The effects of honey bee (Apis mellifera L.) venom and two of its constituents, melittin and phospholipase A2, on the cardiovascular system of the rat

Marsh, Neville; Whaler, B. C.

doi:10.1016/0041-0101(80)90050-1

Cited by 14 publications

(6 citation statements)

References 10 publications

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“…The major components of bee venom are melittin, apamine, polyamines, hyaluronidase and phospholipase. Previous studies have directly examined its eOE ects on the cardiovascular system (Marsh & Whaler 1980 ;Cook & Hof 1988 ; Thomas & Hiley 1988), immune system (Reisma et al 1985 ;Jutel et al 1995 ;Bellinghausen et al 1997), nervous system (Luo et al 1998 ;Ren et al 1999 ;Stocker et al 1999 ;Chen et al 2001) and blood (Pogliani & Cofrancesco 1983). It was noted that apamine and catecholamines such as noradrenaline (norepinephrine) and dopamine caused neurotoxic eOE ects and the degranulation of mast cells (Orlov 1979).…”

Section: Introductionmentioning

confidence: 99%

Effect of honey bee venom on proliferation of K1735M2 mouse melanoma cells in-vitro and growth of murine B16 melanomas in-vivo

Liu

Chen

Xie

et al. 2002

Journal of Pharmacy and Pharmacology

101

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Bee venom has been reported to exhibit antitumour activity in-vitro and in-vivo. Apoptosis, necrosis and lysis of tumour cells were suggested as possible mechanisms by which bee venom inhibited tumour growth. The aim of this study was to investigate potential mechanisms by which bee venom inhibits K1735M2 mouse melanoma cells in-vitro and B16 melanoma, a transplantable solid melanoma in C57BL/6 mice, in-vivo. The proliferation of K1735M2 cells in-vitro was inhibited by bee venom in a concentration- and time-dependent manner. The inhibition was indicated by the arrest of the cell cycle at the G1 stage, as detected by flow cytometric measurements. The bee venom induced apoptosis-like cell death as identified by histological observations and by DNA fragmentation. In the in-vivo experiments, the bee venom (1.0, 3.0, 9.0 mg kg-1 of body weight, on days 1-12) was injected intraperitoneally into mice 24 h after the mice were inoculated with B16 cells. Inhibition of the solid tumour was observed. Apoptosis of the K1735M2 cells was suggested as the possible mechanism by which bee venom inhibited cell proliferation and induced K1735M2 cell differentiation in-vitro. The in-vivo experiment indicated that bee venom could be used as a chemotherapeutic agent against malignant tumours.

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Section: Introductionmentioning

confidence: 99%

Effect of honey bee venom on proliferation of K1735M2 mouse melanoma cells in-vitro and growth of murine B16 melanomas in-vivo

Liu

Chen

Xie

et al. 2002

Journal of Pharmacy and Pharmacology

101

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“…Circulating PLA2 levels correlate directly with the fall in mean arterial blood pressure (MABP) in endotoxin shock in rabbits [1] and gram-negative septic shock in man [4]. Parenteral administration of exogenous PLA2 produces dose-related hypotension in experimental animals [1,[5][6][7][8]. The circulatory collapse caused by both exogenous and endogenous PLA2 is thought to be mediated by generation of vasoactive products of PLA2 hydrolysis, the free fatty acids and lysophosphatides [1][2][3][4].…”

Section: Introductionmentioning

confidence: 99%

Potential therapeutic efficacy of inhibitors of human phospholipase A2 in septic shock

1986

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Soluble phospholipase A2 has been implicated in the pathogenesis of local and systemic inflammatory reactions. Elevated levels of circulating phospholipase A2 (PLA2) correlate with the severity of circulatory collapse and pulmonary dysfunction in gram-negative septic shock. Characterization of septic shock serum PLA2 revealed a calcium-dependent enzyme with absolute 2-acyl specificity with a pH optimum of 7.5. We tested a number of therapeutic agents for their ability to inhibit PLA2 from human septic shock serum. Chloroquine, chlorpromazine, dexamethasone base, dexamethasone sodium phosphate, indomethacin, lidocaine, oleic acid, palmitic acid, promethazine, trans-retinoic acid, rutin and dl-alpha-tocopherol were all studied over the range of 10(-2) to 10(-7) M. All agents, with the sole exception of dexamethasone base, inhibited PLA2 activity at concentrations greater than 10(-3) M. PLA2 inhibition by dexamethasone sodium phosphate was factitious, due to the formation of calcium-phosphate complexes. Of the 11 agents studied, chlorpromazine was the most effective, with an IC50 of 7.5 X 10(-5) M, a membrane concentration achievable within its therapeutic range. Inhibition was non-competitive with an apparent Ki of 5 nM. Since serum PLA2 levels correlate with mortality in both experimental endotoxemia and clinical gram-negative septic shock, and chlorpromazine was previously shown to improve survival in these conditions, we postulate that its therapeutic efficacy resides at least in part in its PLA2-inhibitory activity.

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“…Additionally, at a concentration of 0.1–30 μmol/dL, melittin increased the frequency of contractions of isolated right atria [49]. However, there is also evidence of the irreversible paralysis of isolated rat hearts after using 20–40 μg of melittin [50].…”

Section: Discussionmentioning

confidence: 99%

The Influence of Bee Venom Melittin on the Functioning of the Immune System and the Contractile Activity of the Insect Heart—A Preliminary Study

Lubawy

Urbański

Mrówczyńska

et al. 2019

Toxins

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Melittin (MEL) is a basic polypeptide originally purified from honeybee venom. MEL exhibits a broad spectrum of biological activity. However, almost all studies on MEL activity have been carried out on vertebrate models or cell lines. Recently, due to cheap breeding and the possibility of extrapolating the results of the research to vertebrates, insects have been used for various bioassays and comparative physiological studies. For these reasons, it is valuable to examine the influence of melittin on insect physiology. Here, for the first time, we report the immunotropic and cardiotropic effects of melittin on the beetle Tenebrio molitor as a model insect. After melittin injection at 10−7 M and 10−3 M, the number of apoptotic cells in the haemolymph increased in a dose-dependent manner. The pro-apoptotic action of MEL was likely compensated by increasing the total number of haemocytes. However, the injection of MEL did not cause any changes in the percent of phagocytic haemocytes or in the phenoloxidase activity. In an in vitro bioassay with a semi-isolated Tenebrio heart, MEL induced a slight chronotropic-positive effect only at a higher concentration (10−4 M). Preliminary results indicated that melittin exerts pleiotropic effects on the functioning of the immune system and the endogenous contractile activity of the heart. Some of the induced responses in T. molitor resemble the reactions observed in vertebrate models. Therefore, the T. molitor beetle may be a convenient invertebrate model organism for comparative physiological studies and for the identification of new properties and mechanisms of action of melittin and related compounds.

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The effects of honey bee (Apis mellifera L.) venom and two of its constituents, melittin and phospholipase A2, on the cardiovascular system of the rat

Cited by 14 publications

References 10 publications

Effect of honey bee venom on proliferation of K1735M2 mouse melanoma cells in-vitro and growth of murine B16 melanomas in-vivo

Effect of honey bee venom on proliferation of K1735M2 mouse melanoma cells in-vitro and growth of murine B16 melanomas in-vivo

Potential therapeutic efficacy of inhibitors of human phospholipase A2 in septic shock

The Influence of Bee Venom Melittin on the Functioning of the Immune System and the Contractile Activity of the Insect Heart—A Preliminary Study

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