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| Bromelain is a mixture of enzymes found in pineapples, particularly in the stem and fruit.
key points regarding bromelain and cancer: -Anti-Inflammatory Properties: -Immune System Support: -Direct Anticancer Effects: -Synergistic Effects with Chemotherapy: Biological activity, bromelain has been reported to exhibit a range of effects, including: Anti-inflammatory activity: 10-50 μM Antioxidant activity: 10-100 μM Anti-cancer activity: 50-100 μM Cardiovascular health: 20-50 μM Digestive health: 10-50 μM Cooking can affect the concentration of bromelain in pineapple. Heat can denature the enzymes, making them less active. The extent of the loss of activity depends on the temperature, cooking time, and method of cooking. For example: -Boiling or steaming pineapple for 10-15 minutes can reduce the bromelain activity by 50-70% -Baking or roasting pineapple at 350°F (30-40min) reduce the bromelain activity by 70-90% Bromelain — bromelain is a proteolytic enzyme complex derived mainly from pineapple stem, with lesser related fractions from fruit. It is best classified as a botanical protease mixture / natural product nutraceutical rather than a single defined small molecule. Standard abbreviations include bromelain and BML. Its functional identity is a cysteine-protease-rich mixture with anti-inflammatory, immunomodulatory, mucolytic, and context-dependent anticancer activity. In oncology, the most defensible interpretation is that bromelain is an experimental adjunct with preclinical antitumor and anti-metastatic signals, but without established mainstream systemic anticancer approval or definitive phase III evidence. Primary mechanisms (ranked):
Bioavailability / PK relevance: Oral bromelain shows limited but real absorption of intact enzymatically active material; circulating enzyme is partly bound by antiproteases such as α2-macroglobulin and α1-antichymotrypsin. This supports systemic biological plausibility, but exposure is constrained, heterogeneous, and not well standardized across products. As a protease mixture, batch composition and formulation materially affect PK relevance. In-vitro vs systemic exposure relevance: Many anticancer in-vitro studies use bromelain concentrations that are difficult to map directly onto human systemic exposure because bromelain is a heterogeneous enzyme mixture rather than a single analyte. Therefore, direct translation of cell-culture dose levels to oral human dosing is weak. Mechanistic plausibility exists, but potency in vitro likely overstates predictable systemic anticancer exposure from standard oral supplements. Clinical evidence status: Preclinical evidence is substantial. Human oncology evidence is limited and mostly adjunctive or exploratory, including small supportive studies on immune modulation or treatment side effects, plus early-phase mucinous-tumor work with BromAc rather than bromelain alone. No established standard-of-care systemic anticancer indication is supported at present. Mechanistic relevance in cancer
P: 0–30 min R: 30 min–3 hr G: >3 hr |
| Source: HalifaxProj(inhibit) |
| Type: |
| Cyclooxygenase-2 (COX-2) is an enzyme that plays a critical role in the conversion of arachidonic acid to prostaglandins, which are lipid compounds involved in various physiological processes, including inflammation, pain, and fever. COX-2 is an inducible enzyme, meaning its expression is typically low in normal tissues but can be upregulated in response to inflammatory stimuli, growth factors, and certain oncogenic signals. -Cyclooxygenase-2 (COX-2), the rate-limiting enzyme in prostaglandin biosynthesis, plays a key role in inflammation and circulatory homeostasis. -COX-2 is an inducible enzyme that is upregulated in response to pro-inflammatory signals, including cytokines (e.g., IL-1β, TNF-α) and growth factors. COX-2 is often overexpressed in various tumors, including colorectal, breast, lung, and prostate cancers. The prostaglandins produced by COX-2, particularly prostaglandin E2 (PGE2), have several effects that can facilitate cancer progression: Cell Proliferation: PGE2 can promote the proliferation of cancer cells by activating signaling pathways such as the PI3K/Akt and MAPK pathways. Nonselective NSAIDs, such as aspirin and ibuprofen, inhibit both COX-1 and COX-2. Epidemiological studies have suggested that regular use of NSAIDs may reduce the risk of certain cancers, particularly colorectal cancer. Drugs specifically targeting COX-2, such as celecoxib, have been developed. COX-2 and xanthine oxidase are ROS-producing pro-oxidant enzymes that contribute to inflammation. Elevated COX‑2 levels, often found in inflammatory conditions or certain types of cancers, can contribute to increased production of ROS. |
| 5677- | BML, | Bromelain inhibits nuclear factor kappa-B translocation, driving human epidermoid carcinoma A431 and melanoma A375 cells through G(2)/M arrest to apoptosis |
| - | in-vitro, | Melanoma, | A431 | - | in-vitro, | Melanoma, | A375 |
| 5680- | BML, | Anticancer properties of bromelain: State-of-the-art and recent trends |
| - | Review, | Var, | NA |
| 5683- | BML, | Bromelain inhibits COX-2 expression by blocking the activation of MAPK regulated NF-kappa B against skin tumor-initiation triggering mitochondrial death pathway |
| - | in-vitro, | NA, | NA |
Query results interpretion may depend on "conditions" listed in the research papers. Such Conditions may include : -low or high Dose -format for product, such as nano of lipid formations -different cell line effects -synergies with other products -if effect was for normal or cancerous cells
Filter Conditions: Pro/AntiFlg:% IllCat:% CanType:% Cells:% prod#:216 Target#:66 State#:% Dir#:1
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