Curcumin, a potential inhibitor of up-regulation of TNF-alpha and IL-6 induced by palmitate in 3T3-L1 adipocytes through NF-kappaB and JNK pathway

Biomed Environ Sci. 2009 Feb;22(1):32-9. doi: 10.1016/S0895-3988(09)60019-2.

Abstract

Objective: To investigate the attenuating effect of curcumin, an anti-inflammatory compound derived from dietary spice turmeric (Curcuma longa) on the pro-inflammatory insulin-resistant state in 3T3-L1 adipocytes.

Methods: Glucose uptake rate was determined with the [3H] 2-deoxyglucose uptake method. Expressions of tumor necrosis factor-alpha (TNF-alpha) and interleukin-6 (IL-6) were measured by quantitative RT-PCR analysis and ELISA. Nuclear transcription factor kappaB p65 (NF-kappa p65) and mitogen-activated protein kinase (MAPKs) were detected by Western blot assay.

Results: The basal glucose uptake was not altered, and curcumin increased the insulin-stimulated glucose uptake in 3T3-L1 cells. Curcumin suppressed the transcription and secretion of TNF-alpha and IL-6 induced by palmitate in a concentration-dependent manner. Palmitate induced nuclear translocation of NF-kappaB. The activities of Jun NH2-terminal kinase (JNK), extracellular signal-regulated kinase1/2 (ERK1/2) and p38MAPK decreased in the presence of curcumin. Moreover, pretreatment with SP600125 (inhibitor of JNK) instead of PD98059 or SB203580 (inhibitor of ERK1/2 or p38MAPK, respectively) decreased the up-regulation of TNF-alpha induced by palmitate.

Conclusion: Curcumin reverses palmitate-induced insulin resistance state in 3T3-L1 adipocytes through the NF-kappaB and JNK pathway.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • 3T3-L1 Cells
  • Animals
  • Anthracenes / pharmacology
  • Anti-Inflammatory Agents, Non-Steroidal / pharmacology*
  • Curcumin / pharmacology*
  • Glucose / metabolism
  • Insulin / pharmacology
  • Insulin Resistance
  • Interleukin-6 / genetics
  • Interleukin-6 / metabolism*
  • JNK Mitogen-Activated Protein Kinases / metabolism
  • MAP Kinase Signaling System*
  • Mice
  • NF-kappa B / metabolism*
  • Palmitates / pharmacology*
  • Protein Kinase Inhibitors / pharmacology
  • Tumor Necrosis Factor-alpha / genetics
  • Tumor Necrosis Factor-alpha / metabolism*
  • Up-Regulation

Substances

  • Anthracenes
  • Anti-Inflammatory Agents, Non-Steroidal
  • Insulin
  • Interleukin-6
  • NF-kappa B
  • Palmitates
  • Protein Kinase Inhibitors
  • Tumor Necrosis Factor-alpha
  • pyrazolanthrone
  • JNK Mitogen-Activated Protein Kinases
  • Curcumin
  • Glucose