PMID- 24356300
OWN - NLM
STAT- MEDLINE
DCOM- 20140829
LR  - 20190212
IS  - 1421-9778 (Electronic)
IS  - 1015-8987 (Linking)
VI  - 32
IP  - 6
DP  - 2013
TI  - AOPPs induce MCP-1 expression by increasing ROS-mediated activation of the NF-kappaB 
      pathway in rat mesangial cells: inhibition by sesquiterpene lactones.
PG  - 1867-77
LID - 10.1159/000356619 [doi]
AB  - BACKGROUND: Monocyte chemoattractant protein-1 (MCP-1) plays an important role in 
      extracellular matrix accumulation through macrophage recruitment and activation 
      in the development and progression of diabetic nephropathy. Therefore, this study 
      examined whether advanced oxidation protein products (AOPPs) are involved in 
      nuclear factor-kappaB (NF-kappaB) activation and MCP-1 mRNA and protein expression in 
      mesangial cells (MCs) and evaluated the effects of derivatives of sesquiterpene 
      lactones (SLs) on AOPP-induced renal damage. METHODS: MCP-1 mRNA and protein 
      expression in MCs were determined by quantitative real-time PCR and ELISA, 
      respectively. The level of intracellular reactive oxygen species (ROS) was 
      determined by flow cytometry. The protein expression of tubulin, P47, NF-kappaB p65, 
      phospho-NF-kappaB p65, IkappaB, phospho-IkappaB, IKKbeta and phospho-IKKbeta was evaluated by 
      Western blot. RESULTS: AOPPs caused oxidative stress in MCs and activated the 
      NF-kappaB pathway by inducing IkappaBalpha phosphorylation and degradation. Inhibition of ROS 
      by SOD (ROS inhibitor) blocked the AOPP-mediated NF-kappaB pathway. Moreover, the 
      inhibition of AOPP-induced overproduction of MCP-1 mRNA and protein was 
      associated with inhibition of IkappaBalpha degradation by SLs. CONCLUSION: AOPPs induce 
      MCP-1 expression by activating the ROS/NF-kappaB pathway and can be inhibited by SLs. 
      These findings may provide a novel approach to treat inflammatory and immune 
      renal diseases, including diabetic nephropathy.
CI  - (c) 2014 S. Karger AG, Basel.
FAU - Wang, Jian-Cheng
AU  - Wang JC
AD  - Division of Nephrology, Zhujiang Hospital, Southern Medical University, 
      Guangzhou, Guangdong, P.R. China.
FAU - Zhao, Yan
AU  - Zhao Y
FAU - Chen, Si-Jia
AU  - Chen SJ
FAU - Long, Jing
AU  - Long J
FAU - Jia, Qian-Qian
AU  - Jia QQ
FAU - Zhai, Jia-Dai
AU  - Zhai JD
FAU - Zhang, Quan
AU  - Zhang Q
FAU - Chen, Yue
AU  - Chen Y
FAU - Long, Hai-Bo
AU  - Long HB
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20131220
PL  - Germany
TA  - Cell Physiol Biochem
JT  - Cellular physiology and biochemistry : international journal of experimental 
      cellular physiology, biochemistry, and pharmacology
JID - 9113221
RN  - 0 (Advanced Oxidation Protein Products)
RN  - 0 (Chemokine CCL2)
RN  - 0 (Lactones)
RN  - 0 (NF-kappa B)
RN  - 0 (RNA, Messenger)
RN  - 0 (Reactive Oxygen Species)
RN  - 0 (Sesquiterpenes)
RN  - EC 1.6.3.- (NADPH Oxidases)
RN  - EC 2.7.11.10 (I-kappa B Kinase)
SB  - IM
MH  - Advanced Oxidation Protein Products/*pharmacology
MH  - Animals
MH  - Cells, Cultured
MH  - Chemokine CCL2/genetics/*metabolism
MH  - I-kappa B Kinase/metabolism
MH  - Lactones/chemistry/*pharmacology
MH  - Mesangial Cells/cytology/*drug effects/metabolism
MH  - NADPH Oxidases/metabolism
MH  - NF-kappa B/genetics/*metabolism
MH  - Phosphorylation/drug effects
MH  - RNA, Messenger/metabolism
MH  - Rats
MH  - Reactive Oxygen Species/*metabolism
MH  - Sesquiterpenes/chemistry
MH  - Signal Transduction/drug effects
EDAT- 2013/12/21 06:00
MHDA- 2014/08/30 06:00
CRDT- 2013/12/21 06:00
PHST- 2013/11/26 00:00 [accepted]
PHST- 2013/12/21 06:00 [entrez]
PHST- 2013/12/21 06:00 [pubmed]
PHST- 2014/08/30 06:00 [medline]
AID - 000356619 [pii]
AID - 10.1159/000356619 [doi]
PST - ppublish
SO  - Cell Physiol Biochem. 2013;32(6):1867-77. doi: 10.1159/000356619. Epub 2013 Dec 
      20.