Dr. Weeks’ Comment: Cancer is driven by inflammation. Therefore step #1 is to assess inflammation (hs-CRP, ESR, Galectin-3, IL-6, IL-8, ferritin, NFKB) and step #2 is reduce inflammation (being well hydrated w fluoride free gel state water, aspirin, black cumin seed, curcumin and, of course, honeybee venom.
Therapeutic application of anti-arthritis, pain-releasing, and anti-cancer effects of bee venom and its constituent compounds
Dong Ju Son, … Jin Tae Hong, in Pharmacology & Therapeutics, 2007
https://doi.org/10.1016/j.pharmthera.2007.04.004Get rights and content
Bee venom (BV) therapy (BVT) is the therapeutic application of honeybee venom (HBV) to the treatment of various diseases. BVT has been used as a traditional medicine to treat a variety of conditions, such as arthritis, rheumatism, back pain, cancerous tumors, and skin diseases (Hider, 1988). BV contains at least 18 active components, including enzymes, peptides, and biogenic amines, which have a wide variety of pharmaceutical properties. BV might modify the immune system functions in the body and contribute to the increased production of cortisol (Vick et al., 1972). The healing potency of BV in the treatment of arthritis and rheumatism is initiated after stimulating the production of cortisol in the adrenal glands, which in turn has anti-inflammatory activity (Vick & Shipman, 1972). Recent studies have reported a variety of mechanisms for the anti-arthritis and/or anti-inflammatory effects of BV and its constituents. The decrease in cyclooxygenase (COX)-2 and phospholipase (PL) A2 expression and the decrease in the levels of tumor necrosis factor alpha (TNF-α), interleukin (IL)-1, IL-6, nitric oxide (NO) and oxygen reactive species (ROS) are suggested to be associated with the anti-arthritis effect of melittin (Murakami et al., 1997; Pelletier et al., 1998; Yang et al., 1999; Amin et al., 1999; Cernanec et al., 2002). Adolapin also has anti-inflammatory activity in carrageenan-, prostaglandin (PG)-, and adjuvant-induced rat hind paw edema and adjuvant polyarthritis. The effects of adolapin are presumably due to its ability to inhibit the PG synthesis system through COX inhibitory properties (Shkenderov & Koburova, 1982; Koburova et al., 1985). Apamin, a small conductance Ca2+-activated K+ channel blocker, significantly inhibited both ovalumine-induced tracheal contraction and histamine release from lung tissues, suggesting that this compound reduces allergic airway inflammation through a mast cell stabilizing effect (Ichinose et al., 1995). The mast-cell-degranulating (MCD) peptide has an anti-allergic activity by inhibiting the release of histamine from mast cells (Buku, 1999). The MCD peptide binds to the mast cell receptors in a dose–response manner and has been found to partially inhibit the binding of IgE to this receptor (Buku et al., 2001). Recently, it was found that melittin inhibited the DNA-binding activity of NF-κB, a critical transcriptional factor regulating inflammatory gene expression, by inhibiting IκB phosphorylation (Park et al., 2004, 2007). This result may be critical to understanding the anti-inflammatory and anti-arthritis mechanisms of BV and melittin, its major constituent.
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Effect of bee venom on IL-6, COX-2 and VEGF levels in polycystic ovarian syndrome induced in Wistar rats by estradiol valerate
Abstract
Background
Polycystic ovarian syndrome (PCOS) is a low-grade inflammatory disease characterized by hyperandrogenemia, hirsutism, chronic anovulation and vascular disorder. Interleukin-6 (IL-6), cyclooxygenase-2 (COX-2) and vascular endothelial growth factor (VEGF) are triggered by inflammatory stimuli and lead to angiogenesis and pathogenesis of the ovary. Honeybee venom (HBV) contains an array of biologically active components possessing various pharmaceutical properties. This study was designed to assess the possibility of HBV application as an anti-inflammatory therapeutic agent to suppress levels of the main inflammatory mediators IL-6, COX-2 and VEGF.
To induce PCOS, 1 mg of estradiol valerate (EV) per 100 g of body weight was subcutaneously (SC) injected into eight-week-old rats. After 60 days, 0.5 mg/kg of HBV was administered Intraperitoneal (IP) for 14 consecutive days, and the results of PCOS treatment were investigated. Rats were then anesthetized with CO2, and the ovaries were surgically removed. Serum IL-6 was detected by the ELISA kit. Immunoexpression of COX-2 and VEGF were examined in three groups: EV-induced PCOS, HBV-treated PCOS and control animals.
Results
Thickness of theca layer, number and diameter of cysts and levels of IL-6 significantly decreased in HBV group relative to PCOS group. The immunohistochemical analysis showed an increase in COX-2 and VEGF expression in PCOS group whereas HBV-treated rats presented weak and irregular immunostaining.
Conclusions
Our results suggest that the beneficial effect of HBV may be mediated through its inhibitory effect on serum IL-6 level and ovarian COX-2 and VEGF expression.