PMID- 23936448
OWN - NLM
STAT- MEDLINE
DCOM- 20140401
LR  - 20220410
IS  - 1932-6203 (Electronic)
IS  - 1932-6203 (Linking)
VI  - 8
IP  - 8
DP  - 2013
TI  - Curcumin protects microglia and primary rat cortical neurons against HIV-1 
      gp120-mediated inflammation and apoptosis.
PG  - e70565
LID - 10.1371/journal.pone.0070565 [doi]
LID - e70565
AB  - Curcumin is a molecule found in turmeric root that has anti-inflammatory, 
      antioxidant, and anti-tumor properties and has been widely used as both an herbal 
      drug and a food additive to treat or prevent neurodegenerative diseases. To 
      explore whether curcumin is able to ameliorate HIV-1-associated neurotoxicity, we 
      treated a murine microglial cell line (N9) and primary rat cortical neurons with 
      curcumin in the presence or absence of neurotoxic HIV-1 gp120 (V3 loop) protein. 
      We found that HIV-1 gp120 profoundly induced N9 cells to produce reactive oxygen 
      species (ROS), tumor necrosis factor-alpha (TNF-alpha) and monocyte chemoattractant 
      protein-1 (MCP-1). HIV-1 gp120 also induced apoptosis of primary rat cortical 
      neurons. Curcumin exerted a powerful inhibitory effect against HIV-1 
      gp120-induced neuronal damage, reducing the production of ROS, TNF-alpha and MCP-1 by 
      N9 cells and inhibiting apoptosis of primary rat cortical neurons. Curcumin may 
      exert its biological activities through inhibition of the delayed rectification 
      and transient outward potassium (K(+)) current, as curcumin effectively reduced 
      HIV-1 gp120-mediated elevation of the delayed rectification and transient outward 
      K(+) channel current in neurons. We conclude that HIV-1 gp120 increases ROS, 
      TNF-alpha and MCP-1 production in microglia, and induces cortical neuron apoptosis by 
      affecting the delayed rectification and transient outward K(+) channel current. 
      Curcumin reduces production of ROS and inflammatory mediators in 
      HIV-1-gp120-stimulated microglia, and protects cortical neurons against 
      HIV-1-mediated apoptosis, most likely through inhibition of HIV-1 gp120-induced 
      elevation of the delayed rectification and transient outward K(+) current.
FAU - Guo, Luyan
AU  - Guo L
AD  - Department of Gynaecology and Obstetrics, the First Affiliated Hospital of Sun 
      Yat-sen University, Guangzhou, Guangdong Province, China.
FAU - Xing, Yanyan
AU  - Xing Y
FAU - Pan, Rui
AU  - Pan R
FAU - Jiang, Mingliang
AU  - Jiang M
FAU - Gong, Zheng
AU  - Gong Z
FAU - Lin, Liqing
AU  - Lin L
FAU - Wang, Junbing
AU  - Wang J
FAU - Xiong, Guoyin
AU  - Xiong G
FAU - Dong, Jun
AU  - Dong J
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20130806
PL  - United States
TA  - PLoS One
JT  - PloS one
JID - 101285081
RN  - 0 (HIV Envelope Protein gp120)
RN  - 0 (Inflammation Mediators)
RN  - 0 (Potassium Channels, Voltage-Gated)
RN  - 0 (Reactive Oxygen Species)
RN  - 0 (gp120 protein, Human immunodeficiency virus 1)
RN  - IT942ZTH98 (Curcumin)
RN  - RWP5GA015D (Potassium)
SB  - IM
MH  - Animals
MH  - Apoptosis/*drug effects
MH  - Cell Line
MH  - Cell Survival/drug effects
MH  - Cerebral Cortex/*cytology
MH  - Curcumin/*pharmacology
MH  - Cytoprotection/*drug effects
MH  - HIV Envelope Protein gp120/*metabolism
MH  - Inflammation/metabolism/pathology/prevention & control
MH  - Inflammation Mediators/metabolism
MH  - Mice
MH  - Microglia/*cytology
MH  - Neurons/cytology/*drug effects/metabolism/virology
MH  - Potassium/metabolism
MH  - Potassium Channels, Voltage-Gated/metabolism
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Reactive Oxygen Species/metabolism
PMC - PMC3735595
COIS- Competing Interests: The authors have declared that no competing interests exist.
EDAT- 2013/08/13 06:00
MHDA- 2014/04/02 06:00
PMCR- 2013/08/06
CRDT- 2013/08/13 06:00
PHST- 2012/12/20 00:00 [received]
PHST- 2013/06/24 00:00 [accepted]
PHST- 2013/08/13 06:00 [entrez]
PHST- 2013/08/13 06:00 [pubmed]
PHST- 2014/04/02 06:00 [medline]
PHST- 2013/08/06 00:00 [pmc-release]
AID - PONE-D-13-00008 [pii]
AID - 10.1371/journal.pone.0070565 [doi]
PST - epublish
SO  - PLoS One. 2013 Aug 6;8(8):e70565. doi: 10.1371/journal.pone.0070565. Print 2013.