Dr. Weeks’ Comment:  Apamin and mastcell degenerating peptide (MCD-peptide) have “anti-inflammatory dose/response relationships that correspond to dexamethasone”.

When your doctor says “there is not science supporting that claim, remind him or her to search (as you can!) Pub Med – the national library of science medical branch. A great use of tax dollars…. Shining forth the light of research!   Here are search results which are provocative!

As an example:  Apamin, the worlds most specific calcium dependent potassium blocker is the prime candidate explaining why BVT helps people with MS symptoms.

From BeeWell  The Journal of the American Apitherapy Society,  January 2003  Editor Weeks, B.

Apamin (2% of bee venom) is an 18 amino acid neurotoxin with a molecular weight of 2036 that has been shown to inhibit complement activity (C3) to the degree that produces anti-inflammation without significant compromise of the immunologic defense system. (This in adrenalectomized rats suggesting local response). Apamin also binds to protein of the potassium pump blocking membrane potassium transfer at neuromuscular junctions. This is probably the component operational in the treatment of multiple sclerosis. Apamin also has beta-adrenergic effects not entirely blocked by the drug Propranolol and anti-arrhythmic effects in hearts with intrinsic arrhythmias.

REFERENCES

Banks, B. Possible Therapeutic Use of a Peptide from Bee Venom. Bulletin de L’Institut Pasteur, 1976, 74, p137-44. An excellent summary of current work including: components of bee venom (melittin, melittin-F, apamin, peptide 401, secapin, tertiapin) and demonstrates that peptide 401 is 100 times more potent than hydrocortisone in the rat paw edema test. It is also a better inhibitor than aspirin of the conversion of arachidonic acid to PE2.

Billingham, M. An Anti-Inflammatory Peptide from Bee Venom. Nature. Vol 245, 9/21/73. British researchers produce a definitive paper describing the anti-inflammatory peptide.

“We have also tested the melittin in adjuvant arthritis in rats as it is thought that activity in this test correlated well with efficacy in treating human rheumatoid arthritis. The results are summarized in Fig. 3. The inflammation associated with both the primary and secondary lesions in the established disease was considerable reduced by the treatment of peptide 401 (melittin). The effects of starting the treatment at the same time as the adjuvant injection are much more dramatic, however, as the disease usually failed to develop.”

Chang, Y. Anti-Arthritic Effect of Bee Venom. Agents and Actions 1979 205-11; Bee Venom suppressed carrageen-induced paw edema and adjuvant arthritis in the rat in a dose related manner. Thesis: alteration of immune response and endogenous corticosteroid production. Excellent study showing BV greater efficacy than conventional medications (cyclophosphamide).

Chen, C. Mode of Inhibitory Action of Melittin on Na+-K+-ATPase Activityof the Rat Synaptic Membrane. Biochem Pharm vol 34, No13 p2335-41 1985. Melittin was the most powerful of three agents used (cardiotoxin from Formosa cobra venom and ouabain) as inhibitor of ATPases (Na and Mg).

Toxicon. 1976;14(6):441-7.

Anti-inflammatory effects of apamin.

Ovcharov R, Shkenderov S, Mihailova S.

• PMID: 1014033

2.

Hoppe Seylers Z Physiol Chem. 1980 Apr;361(4):525-35.

[Basic peptides in bee venom, VI. Structure-activity studies on the anti-inflammatory effects of derivatives and fragments of the MCD-peptide (author’s transl)]

[Article in German]

Martin W, Hartter P.

Abstract

Mastcell-degranulating peptide from bee venom exhibits anti-inflammatory activity in the Carrageenine-inflammation model on mice and rats. Its dose/response relationship corresponds to that of dexamethasone. In the 125I-rat serum albumin-test the substance shows an inhibitory effect of 87% on the developing Carrageenine edema at a dose of 1 mg/kg; in contrast the bee venom peptides apamin and melittin exhibit small edema supressing effects. The anti-inflammatory characteristics of MCD-peptide have to be considered with regard to its high basicity and specific molecular structure, determined by two disulfide-bridges for the derivaties with acetylated amino groups respectively with alkylated cysteine residues show no significant activity. A pentapeptide in the C-terminal region of MCD-peptide (Lys-Ile-Cys-Gly-Lys)2 inhibits the carrageenin edema to 55% at a dose of 10 mg/kg.

• PMID: 7380393

3.

Proc Natl Acad Sci U S A. 1992 Feb 15;89(4):1325-9.

Calcium-activated potassium channels mediate prejunctional inhibition of peripheral sensory nerves.

Stretton D, Miura M, Belvisi MG, Barnes PJ.

Department of Thoracic Medicine, National Heart and Lung Institute, London, United Kingdom.

Abstract

Activation of several receptors, including mu-opioid, alpha 2-adrenergic, and neuropeptide Y receptors, inhibits excitatory nonadrenergic noncholinergic (NANC) neural responses in airways, which were mediated by the release of peptides from capsaicin-sensitive sensory nerves. This raises the possibility of a common inhibitory mechanism, which may be related to an increase in K+ conductance in sensory nerves. To examine this hypothesis, we have studied whether K(+)-channel blockers inhibit the effects of neuromodulators of sensory nerves in guinea pig bronchi by using selective K(+)-channel blockers. Charybdotoxin (ChTX; 10 nM), which blocks large conductance Ca(2+)-activated K(+)-channel function, completely blocked and reversed the inhibitory effects of a mu-opioid agonist, neuropeptide Y, and an alpha 2-adrenoceptor agonist on excitatory NANC responses. Neither inhibitors of ATP-sensitive K+ channels (BRL 31660 or glibenclamide, both at 10 microM) nor an inhibitor of small conductance Ca(2+)-activated K+ channels (apamin; 0.1 microM) were effective. This suggests that ChTX-sensitive K(+)-channel activation may be a common mechanism for the prejunctional modulation of sensory nerves in airways. This may have important implications for the control of neurogenic inflammation.

• PMID: 1371356

4.

Br J Pharmacol. 1994 Jul;112(3):958-62.

Involvement of apamin-sensitive K+ channels in antigen-induced spasm of guinea-pig isolated trachea.

Yamauchi H, Miura M, Ichinose M, Ishikawa J, Nakajima N, Tomaki M, Inoue H, Maeyama K, Watanabe T, Shirato K.

First Department of Internal Medicine, Tohoku University School of Medicine, Sendai, Japan.

Abstract

1. In order to examine whether K+ channels play a role in antigen-induced airway responses, the effect of K+ channel blockers on antigen-induced airway smooth muscle contraction and mediator release was examined in vitro in guinea-pigs actively sensitized with ovalbumin (OA). 2. Tracheal strips from sensitized animals were suspended in organ baths under a resting tension of 1 g and isometric tension was continuously measured. Cumulative concentration-response curves to OA (0.1-1000 ng ml-1) or histamine (10 nM-1 mM) were obtained in the presence and absence of K+ channel blockers. 3. OA (10, 100 or 1000 ng ml-1) was incubated with minced lung tissues from the same animals for 15 min in the presence and absence of K+ channel blockers, and released histamine and leukotriene C4 (LTC4) in the incubating medium were measured. 4. Apamin, a small conductance Ca(2+)-activated K+ channel (PK,Ca) blocker, (0.1, 0.3 and 1 microM) significantly inhibited OA-induced smooth muscle contraction, while charybdotoxin (ChTX, 10 nM), an intermediate and large conductance PK,Ca blocker, and iberiotoxin (IbTX, 3 nM), a large conductance PK,Ca blocker, were without effect. Apamin (0.3 microM) had no effect on exogenously administered histamine-induced airway smooth muscle contraction, suggesting that the inhibition of OA-induced contraction by apamin did not occur at the smooth muscle level. 5. The inhibition of OA-induced contraction by apamin (0.3 microM) was not significantly affected by pretreatment with a leukotriene antagonist, ONO-1078 (10 microM), but was abolished by pretreatment with a histamine H1-receptor blocker, pyrilamine (1 microM). 6. Apamin by itself (up to 0.1 MicroM) had no effect on spontaneous histamine release from minced lung tissues. Histamine release induced by low and intermediate concentrations of OA (10 and 100 ng ml-1)was significantly suppressed by apamin pretreatment (P<0.05 and P<0.001), whereas LTC4 release was not affected. ChTX (0.1 MicroM) and IbTX (10 nM) had no significant effect on either spontaneous or OA (100 ng ml-1)-induced histamine release.7. These results suggest that apamin partially but substantially inhibits antigen-induced smooth muscle contraction, presumably by inhibiting antigen-induced histamine release from airway mast cells through small conductance PKca closure.

PMID: 7522863

5.

Neuroscience. 2006;138(2):631-40. Epub 2006 Jan 30.

Effects of bee venom peptidergic components on rat pain-related behaviors and inflammation.

Chen YN, Li KC, Li Z, Shang GW, Liu DN, Lu ZM, Zhang JW, Ji YH, Gao GD, Chen J.

Institute for Functional Brain Disorders and Institute for Biomedical Sciences of Pain, Tangdu Hospital, Fourth Military Medical University, #1 Xinsi Road, Baqiao, Xi’an 710038, PR China.

Abstract

To identify the active components of honeybee venom in production of inflammation and pain-related behaviors, five major peptidergic subfractions were separated, purified and identified from the whole honeybee venom. Among them, four active peptidergic components were characterized as apamin, mast-cell degranulating peptide (MCDP), phospholipase A(2) (PLA(2))-related peptide and melittin, respectively. All five subfractions were effective in production of local inflammatory responses (paw edema) in rats although the efficacies were different. Among the five identified subfractions, only MCDP, PLA(2)-related peptide and melittin were able to produce ongoing pain-related behaviors shown as paw flinches, while only apamin and melittin were potent to produce both thermal and mechanical hypersensitivity. As shown in our previous report, melittin was the most potent polypeptide in production of local inflammation as well as ongoing pain and hypersensitivity. To further explore the peripheral mechanisms underlying melittin-induced nociception and hypersensitivity, a single dose of capsazepine, a blocker of thermal nociceptor transient receptor potential vanilloid receptor 1, was treated s.c. prior to or after melittin administration. The results showed that both pre- and post-treatment of capsazepine could significantly prevent and suppress the melittin-induced ongoing nociceptive responses and thermal hypersensitivity, but were without influencing mechanical hypersensitivity. The present results suggest that the naturally occurring peptidergic substances of the whole honeybee venom have various pharmacological potencies to produce local inflammation, nociception and pain hypersensitivity in mammals, and among the five identified reverse-phase high pressure liquid chromatography subfractions (four polypeptides), melittin, a polypeptide occupying over 50% of the whole honeybee venom, plays a central role in production of local inflammation, nociception and hyperalgesia or allodynia following the experimental honeybee’s sting. Peripheral transient receptor potential vanilloid receptor 1 is likely to be involved in melittin-produced ongoing pain and heat hyperalgesia, but not mechanical hyperalgesia, in rats.

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IH current generates the afterhyperpolarisation following activation of subthreshold cortical synaptic inputs to striatal cholinergic interneurons.

Oswald MJ, Oorschot DE, Schulz JM, Lipski J, Reynolds JN.

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SK channel blockade promotes burst firing in dorsal raphe serotonergic neurons.

Rouchet N, Waroux O, Lamy C, Massotte L, Scuvée-Moreau J, Liégeois JF, Seutin V.

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Accumulation of cytoplasmic calcium, but not apamin-sensitive afterhyperpolarization current, during high frequency firing in rat subthalamic nucleus cells.

Teagarden M, Atherton JF, Bevan MD, Wilson CJ.

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Calcium-dependent fast depolarizing afterpotentials in vasopressin neurons in the rat supraoptic nucleus.

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Lateral habenula stimulation inhibits rat midbrain dopamine neurons through a GABA(A) receptor-mediated mechanism.

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Apamin-sensitive calcium-activated potassium currents (SK) are activated by persistent calcium currents in rat motoneurons.

Li X, Bennett DJ.

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Acute tissue-type plasminogen activator release in human microvascular endothelial cells: the roles of Galphaq, PLC-beta, IP3 and 5,6-epoxyeicosatrienoic acid.

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Opposing effects of spinal nerve ligation on calcium-activated potassium currents in axotomized and adjacent mammalian primary afferent neurons.

Sarantopoulos CD, McCallum JB, Rigaud M, Fuchs A, Kwok WM, Hogan QH.

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Electromechanical and pharmacomechanical signalling pathways for conducted vasodilatation along endothelium of hamster feed arteries.

Domeier TL, Segal SS.

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Do gap junctions play a role in nerve transmissions as well as pacing in mouse intestine?

Daniel EE, Yazbi AE, Mannarino M, Galante G, Boddy G, Livergant J, Oskouei TE.

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Solution structure of IsTX. A male scorpion toxin from Opisthacanthus madagascariensis (Ischnuridae).

Yamaji N, Dai L, Sugase K, Andriantsiferana M, Nakajima T, Iwashita T.

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Involvement of purinergic nerves in the NANC inhibitory junction potentials in pigeon oesophageal smooth muscle.

Vetri T, Postorino A, Fileccia R, Bonvissuto F, Abbadessa Urso S.

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Effects of intracellular stores and extracellular Ca(2+) on Ca(2+)-activated K(+) currents in mature mouse inner hair cells.

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Electrophysiological properties of inhibitory junction potential in murine lower oesophageal sphincter.

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Characterization of an apamin-sensitive potassium current in suprachiasmatic nucleus neurons.

Teshima K, Kim SH, Allen CN.

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Biophysical and pharmacological characterization of voltage-gated calcium currents in turtle auditory hair cells.

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Ionic currents in isolated and in situ squid Schwann cells.

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Differential regulation of SK and BK channels by Ca(2+) signals from Ca(2+) channels and ryanodine receptors in guinea-pig urinary bladder myocytes.

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TEA- and apamin-resistant K(Ca) channels in guinea-pig myenteric neurons: slow AHP channels.

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Spontaneous apamin-sensitive hyperpolarizations in dopaminergic neurons of neonatal rats.

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