SIMPLE & 100% NATURAL COMPOSITION
ReJoint™ is comprised of 5 very carefully sourced, extracted,
and balanced herbs-hence its unusually remarkable effectiveness.
PATHWAYS OF INFLAMMATION
- •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 possesses weak diuretic properties, and therefore reduces the swelling of inflamed tissues, thereby reducing pressure on adjacent nerves
- •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)
- •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
- •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.