PMID- 22427564
OWN - NLM
STAT- MEDLINE
DCOM- 20120706
LR  - 20131121
IS  - 1552-5783 (Electronic)
IS  - 0146-0404 (Linking)
VI  - 53
IP  - 4
DP  - 2012 Apr 30
TI  - Effect of berberine on proinflammatory cytokine production by ARPE-19 cells 
      following stimulation with tumor necrosis factor-alpha.
PG  - 2395-402
LID - 10.1167/iovs.11-8982 [doi]
AB  - PURPOSE: Berberine (BBR) is a well-known drug used in traditional medicine and 
      has been shown to possess anti-inflammatory properties. Whether it can affect the 
      production of inflammatory cytokines by RPE cells is not yet clear and was 
      therefore the subject of our study. METHODS: ARPE-19 cells were cultured with 
      TNF-alpha in the presence or absence of BBR to different time points. Concentrations 
      of IL-6, IL-8, and monocyte chemoattractant protein-1 (MCP-1) in the supernatant 
      were measured by using an ELISA. The mRNA expression of these cytokines was 
      measured by real-time PCR. Phosphorylation of p38 mitogen-activated protein 
      kinase (MAPK), extracellular signal-regulated kinase (ERK1/2), and c-Jun 
      N-terminal kinase (JNK) was measured by Western blot assay. The signal 
      transduction mechanisms involved in cytokine production were evaluated using 
      various inhibitors for p38, ERK1/2, and JNK. RESULTS: TNF-alpha significantly 
      increased the expression of IL-6, IL-8, and MCP-1 in ARPE-19 cells at both the 
      protein and mRNA levels. It promoted the phosphorylation of p38, ERK1/2, and JNK. 
      Inhibitory experiments showed that IL-6 was modulated by p38, whereas IL-8 and 
      MCP-1 were modulated by p38, ERK1/2, and JNK signal pathways. BBR inhibited the 
      expression of IL-6, IL-8, and MCP-1 remarkably at both protein and mRNA levels 
      and down-regulated the phosphorylation of p38, ERK1/2, and JNK upon stimulation 
      with TNF-alpha. CONCLUSIONS: The present results suggested that BBR significantly 
      inhibits the expression of inflammatory cytokines in ARPE-19 cells and that the 
      inhibitory effect is mediated by down-regulation of the p38, ERK1/2, and JNK 
      pathways.
FAU - Wang, Qian
AU  - Wang Q
AD  - the First Affiliated Hospital of Chongqing Medical University, Chongqing Key 
      Laboratory of Ophthalmology, Chongqing Eye Institute, Chongqing, People's 
      Republic of China; Second Affiliated Hospital of Chongqing Medical University, 
      Chongqing, People's Republic of China.
FAU - Qi, Jian
AU  - Qi J
FAU - Hu, Ranran
AU  - Hu R
FAU - Chen, Ying
AU  - Chen Y
FAU - Kijlstra, Aize
AU  - Kijlstra A
FAU - Yang, Peizeng
AU  - Yang P
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20120430
PL  - United States
TA  - Invest Ophthalmol Vis Sci
JT  - Investigative ophthalmology & visual science
JID - 7703701
RN  - 0 (Chemokine CCL2)
RN  - 0 (Interleukin-6)
RN  - 0 (Interleukin-8)
RN  - 0 (RNA, Messenger)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 0I8Y3P32UF (Berberine)
RN  - EC 2.7.11.24 (Extracellular Signal-Regulated MAP Kinases)
RN  - EC 2.7.11.24 (JNK Mitogen-Activated Protein Kinases)
RN  - EC 2.7.11.24 (p38 Mitogen-Activated Protein Kinases)
SB  - IM
MH  - Berberine/*pharmacology
MH  - Blotting, Western
MH  - Chemokine CCL2/*metabolism
MH  - Enzyme-Linked Immunosorbent Assay
MH  - Extracellular Signal-Regulated MAP Kinases/metabolism
MH  - Humans
MH  - Interleukin-6/*metabolism
MH  - Interleukin-8/*metabolism
MH  - JNK Mitogen-Activated Protein Kinases/metabolism
MH  - Phosphorylation
MH  - RNA, Messenger/metabolism
MH  - Real-Time Polymerase Chain Reaction
MH  - Retinal Pigment Epithelium/drug effects/*metabolism
MH  - Tumor Necrosis Factor-alpha/pharmacology
MH  - p38 Mitogen-Activated Protein Kinases/metabolism
EDAT- 2012/03/20 06:00
MHDA- 2012/07/07 06:00
CRDT- 2012/03/20 06:00
PHST- 2012/03/20 06:00 [entrez]
PHST- 2012/03/20 06:00 [pubmed]
PHST- 2012/07/07 06:00 [medline]
AID - iovs.11-8982 [pii]
AID - 10.1167/iovs.11-8982 [doi]
PST - epublish
SO  - Invest Ophthalmol Vis Sci. 2012 Apr 30;53(4):2395-402. doi: 10.1167/iovs.11-8982.