Curcumin Inhibits Monocyte Chemoattractant Protein-1 Expression in TNF-α induced Astrocytes Through AMPK Pathway.
Neurochem Res
; 43(4): 775-784, 2018 Apr.
Article
em En
| MEDLINE
| ID: mdl-29460119
ABSTRACT
Curcumin, a phenolic pigment, plays an inhibitory role in astrocytes activation, a key step for neuropathic pain (NP). The present study aimed to investigate the mechanism behind the therapeutic effect of Curcumin on NP in vitro. Specifically, we investigated the inhibitory effect of Curcumin on tumor necrosis factor-α (TNF-α)-induced astrocyte migration. We also studied the effects of Curcumin on monocyte chemoattractant protein-1(MCP-1) expression and activity, as well as super oxide dismutase-2 (SOD2) expression and activity in TNF-α-induced astrocytes. Additionally, we investigated whether the adenosine-monophosphate-activated protein kinase signaling (AMPK) pathway was involved in this process. Our data demonstrated that Curcumin inhibited TNF-α-induced astrocytes migration, decreased MCP-1 expression, and up-regulated SOD2 expression in TNF-α-induced astrocytes in vitro. Our study also indicated that this process was mediated through the AMPK signaling pathway, as addition of Curcumin significantly increased the level of phosphorylated AMPK protein. Furthermore, the specific AMPK activator AICAR (5-aminoimidazole-4-carboxamide 1-D-ribofuranoside) mimicked the effects of Curcumin, whereas a selective AMPK inhibitor Compound C (also called dorsomorphin) partially blocked its function. These results could shed light on understanding of the molecular basis for the inhibition of Curcumin on MCP-1 expression during the process of astrocyte activation, and provide a molecular mechanism for using Curcumin in neuropathic pain.
Palavras-chave
Texto completo:
1
Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Astrócitos
/
Fator de Necrose Tumoral alfa
/
Quimiocina CCL2
/
Sistema de Sinalização das MAP Quinases
/
Curcumina
Limite:
Animals
Idioma:
En
Ano de publicação:
2018
Tipo de documento:
Article