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BR-102024017625-A2 - Use of Africanized bee venom for the treatment of depression.

BR102024017625A2BR 102024017625 A2BR102024017625 A2BR 102024017625A2BR-102024017625-A2

Abstract

This invention relates to the use of Africanized bee venom (Apis mellifera Linnaeus) as an active component in pharmaceutical formulations intended for the treatment of depressive disorder. To evaluate the therapeutic potential of the venom, an experiment was conducted using a validated animal model, in which Swiss mice with reserpine-induced depressive-like behavior were analyzed. This invention seeks to meet both a pharmaceutical and technological need by introducing Africanized bee venom as an active ingredient in pharmaceutical treatments, while also proposing improvements in the product's bioavailability. Thus, the invention offers an innovative alternative for the treatment of depression, potentially expanding available therapeutic options and contributing to advances in integrative medicine.

Inventors

  • CAMILA GOMES DANTAS
  • RAYANE GOIS SOUTO
  • Edna Aragão Farias Cândido

Assignees

  • INSTITUTO DE TECNOLOGIA E PESQUISA
  • UNIVERSIDADE TIRADENTES

Dates

Publication Date
20260310
Application Date
20240827

Claims (8)

  1. 1. USE OF BEE VENOM FOR THE TREATMENT OF DEPRESSION, characterized by its use in doses of VA 0.5 mg.Kg-1; VA 1.0 mg.Kg-1 and VA 1.5 mg.Kg-1 for the treatment of depressive disorder.
  2. 2. USE OF BEE VENOM FOR THE TREATMENT OF DEPRESSION, according to claim 1, characterized in that the bee venom is from the species Apis mellifera Linnaeus.
  3. 3. USE OF BEE VENOM according to claim 1, characterized in that the venom is used as an active ingredient in pharmaceutical compositions.
  4. 4. USE OF BEE VENOM, according to claim 1, characterized in that the venom is obtained by electrical extraction.
  5. 5. USE OF BEE VENOM, according to claim 1, characterized by diluting Africanized bee venom in 40 μL of saline solution;
  6. 6. USE OF BEE VENOM, according to claim 1, characterized by the dosage of bee venom being VA 1.0 mg.Kg- 1, applied subcutaneously, daily, for 10 days.
  7. 7. USE OF BEE VENOM according to claim 1, characterized by having anti-inflammatory and neuroprotective properties, exhibiting a broad spectrum of action on the Central Nervous System,
  8. 8. USE OF BEE VENOM according to claim 1, characterized by acting on the pathophysiology of diseases, to treat the symptoms of depressive and emotional behavior.

Description

FIELD OF THE INVENTION 001. This Invention Patent (PI) refers to the use of bee venom from the species Apis mellifera Linnaeus, whose chemical profile differs from that of European bees, as an active element in pharmaceutical compositions for the treatment of depressive disorder. In this invention, the therapeutic effect of bee venom was evaluated through the behavior of mice treated with reserpine, which acts on low-conductance calcium-activated potassium channels and on the dopaminergic, glutamatergic, and serotonergic systems. Currently available studies for this purpose are based on the use of venom from European bees, due to the origin of the research groups, the availability, and easy access to the extracted venom. The proposed invention aims to fill a pharmaceutical and technological gap in the application of Africanized bee venom as an active element in pharmaceutical compositions, in addition to proposing improvements in the bioavailability of this product, offering an innovative therapeutic alternative. FUNDAMENTALS OF THE TECHNIQUE 002. Depression is a mental disorder characterized by frequent sadness, affecting more than 300 million people worldwide, regardless of age. In Brazil, this disorder affects approximately 11.5 million individuals, which corresponds to 5.8% of the population (Pan American Health Organization & World Health Organization. Depression: What you need to know. Brasília, 2017; LEÃO, A. H.; MEURER, Y. S.; DA SILVA, A. F.; MEDEIROS, A. M.; CAMPÊLO, C. L.; ABÍLIO, V. C.; ENGELBERTH, R. C.; CAVALCANTE, J. S.; IZÍDIO, G. S.; RIBEIRO, A. M.; SILVA, R. H. Spontaneously hypertensive rats (SHR) are resistant to a progressive reserpine-induced model of Parkinson's disease: differences in motor behavior, tyrosine hydroxylase and α-synuclein expression. Frontiers in Aging Neuroscience, v. 9, n.78, 2017). 003. This disorder is characterized by mood swings, restlessness, anxiety, and feelings of worthlessness, which reduces quality of life and is currently one of the leading causes of mortality in the world (HAO, Y.; GE, H.; SUN, M.; GAO, Y. Selecting an appropriate animal model of depression. International Journal of Molecular Sciences, v. 20, n. 19, p. 4827, 2019; OLIFFE, J. L.; ROSSNAGEL, E.; SEIDLER, Z. E.; KEALY, D.; OGRODNICZUK, J. S.; RICE, S. M. Men's Depression and suicide. Current Psychiatry Reports, v. 2, n.10, p.103, 2019; SILVA, M. R. G; MARCOLAN J. F. Working conditions and depression in hospital emergency service nurses. Revista Brasileira de Enfermagem, São Paulo, v. 73, 2020). 004. Its etiology is not yet fully understood, although it is estimated to be related to social, genetic and environmental factors (DUMAN, R. S.; AGHAJANIAN, G. K.; SANACORA, G.; KRYSTAL, J. H. Synaptic plasticity and depression: new insights from stress and rapid-acting antidepressants. Nature Medicine, v. 22, n.3, p. 238-249, 2016; MALHI, G. S.; MANN, J. J. Depression. Lancet, v. 392, n. 10161, p. 2299-2312, 2018). 005. The pathophysiology of the disease consists of decreased functioning of monoaminergic neurotransmitters, such as serotonin, dopamine, and norepinephrine, which are involved in motor control and social behavior (KRISHNAN, V.; NESTLER, E. J. The molecular neurobiology of depression. Nature, v. 455, p. 894-902, 2018; VIGNET, C.; TRENKEL, V. M.; VOUILLARMET, A.; BRICCA, G.; BEGOUT, M.L.; PRIMO, X. Changes in brain monoamines underlie behavioural disruptions after zebrafish diet exposure to polycyclic aromatic hydrocarbons environmental mixtures. International Journal of Molecular Sciences, v.18, n. 3, p. 560, 2017). 006. The monoaminergic theory points to a decrease in cerebral catecholamines and consequent dysregulation of neurotransmitters, resulting in a deficiency of serotonin, dopamine, and norepinephrine, and/or a quantitative reduction in their receptors, or even in their inefficiency (PARK, L. T.; ZARATE, C. A. Jr. Depression in the primary care setting. The New England Journal of Medicine, v. 380, n. 6, p. 559-568, 2019). However, reserpine irreversibly blocks the vesicular monoamine transporter-2 in the adrenergic neurotransmission pathway, thereby causing depletion of cytoplasmic monoamine oxidase in peripheral and central synapses (SHAMON, S. D.; PEREZ, M. I. Blood pressure-lowering efficacy of reserpine for primary hypertension. Cochrane Database of Systematic Reviews, n. 12, 2016; LEÃO, A. H.; MEURER, Y. S.; DA SILVA, A. F.; MEDEIROS, A. M.; CAMPÊLO, C. L.; ABÍLIO, V.C.; ENGELBERTH, R.C.; CAVALCANTE, J. S.; IZÍDIO, G. S.; RIBEIRO, A. M.; SILVA, R.H. Spontaneously hypertensive rats (SHR) are resistant to a progressive reserpine-induced model of Parkinson's disease: differences in motor behavior, tyrosine hydroxylase and α-synuclein expression. Frontiers in Aging Neuroscience, v. 9, n. 78, 2017). In this sense, monoamine iodide (MAO) neurotransmitter deficiency is one of the main causative factors of depression (WANG, Y. N.; HOU, Y. Y.; SUN, M. Z.; ZHANG, C. Y.; BAI, G.; ZHAO