Stem bromelain

Stem bromelain is ultimately a mixture of a number of thiol endopeptidases and other elements including phosphatases, glucosidase, peroxidases, cellulases, glycoproteins, carbohydrates, and various protease inhibitors. The many different substrates and reactions that these varied enzymes can catalyze results in a number of different and possible mechanisms of action.

Stem bromelain is currently principally used as a topical agent for debridement of necrotic tissue from wounds or second to third-degree burns. As bromelain can contain escharase as one of its component enzymes, it is thought that various stem bromelain creams or gels can accelerate the healing process of wounds by facilitating the rapid removal of necrotic layers of dermis while preserving unburned/unharmed tissues and/or perhaps by accelerating the recovery of blood perfusion in wound tissue, control the expression of TNF-alpha, and raise the expression of TGT-beta, as demonstrated in the pig animal model. This kind of enzymatic debridement is ultimately preferred to surgical debridement as physical, surgical procedures are naturally painful, non-selective, and involve the possibility of repeat or excessive anesthesia and/or bleeding.

With regards to cardiovascular health, certain studies suggest that stem bromelain is capable of breaking down cholesterol plaques, eliciting a strong fibrinolytic activity, and inhibiting blood platelet aggregation - all of which protect against ischemia/reperfusion injury in skeletal muscle and minimize the risk of arterial thrombosis and embolism. Additionally, stem bromelain has also been shown to attenuate allergic airway disease by altering CD4+ and CD8+ T lymphocyte populations - an action that may be beneficial in treating human asthma or hypersensitivity disorders. Finally, stem bromelain has also been used to induce cardioprotection against ischemia-reperfusion injury via the Akt/Foxo pathway in rat model myocardium.

In the treatment of osteoarthritis, it is believed that stem bromelain has analgesic properties which are thought to be the result of direct influence on pain mediators such as bradykinin. In addition, various trials suggest that the medication could be useful in reducing swelling, bruising, and pain in women having surgery like episiotomy. Moreover, stem bromelain may also be used for treating acute inflammation and sports injuries.

Furthermore, stem bromelain has also been studied as an adjuvant therapy for chronic inflammatory, malignant, and autoimmune diseases. Certain in vitro experiments have demonstrated that stem bromelain can modulate surface adhesion molecules on T cells, macrophages, and natural killer cells and also cause the secretion of IL-1B, IL-6, and Tumor Necrosis Factor-alpha (TNF-alpha) via peripheral blood mononuclear cells. The agent has also been able to block the Raf-1/extracellular-regulated-kinase-2 (ERK-2) pathways by preventing T cell signal transduction. In particular however, treating cells with stem bromelain decreases the activation of CD4(+) T cells and reduces the expression of CD25. Additionally, there is also evidence to suggest that oral therapy with stem bromelain produces certain analgesic and anti-inflammatory effects in patients with rheumatoid arthritis, which is a particularly common autoimmune disease.

Stem bromelain also affects blood coagulation by increasing the serum fibrinolytic ability and by preventing the synthesis of fibrin, a protein involved in blood clotting. In the rat animal model, the reduction of serum fibrinogen level seems to be dose-dependent when both prothrombin time and activated partial thromboplastin time become markedly prolonged at higher concentrations of administered stem bromelain. In vitro and in vivo studies also suggest stem bromelain can act as an effective fibrinolytic agent since it stimulates the conversion of plasminogen to plasmin, causing an increased fibrinolysis by degrading fibrin.

In terms of potential antimicrobial effects of stem bromelain, there are varying observations regarding its specific mechanism of action. When counteracting the effects of some intestinal pathogens like Vibrio cholera or Escherichia coli (whose enterotoxin causes diarrhea in animals), some studies suggest that stem bromelain interacts with intestinal secretory signaling pathways like adenosine 3':5'-cyclic monophosphatase, guanosine 3':5'-cyclic monophosphatase, and/or calcium-dependent signaling cascades. Conversely, other studies propose that stem bromelain supplementation can lead to antiadhesion effects which prevent E. coli bacteria from attaching to particular glycoprotein receptors on the intestinal mucosa by proteolytically modifying those receptor attachment sites.

Additionally, various studies have shown that stem bromelain also possesses anticancer activity. In particular, the agent has been found to increase the expression of p53 and Bax in mouse skin, both of which are well-known apoptosis activators. Stem bromelain can also evidently decrease the activity of cell survival regulators like Akt and Erk, therefore inducing apoptotic tumor cell death. Finally, stem bromelain has also been observed to downregulate NF-kB and Cox-2 expression in mouse papillomas and in models of skin tumorigenesis. It has also demonstrated the capability to inhibit bacterial endotoxin (LPS)-induced NF-kB activity as well as the expression of PGE2 and Cox-2 in human monocytic leukemia and murine microglial cell lines.