We call diabetes the “turkey disease” because it is insidious, it is stealthy and it lead to you being carved up, like a turkey. Inflammation drives diabetes as it does all chronic degenerative illnesses but bee venom has many healing peptides and some very powerful anti-inflammatory agents like mellitin… and as noted below, bee venom “significantly enhanced wound closure in diabetic mice by increasing collagen production and restoring the levels of inflammatory cytokines, free radical, TGF-β, and VEGF.” That is POWERFUL and HIGHLY beneficial stuff.
Here are 5 powerful peer reviewed scientific articles endorsing bee venom therapy for helping diabetic wounds heal.
Mol Immunol.2018 Nov;103:322-335. doi: 10.1016/j.molimm.2018.10.016. Epub 2018 Oct 23.
Impaired wound healing is a serious complication of diabetes that negatively affects the patient’s socioeconomic life. Multiple mechanisms contribute to impaired diabetic wound healing including deficient recruitment of wound macrophages/neutrophils and impaired neovascularization. Bee venom (BV) has been used as an anti-inflammatory agent for the treatment of several diseases. Nevertheless, the impacts of BV on the diabetic wound healing have been poorly studied. In the present study, we investigated the molecular mechanisms underlying BV treatment on diabetic wound healing in a type I diabetic mouse model. Three experimental groups were used: group 1, non-diabetic control mice; group 2, vehicle-diabetic mice; and group 3, BV-treated diabetic mice. We found that the diabetic mice exhibited impaired wound closure characterized by a significant decrease in collagen and β-defensin-2 (BD-2) expression compared to control non-diabetic mice. The impairment of diabetic wound healing is attributed to increased ROS levels and abolished antioxidant enzymes activity in the wounded tissues. Additionally, wounded tissue in diabetic mice revealed aberrantly decreased levels of Ang-1 and Nrf2 (the agonist ligands of Tie-2) followed by a marked reduction in the phosphorylation of Tie2 and downstream signaling eNOS, AKT and ERK. Impaired diabetic wound healing was also characterized by a significant reduction in activities of total antioxidant enzymes followed by a marked reduction in the levels of CCL2, CCL3 and CXCL2; which led to impaired recruitment and functions of wound macrophages/neutrophils; and significant reduction in the expression of CD31, a marker for neovascularization and angiogenesis of the injured tissue. Interestingly, BV treatment significantly enhanced wound closure in diabetic mice by increasing collagen and BD-2 expression and restoring the levels of Ang-1 and Nrf2 and hence enhancing the Tie-2 downstream signaling. Most importantly, treatment of diabetic mice with BV significantly restored the activities of wounded tissue antioxidant enzymes and the levels of chemokines, and subsequently rescued wound macrophages from mitochondrial membrane potential-induced apoptosis. Our findings reveal the immune-enhancing effects of BV for improving healing process of diabetic wounds and provide the first insight concerning the underlying molecular mechanisms.
BMC Immunol.2017 Jun 21;18(Suppl 1):23. doi: 10.1186/s12865-017-0207-y.
There is now good evidence that cytokines and growth factors are key factors in tissue repair and often exert anti-infective activities. However, engineering such factors for global use, even in the most remote places, is not realistic. Instead, we propose to examine how such factors work and to evaluate the reparative tools generously provided by ‘nature.’ We used two approaches to address these objectives. The first approach was to reappraise the internal capacity of the factors contributing the most to healing in the body, i.e., blood platelets. The second was to revisit natural agents such as whey proteins, (honey) bee venom and propolis. The platelet approach elucidates the inflammation spectrum from physiology to pathology, whereas milk and honey derivatives accelerate diabetic wound healing. Thus, this review aims at offering a fresh view of how wound healing can be addressed by natural means.
J Cell Physiol.2016 Oct;231(10):2159-71. doi: 10.1002/jcp.25328. Epub 2016 Feb 15.
Bee Venom Accelerates Wound Healing in Diabetic Mice by Suppressing Activating Transcription Factor-3 (ATF-3) and Inducible Nitric Oxide Synthase (iNOS)-Mediated Oxidative Stress and Recruiting Bone Marrow-Derived Endothelial Progenitor Cells.
Multiple mechanisms contribute to impaired diabetic wound healing including impaired neovascularization and deficient endothelial progenitor cell (EPC) recruitment. Bee venom (BV) has been used as an anti-inflammatory agent for the treatment of several diseases. Nevertheless, the effect of BV on the healing of diabetic wounds has not been studied. Therefore, in this study, we investigated the impact of BV on diabetic wound closure in a type I diabetic mouse model. Three experimental groups were used: group 1, non-diabetic control mice; group 2, diabetic mice; and group 3, diabetic mice treated with BV. We found that the diabetic mice exhibited delayed wound closure characterized by a significant decrease in collagen production and prolonged elevation of inflammatory cytokines levels in wounded tissue compared to control non-diabetic mice. Additionally, wounded tissue in diabetic mice revealed aberrantly up-regulated expression of ATF-3 and iNOS followed by a marked elevation in free radical levels. Impaired diabetic wound healing was also characterized by a significant elevation in caspase-3, -8, and -9 activity and a marked reduction in the expression of TGF-β and VEGF, which led to decreased neovascularization and angiogenesis of the injured tissue by impairing EPC mobilization. Interestingly, BV treatment significantly enhanced wound closure in diabetic mice by increasing collagen production and restoring the levels of inflammatory cytokines, free radical, TGF-β, and VEGF. Most importantly, BV-treated diabetic mice exhibited mobilized long-lived EPCs by inhibiting caspase activity in the wounded tissue. Our findings reveal the molecular mechanisms underlying improved diabetic wound healing and closure following BV treatment. J. Cell. Physiol. 231: 2159-2171, 2016.
Arch Pharm Res.2014 Aug;37(8):1016-31. doi: 10.1007/s12272-013-0308-y. Epub 2013 Nov 30.
Diabetes is one of the leading causes of impaired wound healing. The objective of this study was to develop a bee venom-loaded wound dressing with an enhanced healing and anti-inflammatory effects to be examined in diabetic rats. Different preparations of polyvinyl alcohol (PVA), chitosan (Chit) hydrogel matrix-based wound dressing containing bee venom (BV) were developed using freeze-thawing method. The mechanical properties such as gel fraction, swelling ratio, tensile strength, percentage of elongation and surface pH were determined. The pharmacological activities including wound healing and anti-inflammatory effects in addition to primary skin irritation and microbial penetration tests were evaluated. Moreover, hydroxyproline, glutathione and IL-6 levels were measured in the wound tissues of diabetic rats. The bee venom-loaded wound dressing composed of 10 % PVA, 0.6 % Chit and 4 % BV was more swellable, flexible and elastic than other formulations. Pharmacologically, the bee venom-loaded wound dressing that has the same previous composition showed accelerated healing of wounds made in diabetic rats compared to the control. Moreover, this bee venom-loaded wound dressing exhibited anti-inflammatory effect that is comparable to that of diclofenac gel, the standard anti-inflammatory drug. Simultaneously, wound tissues covered with this preparation displayed higher hydroxyproline and glutathione levels and lower IL-6 levels compared to control. Thus, the bee venom-loaded hydrogel composed of 10 % PVA, 0.6 % Chit and 4 % BV is a promising wound dressing with excellent forming and enhanced wound healing as well as anti-inflammatory activities.
J Korean Med Sci.1999 Dec;14(6):648-52.
To investigate whether BCG, lymphtoxin (LT) or bee venom (BV) can prevent insulitis and development of diabetes in non-obese diabetic (NOD) mice, we measured the degree of insulitis and incidence of diabetes in 24 ICR and 96 female NOD mice. NOD mice were randomly assigned to control, BCG-, LT-, and BV-treated groups. The BCG was given once at 6 weeks of age, and LT was given in 3 weekly doses from the age of 4 to 10 weeks. The BV was injected in 2 weekly doses from the age of 4 to 10 weeks. Diabetes started in control group at 18 weeks of age, in BCG group at 24 weeks of age, and in LT- or BV-treated group at 23 weeks of age. Cumulative incidences of diabetes at 25 weeks of age in control, BCG-, LT-, and BV-treated NOD mice are 58, 17, 25, and 21%, respectively. Incidence and severity of insulitis were reduced by BCG, LT and BV treatment. In conclusion, these results suggest that BCG, LT or BV treatment in NOD mice at early age inhibit insulitis, onset and cumulative incidence of diabetes.