    Tian Tian
    Lingling Hou
    Jinhua Zhang
    Journal of Molecular Medicine, 2022, 100 : 1071 - 1085
  • [7] Regulation of Nur77-TLR4/MyD88 signaling pathway is required for Ginsenoside Rc ameliorates hepatic fibrosis regression by deactivating hepatic stellate cells
    Qin, Bo-Feng
    Gao, Shan
    Feng, Qi-yuan
    Chen, Wei
    Sun, Hai-Ming
    Song, Jian
    ACTA HISTOCHEMICA, 2023, 125 (07)
  • [8] Disruption of MYD88 Pathway Signaling Leads to Loss of Constitutive IRAK1, NF-κβ and JAK/STAT Signaling and Induces Apoptosis of Cells Expressing the MYD88 L265P Mutation in Waldenstrom's Macroglobalinemia
    Yang, Guang
    Zhou, Yangsheng
    Liu, Xia
    Cao, Yang
    Hunter, Zachary
    Treon, Steven P.
    BLOOD, 2011, 118 (21) : 274 - 275
  • [9] NaAsO2 regulates TLR4/MyD88/NF-κB signaling pathway through DNMT1/SOCS1 to cause apoptosis and inflammation in hepatic BRL-3A cells
    Sheng Li
    Jingyi Zhang
    Mingxiao Ma
    Mengyao Zhang
    Linzhi Li
    Weixin Chen
    Shugang Li
    Biological Trace Element Research, 2024, 202 : 258 - 267
  • [10] NaAsO2 regulates TLR4/MyD88/NF-κB signaling pathway through DNMT1/SOCS1 to cause apoptosis and inflammation in hepatic BRL-3A cells
    Li, Sheng
    Zhang, Jingyi
    Ma, Mingxiao
    Zhang, Mengyao
    Li, Linzhi
    Chen, Weixin
    Li, Shugang
    BIOLOGICAL TRACE ELEMENT RESEARCH, 2024, 202 (01) : 258 - 267