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1.
Yale J Biol Med ; 97(2): 205-224, 2024 Jun.
Artigo em Inglês | MEDLINE | ID: mdl-38947104

RESUMO

Neuroinflammation, toxic protein aggregation, oxidative stress, and mitochondrial dysfunction are key pathways in neurodegenerative diseases like Alzheimer's disease (AD). Targeting these mechanisms with antioxidants, anti-inflammatory compounds, and inhibitors of Aß formation and aggregation is crucial for treatment. Marine algae are rich sources of bioactive compounds, including carbohydrates, phenolics, fatty acids, phycobiliproteins, carotenoids, fatty acids, and vitamins. In recent years, they have attracted interest from the pharmaceutical and nutraceutical industries due to their exceptional biological activities, which include anti-inflammation, antioxidant, anticancer, and anti-apoptosis properties. Multiple lines of evidence have unveiled the potential neuroprotective effects of these multifunctional algal compounds for application in treating and managing AD. This article will provide insight into the molecular mechanisms underlying the neuroprotective effects of bioactive compounds derived from algae based on in vitro and in vivo models of neuroinflammation and AD. We will also discuss their potential as disease-modifying and symptomatic treatment strategies for AD.


Assuntos
Doença de Alzheimer , Microalgas , Alga Marinha , Doença de Alzheimer/tratamento farmacológico , Doença de Alzheimer/metabolismo , Humanos , Microalgas/química , Microalgas/metabolismo , Alga Marinha/química , Animais , Fármacos Neuroprotetores/farmacologia , Fármacos Neuroprotetores/uso terapêutico , Produtos Biológicos/farmacologia , Produtos Biológicos/uso terapêutico , Produtos Biológicos/isolamento & purificação , Antioxidantes/farmacologia
2.
Fitoterapia ; 176: 106025, 2024 Jul.
Artigo em Inglês | MEDLINE | ID: mdl-38768797

RESUMO

Algae and its metabolites have been a popular subject of research in numerous fields over the years. Various reviews have been written on algal bioactive components, but a specific focus on Antarctic-derived algae is seldom reviewed. Due to the extreme climate conditions of Antarctica, it is hypothesized that the acclimatized algae may have given rise to a new set of bioactive compounds as a result of adaptation. Although most studies done on Antarctic algae are based on ecological and physiological studies, as well as in the field of nanomaterial synthesis, some studies point out the potential therapeutic properties of these compounds. As an effort to shed light on a different application of Antarctic algae, this review focuses on evaluating its different medicinal properties, including antimicrobial, anticancer, antioxidative, anti-inflammatory, and skin protective effects.


Assuntos
Antioxidantes , Regiões Antárticas , Antioxidantes/farmacologia , Antioxidantes/isolamento & purificação , Anti-Inflamatórios/farmacologia , Anti-Inflamatórios/isolamento & purificação , Humanos , Anti-Infecciosos/farmacologia , Anti-Infecciosos/isolamento & purificação , Antineoplásicos/farmacologia , Antineoplásicos/isolamento & purificação , Produtos Biológicos/farmacologia , Produtos Biológicos/isolamento & purificação , Estrutura Molecular
3.
PeerJ ; 10: e13657, 2022.
Artigo em Inglês | MEDLINE | ID: mdl-35811814

RESUMO

Background: Curcumin is an active compound derived from turmeric, Curcuma longa, and is known for its benefits to human health. The amoebicidal activity of curcumin against Acanthamoeba triangularis was recently discovered. However, a physiological change of intracellular pathways related to A. triangularis encystation mechanism, including autophagy in the surviving amoeba after curcumin treatment, has never been reported. This study aims to investigate the effect of curcumin on the survival of A. triangularis under nutrient starvation and nutrient-rich condition, as well as to evaluate the A. triangularis encystation and a physiological change of Acanthamoeba autophagy at the mRNA level. Methods: In this study, A. triangularis amoebas were treated with a sublethal dose of curcumin under nutrient starvation and nutrient-rich condition and the surviving amoebas was investigated. Cysts formation and vacuolization were examined by microscopy and transcriptional expression of autophagy-related genes and other encystation-related genes were evaluated by real-time PCR. Results: A. triangularis cysts were formed under nutrient starvation. However, in the presence of the autophagy inhibitor, 3-methyladenine (3-MA), the percentage of cysts was significantly reduced. Interestingly, in the presence of curcumin, most of the parasites remained in the trophozoite stage in both the starvation and nutrient-rich condition. In vacuolization analysis, the percentage of amoebas with enlarged vacuole was increased upon starvation. However, the percentage was significantly declined in the presence of curcumin and 3-MA. Molecular analysis of A. triangularis autophagy-related (ATG) genes showed that the mRNA expression of the ATG genes, ATG3, ATG8b, ATG12, ATG16, under the starvation with curcumin was at a basal level along the treatment. The results were similar to those of the curcumin-treated amoebas under a nutrient-rich condition, except AcATG16 which increased later. On the other hand, mRNA expression of encystation-related genes, cellulose synthase and serine proteinase, remained unchanged during the first 18 h, but significantly increased at 24 h post treatment. Conclusion: Curcumin inhibits cyst formation in surviving trophozoites, which may result from its effect on mRNA expression of key Acanthamoeba ATG-related genes. However, further investigation into the mechanism of curcumin in A. triangularis trophozoites arrest and its association with autophagy or other encystation-related pathways is needed to support the future use of curcumin.


Assuntos
Acanthamoeba , Amoeba , Curcumina , Animais , Humanos , Acanthamoeba/genética , Curcumina/farmacologia , Trofozoítos/fisiologia
4.
J Cell Mol Med ; 26(5): 1434-1444, 2022 03.
Artigo em Inglês | MEDLINE | ID: mdl-35106914

RESUMO

Alzheimer's disease (AD), the major cause of dementia, affects the elderly population worldwide. Previous studies have shown that depletion of receptor-interacting protein kinase 1 (RIPK1) expression reverted the AD phenotype in murine AD models. Necroptosis, executed by mixed lineage kinase domain-like (MLKL) protein and activated by RIPK1 and RIPK3, has been shown to be involved in AD. However, the role of RIPK1 in beta-amyloid (Aß)-induced necroptosis is not yet fully understood. In this study, we explored the role of RIPK1 in the SH-SY5Y human neuroblastoma cells treated with Aß 1-40 or Aß 1-42. We showed that Aß-induced neuronal cell death was independent of apoptosis and autophagy pathways. Further analyses depicted that activation of RIPK1/MLKL-dependant necroptosis pathway was observed in vitro. We demonstrated that inhibition of RIPK1 expression rescued the cells from Aß-induced neuronal cell death and ectopic expression of RIPK1 was found to enhance the stability of the endogenous APP. In summary, our findings demonstrated that Aß can potentially drive necroptosis in an RIPK1-MLKL-dependent manner, proposing that RIPK1 plays an important role in the pathogenesis of AD.


Assuntos
Doença de Alzheimer , Síndromes Neurotóxicas , Idoso , Doença de Alzheimer/genética , Peptídeos beta-Amiloides/metabolismo , Peptídeos beta-Amiloides/toxicidade , Animais , Apoptose , Morte Celular , Humanos , Camundongos , Necroptose , Proteínas Quinases/genética , Proteína Serina-Treonina Quinases de Interação com Receptores/genética , Proteína Serina-Treonina Quinases de Interação com Receptores/metabolismo
5.
Stem Cell Investig ; 6: 25, 2019.
Artigo em Inglês | MEDLINE | ID: mdl-31559312

RESUMO

Cancer is a genetic disease which results in a functional imbalance between tumour-repressive and oncogenic signals. The WHO highlights the burden of this indomitable disease, listing it as the second leading cause of death globally. The major cause of cancer-related death is rarely the effect of the primary tumour itself, but rather, the devastating spread of cancer cells in metastases. Epithelial-mesenchymal plasticity (EMP)-termed as the ability of cells to maintain its plasticity and transit between epithelial-mesenchymal transition (EMT) and mesenchymal-epithelial transition (MET) states-plays a fundamental role in cancer metastasis. These cell transitions allow them migrate from the primary tumour and invade the secondary site. EMP is associated with migration, invasion, colonisation, self-renewal and drug resistance. This review briefly elucidates the mechanism of EMP and the association between cancer stem cells (CSCs) and circulating tumour cells (CTCs), biomarkers and signalling pathways involved in EMP as well as drug resistance and therapeutic targeting.

6.
Plant Foods Hum Nutr ; 74(1): 18-27, 2019 Mar.
Artigo em Inglês | MEDLINE | ID: mdl-30535971

RESUMO

Cancer is a preventable and treatable disease, however, the incidence rates are on the rise. Classical treatment modalities for cancer include surgery, radiotherapy and chemotherapy. However, these are associated with detrimental side effects such as nausea and emesis. Therefore, researchers currently vest interest in complementary and alternative medicines for cancer treatment and prevention. Plants such as Syzygium sp. are a common basis of complementary medicines due to its abundance of bioactive phytochemicals. Numerous natural compounds derived from Syzygium sp., such as phenolics, oleanolic acids, and betulinic acids, and dimethyl cardamonins, were reported to have anticancer effects. Many possess the ability to inhibit cell proliferation and induce apoptosis. In this review, we discuss the vast potential Syzygium sp. harbours as a source of anticancer natural compounds due to its abundance, easy acceptability, affordability and safety for regular consumption.


Assuntos
Antineoplásicos Fitogênicos/farmacologia , Compostos Fitoquímicos/farmacologia , Syzygium/química , Chalconas/farmacologia , Humanos , Ácido Oleanólico/farmacologia , Triterpenos Pentacíclicos , Fenóis/farmacologia , Plantas Medicinais , Triterpenos/farmacologia , Ácido Betulínico
7.
Stem Cell Investig ; 4: 96, 2017.
Artigo em Inglês | MEDLINE | ID: mdl-29270422

RESUMO

Breast cancer is marked as one of the leading causes of malignancy-related morbidities worldwide. In spite of aggressive interventions, the inevitability of relapse and metastasis severely impede survival rates. Mounting evidence highlight the insidious role of cancer stem cells (CSCs), a small but significant subpopulation of undifferentiated cells that drive tumour progression, spread and resistance to conventional therapy. The nature and significance of breast CSCs remains poorly understood, and even disputed by many researchers. This review discusses the origins, biomarkers, signalling pathways, regulatory mechanisms, and targeted therapy of breast CSCs.

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