4.3 Article

Berberine inhibits the expression of TNFα, MCP-1, and IL-6 in AcLDL-stimulated macrophages through PPARγ pathway

Journal

ENDOCRINE
Volume 33, Issue 3, Pages 331-337

Publisher

SPRINGER
DOI: 10.1007/s12020-008-9089-3

Keywords

Berberine; Macrophage; Acetylated low-density lipoprotein; Inflammation; Peroxisome proliferator-activated receptor gamma

Funding

  1. Key Project of National Science Foundation of China [30230380]
  2. National Nature Science Foundation of China [39900072, 30670999, 30711120573, 30870954]
  3. High Tech Program [2002BA711A05, 2001AA221201]
  4. National Key Basic Research and Development Program [2002CB713703]
  5. Shanghai Commission for Science and Technology [O1JC14026, 07ZR14071]

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Macrophages are the main source of cytokines in atherosclerotic plaques. Modified low-density lipoproteins may stimulate macrophages to produce large quantities of proinflammatory cytokines that promote athcrosclerosis. Berberine is the main component of the traditional Chinese medicine umbellatine, which has a widespread effect and was used to treat many diseases clinically. Our previous Study found that berberine could increase adipophilin expression in macrophages, which is a target gene of PPAR gamma, PPAR gamma agonist could decrease proinflammatory cytokines in macrophage. In this study, we investigated the effects and the mechanism of action of berberine on the expression and secretion of TNF alpha, MCP-1, and IL-6 in vitro to identify new pharmacological actions of berberine. The results of RT-PCR and ELISA shows that berberine may inhibit the expression and secretion of the tumor necrosis factor alpha (TNF alpha), monocyte chemoattractant protein 1 (MCP-1), and interleukin-6 (IL-6) in macrophages stimulated by acetylated low-density lipoprotein (AcLDL), whereas the peroxisome proliferator-activated receptor gamma (PPAR gamma) inhibitor GW9662 could attenuate this effect of berberine. This study demonstrates that berberine may inhibit the expression and production of TNF-alpha, MCP-1, and IL-6 in AcLDL-stimulated macrophages. This effect might be partially mediated through PPAR gamma activity.

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