Health Benefits of Broccoli Extract

Health Benefits of Broccoli Extract

Broccolis, belonging to the cruciferous family of plants, have long been known to have extensive health benefits – due especially to sulfur containing compounds that can detoxify the body. These so called glucosinolates are known as chemoprotective agents since, among other functions, they reduce the presence of carcinogens in the body. Of immediate concern are cigarette smoke, alcohol, synthetic and naturally occurring carcinogens, radiation, drug, infectious agents and more. A less than ideal diet can provide numerous carcinogenic substances (grilled meat, etc) on a daily basis. Studies have shown that a diet including very high levels of yellow and green vegetables especially of the cruciferous family reduce the risk of developing various organ cancers. Since getting a daily supply of the crucial vegetables is not always possible, or if more than a minimal amount is desired, having a daily supplement of the active detoxifying broccoli substances is clearly very important.  Broccoli Plus is a true nutritional supplement that can significantly enhance the quality of your daily diet.

However, glucoraphanin, the most important of the glucosinolates, a precursor of the active enzyme, needs to be digested by the enzyme myrosinase to the active sulforaphane. Broccoli sprouts are added to the formula since they naturally contain the myrosinase enzyme. Thus the desired maximum benefits are obtained.

Glucoraphanin

Figure 1 Glucoraphanin (from Wikipedia)

Wikipedia Sulforaphane

Sulforaphane (from Wikipedia)

 

 

 

 

 

The main benefits of sulforaphanes of broccoli are:

  • Reduce, detoxify, carcinogens in the body thereby reducing the chance of getting cancer.
  • Liver detoxification (VIP: the active sulforaphanes are selective phase 2 detoxifying enzyme inducers without inducing the phase 1 enzyme induction – ex. cytochrome P450). Anti-carcinogens have been directly linked to their ability to induce, increase the activity of phase 2 enzymes.
  • Trigger an increase in the activity of Antioxidant enzymes that fight inflammation and thus promote a healthy inflammatory response
  • Promotes Glutathione- the most prevalent intra-cellular antioxidant
  • Allows DNA to protect/repair itself
  • Keeping the ulcer causing bacteria H. pylori at a beneficial level (it is absolutely needed to a certain extent but not to the point where it causes stomach ulcers)

Emotional benefits:

  • Just as Cruciferous plants contribute on a physiological level to remove unwanted toxins on a mental level they help to overcome a feeling of stagnation, the experience of not being able to resolve “road blocks”      

More on Sulforaphane – Mechanism of Action:

Sulforaphane induces the Nrf-2 pathway and triggers the release of antioxidants and detoxifiers called phase 2 enzymes. These enzymes maintain cellular redox balance (or cellular homeostasis) by inactivating and excreting potentially dangerous substances.14 Though some studies show an additional anti-inflammatory benefit of sulforaphane independent of the Nrf-2 pathway,15 the main mechanism responsible for dampening the inflammatory pathway occurs via the inhibition of nuclear factor kappa-light-chain-enhancer of activated B cells (NF-KB). 16 Inhibition of the NF-kB pathway by sulforaphane has been shown to impede prostaglandin E2 (PGE2) synthesis and down-regulate the subsequent cascade of inflammatory cytokines, including interleukin-1B (IL-1B) 17, interleukin-17 (IL-17), and tumor necrosis factor alpha (TNF-α). 16

Summary of In Vitro Studies

In 2005, Healy et al. found that phase 2 enzyme inducers negate the shear-mediated repression of antioxidant response element (ARE)-regulated enzyme activity and apoptosis in human chondrocytes.27 In 2012, Fragoulis et al. demonstrated that SF treatment decreased inflammation and the production of the inflammatory cytokines IL-17 and TNF-α in a dose-dependent manner in inflamed synovial joint cells (synoviocytes). They further found that sullforaphane induced Nrf2 in naïve synoviocytes, whereas it induced apoptosis in inflamed synoviocytes.28 In another study, researchers found that sulforaphane inhibited synovial hyperplasia, T cell proliferation, and the production of the inflammatory cytokines IL-17 and TNF-α by rheumatoid T cells.29 Davidson et al. found that sulforaphane blocked inflammation at the level of NF-κB in a bovine cartilage explant model, in a destabilization of medial meniscus murine model of osteoarthritis, as well as in whole animal models.16

Summary of In Vivo Studies

In 2012, sulforaphane treatment was shown to improve hind limb locomotion in rats after spinal cord injury, reduce the inflammatory cytokines IL-17, TNF- α, and IL-6, and improve the clinical severity of arthritis.30 In 2010, sulforaphane was shown to decrease the expression of two inflammatory mediators: TNF-α and metalloproteinase (MMP)-9 following spinal cord injury in mice.15 In 2011, researchers showed that sulforaphane activated Nrf2 in impaired spinal cord tissue and spinal cord injury resulting in reduced inflammatory damage, histologic injury, dying neurons count, and spinal cord edema.31 In 2013, Galuppo et al. found that glucoraphanin bioactivated with myrosinase significantly decreased histological damage of proinflammatory events, and was neuroprotective in a mouse model following spinal cord injury. 32 In mice with synovial hyperplasia, which characterizes rheumatoid arthritis, anti-CII antibody-induced arthritis in mice was also alleviated by sulforaphane injection.29

The goal of current therapeutic strategies both for rheumatoid arthritis and osteoarthritis is to block the NF-kB-triggered release of inflammatory prostaglandins (PGE2) and cytokines (Il-1B).13 Sulforaphane provides an alternative to NSAIDS for suppressing inflammation and avoids the risk of potential life-threatening side effects of chronic NSAID use such as gastrointestinal bleeding and renal disease .17

References:

  1. Shapiro TA, Fahey JW, Wade KK, et al. Human metabolism and excretion of cancer chemoprotective glucosinolates and isothiocyanates of crucerifous vegetables. Cancer Epidemiol Biomarkers Prev 1998;7:1091-1100.
  2. James D, Devaraj S, Bellur P, Lakkanna S, Vicini J, Boddupalli S. Novel concepts of broccoli sulforaphanes and disease: induction of phase II antioxidant and detoxification enzymes by enhanced-glucoraphanin broccoli. Nutr Rev 2012;70(11):654-665. doi: 10.1111/j.1753-4887.2012.00532.x. Epub 2012 Oct 12.
  3. Turpaey KT. Keap 1-Nrf2 signaling pathway: mechanisms of regulation and role in protection of cells against toxicity caused by xenobiotics and electrophiles. Biochemistry (Mosc) 2013;78(2):111-126. doi: 10.1134/S0006297913020016.
  4. Lugrin J, Rosenblatt-Velin N, Parapanov R, Liaudet L. The role of oxidative stress during inflammatory processes. Biol Chem 2013 Oct 12. pii: /j/bchm.just-accepted/hsz-2013-0241/hsz-2013-0241.xml. doi: 10.1515/hsz-2013-0241.
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  6. Vauzour D, Buonfiglio M, Corona G, et al. Sulforaphane protects cortical neurons against 5-S-cysteinyldopamine-induced toxicity through the activation of ERKl/2, Nrf-2 and the upregulation of detoxification enzymes. Mol Nutr Food Res 2010;54:532-542.
  7. Tarozzi A, Morroni F, Merlicco A, et al. Sulforphane as an inducer of glutathione prevents oxidative stress-induced cell death in dopaminergic-like neuroblastoma cell line. J Neuroehem 2009:111:1161-1171.
  8. Han JM, Lee YJ, Lee SY, et al. Protective effect of sulforaphane against dopaminergic cell death. J Pharmaeol Exp Ther 2007;321:249-256.
  9. Alfieri A et al. Sulforaphane preconditioning of the Nrf2/HO-1 defense pathway protects the cerebral vasculature against blood-brain barrier disruption and neurological deficits in stroke. Free Radic Biol Med 2013 Sep 7;65C:1012-1022. doi: 10.1016/j.freeradbiomed.2013.08.190.
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  15. Mao L, Wang HD, Wang XL, Qiao L, Yin HX. Sulforaphane attenuates matrix metalloproteinase-9-expression following spinal cord injury in mice. Ann Clin Lab Sci 2010;40(4):354-360.
  16. Davidson RK et al. Sulforaphane represses matrix-degrading proteases and protects cartilage from destruction in vitro and in vivo. Arthritis Rheum. 2013 Aug 27. doi: 10.1002/art.38133. [Epub ahead of print].
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  21. Bahadoran Z, Mirmiran P, Azizi F. Potential efficacy of broccoli sprouts as a unique supplement for management of type 2 diabetes and its complications. J Med 2013; 16(5): 375-382.
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  27. Healy ZR et al. Divergent responses of chondrocytes and endothelial cells to shear stress: cross-talk among COX-2, the phase 2 response, and apoptosis. PNAS 2005;102(39):14010-14015.
  28. Fragoulis A, et al.Sulforaphane has opposing effects on TNF-alpha stimulated and unstimulated synoviocytes. Arthritis Res Ther. 2012 Oct 27;14(5):R220.