Cellular and molecular mechanisms of anti-inflammatory effect of Aflapin: a novel Boswellia serrata extract

Mol Cell Biochem. 2011 Aug;354(1-2):189-97. doi: 10.1007/s11010-011-0818-1. Epub 2011 Apr 11.


There is significant number of evidences suggesting the anti-inflammatory properties of gum resin extracts of Boswellia serrata containing 3-O-acetyl-11-keto-β-boswellic acid (AKBA) and their promising potential as therapeutic interventions against inflammatory diseases such as osteoarthritis (OA). Unfortunately, the poor bioavailability of AKBA following oral administration might limit the anti-inflammatory efficacy of standardized Boswellia extract(s). To address this issue, we describe a novel composition called Aflapin, which contains B. serrata extract enriched in AKBA and non-volatile oil portion of B. serrata gum resin. Our observations show that the availability of AKBA in systemic circulation of experimental animals is increased by 51.78% in Aflapin-supplemented animals, in comparison with that of 30% AKBA standardized extract or BE-30 (5-Loxin(®)). Consistently, Aflapin confers better anti-inflammatory efficacy in Freund's Complete Adjuvant (FCA)-induced inflammation model of Sprague-Dawley rats. Interestingly, in comparison with BE-30, Aflapin(®) also provides significantly better protection from IL-1β-induced death of human primary chondrocytes and improves glycosaminoglycans production in human chondrocytes. In Tumor necrosis factor alpha (TNFα)-induced human synovial cells, the inhibitory potential of Aflapin (IC(50) 44.736 ng/ml) on matrix metalloproteinase-3 (MMP-3) production is 14.83% better than that of BE-30 (IC(50) 52.528 ng/ml). In summary, our observations collectively suggest that both the Boswellia products, BE-30 (5-Loxin(®)) and Aflapin, exhibit powerful anti-inflammatory efficacy and anti-arthritic potential. In particular, in comparison with BE-30, Aflapin provides more potential benefits in recovering articular cartilage damage or protection from proteolytic degradation due to inflammatory insult in arthritis such as osteoarthritis or rheumatoid arthritis.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Anti-Inflammatory Agents, Non-Steroidal / pharmacokinetics
  • Anti-Inflammatory Agents, Non-Steroidal / pharmacology*
  • Anti-Inflammatory Agents, Non-Steroidal / therapeutic use
  • Arachidonate 5-Lipoxygenase / metabolism
  • Biological Availability
  • Boswellia*
  • Cell Culture Techniques
  • Cell Death
  • Cell Line, Tumor
  • Cell Proliferation
  • Cells, Cultured
  • Female
  • Foot / pathology
  • Freund's Adjuvant
  • Glycosaminoglycans / metabolism
  • Hindlimb / pathology
  • Humans
  • Inflammation / chemically induced
  • Inflammation / drug therapy
  • Interleukin-1beta
  • Lipoxygenase Inhibitors / pharmacokinetics
  • Lipoxygenase Inhibitors / pharmacology*
  • Lipoxygenase Inhibitors / therapeutic use
  • Male
  • Matrix Metalloproteinase 3 / metabolism
  • Osteoarthritis / drug therapy*
  • Phytotherapy*
  • Plant Extracts / pharmacokinetics
  • Plant Extracts / pharmacology*
  • Plant Extracts / therapeutic use
  • Rats
  • Rats, Sprague-Dawley
  • Rats, Wistar
  • Triterpenes / pharmacokinetics
  • Triterpenes / pharmacology*
  • Triterpenes / therapeutic use
  • Tumor Necrosis Factor-alpha / metabolism


  • Aflapin
  • Anti-Inflammatory Agents, Non-Steroidal
  • Glycosaminoglycans
  • Interleukin-1beta
  • Lipoxygenase Inhibitors
  • Plant Extracts
  • Triterpenes
  • Tumor Necrosis Factor-alpha
  • acetyl-11-ketoboswellic acid
  • Freund's Adjuvant
  • Arachidonate 5-Lipoxygenase
  • MMP3 protein, human
  • Matrix Metalloproteinase 3