Pathways of Inflammation


Mechanisms of Anti-inflammatory Action*

Boswellia Serrata

  • Inhibits TNF-alpha-induced inflammatory response
  • Inhibit enzymes (MMP) which catalyze connective tissue breakdown
  • Acetyl-11-keto-beta-boswellic acid (AKBA) inhibits NF-kappaB which activates many genes involved in inflammatory responses.
  • Inhibits the formation and release of certain inflammatory leukotrienes.
  • Inhibits conversion of arachidonic acid to inflammatory leukotrienes.
  • Reduces complement activity, known to trigger inflammatory mediators.
  • Prevents the breakdown of connective tissue in inflammatory arthritic conditions by reducing glycosaminoglycan (GAG) degradation
  • Reduces enzymes that are elevated in inflammatory conditions like arthritis (such as glutamic pyruvic transaminase, glycohydrolase, and beta-glucuronidase)

Horsetail

  • Horsetail possesses weak diuretic properties, and therefore reduces the swelling of inflamed tissues, thereby reducing pressure on adjacent nerves

Stinging Nettle

  • Potently suppresses human leukocyte elastase (HLE), one of the most destructive enzymes released by certain white blood cells during the inflammatory process
  • Inhibits TNF-alpha, NF-Kappa B, Leukotiene and Prostaglandin synthesis
  • Lowers levels of interleukin-6 and high-sensitivity C-reactive protein (hs-CRP)

Celery

  • Inhibits mRNA expression of COX-2 in inflammatory responses
  • Suppresses inflammatory mediator release by blocking nuclear factor (NF)-kappaB activation pathways
  • Reduces LPS-induced interleukin (IL)-6 production in the brain
  • Celery possesses weak diuretic properties, and reduces iNOS, an inflammatory mediator

Garlic

  • Enhances phagocytosis, white blood cell production, natural killer cell activity and prevents immune suppression

*Above based on Natural Standard database, and a review by Clarke and Mullin, which   investigated the immunomodulatory effects of various alternative and complementary therapies, including Boswellia, and the variety of mechanisms by which they disrupt the pro-inflammatory cascade.