Cardiospermum halicacabum ethanol extract inhibits LPS induced COX-2, TNF-alpha and iNOS expression, which is mediated by NF-kappaB regulation, in RAW264.7 cells

J Ethnopharmacol. 2009 Jul 6;124(1):39-44. doi: 10.1016/j.jep.2009.04.020. Epub 2009 Apr 23.

Abstract

Aim of this study: Cardiospermum halicacabum L. is well known for its anti-inflammatory, analgesic and antipyretic activities. It has been used in Ayurveda and folk medicine for the treatment of rheumatism, fever and earache. But its mechanism of anti-inflammatory and analgesic action is still unclear, hence in this context, the objective of our study is to reveal the mechanism of anti-inflammatory and analgesic activity of Cardiospermum halicacabum L. which would form an additional proof to the traditional knowledge of Cardiospermum halicacabum L.

Materials and methods: In this study the ethanolic extract of the whole plant was used to evaluate the anti-inflammatory action in mouse macrophage cell line RAW264.7 cells. The expression levels of cyclooxygenase (COX)-1, COX-2, tumor necrosis factor-alpha (TNF-alpha), inducible nitric oxide synthase (iNOS) and COX-2 protein expression by semi-quantitative reverse transcriptase-polymerase chain reaction (RT-PCR) and western blot and nuclear factor kappa-B (NF-kappaB) binding activity by electrophoretic mobility shift assay (EMSA).

Results: We found that the ethanol extract dose dependently inhibit mRNA expression of COX-2, TNF-alpha, iNOS and COX-2 protein expression. But the extract did not affect the expression of COX-1 mRNA expression. Furthermore, Cardiospermum halicacabum L. ethanol extract inhibited the TNF-alpha induced DNA binding activity of NF-kappaB, which was associated with decreased p65 protein level in the nucleus in Jurkat cells.

Conclusion: These results enabled to understand the mechanisms behind the anti-inflammatory and analgesic activity of Cardiospermum halicacabum L.

Publication types

  • Evaluation Study
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Anti-Inflammatory Agents / pharmacology*
  • Carrier Proteins / metabolism
  • Cell Line
  • Cyclooxygenase 1 / biosynthesis
  • Cyclooxygenase 1 / genetics
  • Cyclooxygenase 2 / biosynthesis*
  • Cyclooxygenase 2 / genetics
  • Lipopolysaccharides
  • Macrophages / drug effects
  • Mice
  • NF-kappa B / metabolism*
  • Neoplasm Proteins / metabolism
  • Nitric Oxide Synthase Type II / biosynthesis*
  • Plant Extracts / pharmacology*
  • RNA, Messenger / biosynthesis
  • Sapindaceae*
  • Transcription Factor RelA
  • Tumor Necrosis Factor-alpha / biosynthesis*
  • Tumor Necrosis Factor-alpha / genetics

Substances

  • Anti-Inflammatory Agents
  • Carrier Proteins
  • Lipopolysaccharides
  • NF-kappa B
  • Neoplasm Proteins
  • Plant Extracts
  • RNA, Messenger
  • Rela protein, mouse
  • Transcription Factor RelA
  • Tumor Necrosis Factor-alpha
  • Nitric Oxide Synthase Type II
  • Cyclooxygenase 1
  • Cyclooxygenase 2