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1.
Bone Rep ; 20: 101740, 2024 Mar.
Artigo em Inglês | MEDLINE | ID: mdl-38304620

RESUMO

Nowadays, there is an increasing prevalence of bone diseases and defects caused by trauma, cancers, infections, and degenerative and inflammatory conditions. The restoration of bone tissue lost due to trauma, fractures, or surgical removal resulting from locally invasive pathologies requires bone regeneration. As an alternative to conventional treatments, sustainable materials based on natural products, such as honeybee-derived products (honey, propolis, royal jelly, bee pollen, beeswax, and bee venom), could be considered. Honeybee-derived products, particularly honey, have long been recognized for their healing properties. There are a mixture of phytochemicals that offer bone protection through their antimicrobial, antioxidant, and anti-inflammatory properties. This review aims to summarize the current evidence regarding the effects of honeybee-derived products on bone regeneration. In conclusion, honey, propolis, royal jelly, beeswax, and bee venom can potentially serve as natural products for promoting bone health.

2.
Inflammopharmacology ; 29(5): 1291-1306, 2021 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-34424482

RESUMO

Autoimmune diseases (ADs) are conditions in which the immune system cannot distinguish self from non-self and, as a result, tissue injury occurs primarily due to the action of various inflammatory mediators. Different immunosuppressive agents are used for the treatment of patients with ADs, but some clinical cases develop resistance to currently available therapies. The proteasome inhibitor bortezomib (BTZ) is an approved agent for first-line therapy of people with multiple myeloma. BTZ has been shown to improve the symptoms of different ADs in animal models and ameliorated symptoms in patients with systemic lupus erythematous, rheumatoid arthritis, myasthenia gravis, neuromyelitis optica spectrum disorder, Chronic inflammatory demyelinating polyneuropathy, and autoimmune hematologic diseases that were nonresponsive to conventional therapies. Proteasome inhibition provides a potent strategy for treating ADs. BTZ represents a proteasome inhibitor that can potentially be used to treat AD patients resistant to conventional therapies.


Assuntos
Doenças Autoimunes/tratamento farmacológico , Bortezomib/farmacologia , Inibidores de Proteassoma/farmacologia , Animais , Antineoplásicos/farmacologia , Doenças Autoimunes/fisiopatologia , Modelos Animais de Doenças , Resistência a Medicamentos , Humanos , Mieloma Múltiplo/tratamento farmacológico
3.
J Appl Biomed ; 17(2): 99-106, 2019 Jun.
Artigo em Inglês | MEDLINE | ID: mdl-34907731

RESUMO

Brain ischemia is a leading cause of death and disability worldwide that occurs when blood supply of the brain is disrupted. Brain-derived neurotrophic factor (BDNF) is a protective factor in neurodegenerative conditions. Nevertheless, there are some problems when exogenous BDNF is to be used in the clinic. 14-3-3ζ is a pro-survival highly-expressed protein in the brain that protects neurons against death. This study evaluates 14-3-3ζ effects on BDNF transcription at early time point after ischemia and its possible protective effects against ischemia damage. Human 14-3-3ζ protein was purified after expression. Rats were assigned into four groups, including sham, ischemia, and two treatment groups. Stereotaxic cannula implantation was carried out in the right cerebral ventricle. After one week, rats underwent middle cerebral artery occlusion (MCAO) surgery and received 14-3-3ζ (produced in our laboratory or standard form as control) in the middle of ischemia time. At 6 h of reperfusion after ischemia, brain parts containing the hippocampus, the cortex, the piriform cortex-amygdala and the striatum were collected for real time PCR analysis. At 24 h of reperfusion after ischemia, neurological function evaluation and infarction volume measurement were performed. The present study showed that 14-3-3ζ could up-regulate BDNF mRNA at early time point after ischemia in the hippocampus, in the cortex and in the piriform cortex-amygdala and could also improve neurological outcome and reduce infarct volume. It seems that 14-3-3ζ could be a candidate factor for increasing endogenous BDNF in the brain and a potential therapeutic factor against brain ischemia.

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