RESUMEN
Inflammation is a defense mechanism of the body in response to harmful stimuli such as pathogens, damaged cells, toxic compounds or radiation. However, chronic inflammation plays an important role in the pathogenesis of a variety of diseases. Multiple anti-inflammatory drugs are currently available for the treatment of inflammation, but all exhibit less efficacy. This drives the search for new anti-inflammatory compounds focusing on natural resources. Marine organisms produce a broad spectrum of bioactive compounds with anti-inflammatory activities. Several are considered as lead compounds for development into drugs. Anti-inflammatory compounds have been extracted from algae, corals, seaweeds and other marine organisms. We previously reviewed anti-inflammatory compounds, as well as crude extracts isolated from echinoderms such as sea cucumbers, sea urchins and starfish. In the present review, we evaluate the anti-inflammatory effects of compounds from other marine organisms, including macroalgae (seaweeds), marine angiosperms (seagrasses), medusozoa (jellyfish), bryozoans (moss animals), mollusks (shellfish) and peanut worms. We also present a review of the molecular mechanisms of the anti-inflammatory activity of these compounds. Our objective in this review is to provide an overview of the current state of research on anti-inflammatory compounds from marine sources and the prospects for their translation into novel anti-inflammatory drugs.
Asunto(s)
Antozoos , Briozoos , Escifozoos , Algas Marinas , Animales , Arachis , Organismos Acuáticos , Antiinflamatorios/farmacología , Inflamación/tratamiento farmacológico , MariscosRESUMEN
Cardiovascular diseases (CVDs) are one of the leading causes of death worldwide. Accumulating evidences have highlighted the importance of exosomes and non-coding RNAs (ncRNAs) in cardiac physiology and pathology. It is in general consensus that exosomes and ncRNAs play a crucial role in the maintenance of normal cellular function; and interestingly it is envisaged that their potential as prospective therapeutic candidates and biomarkers are increasing rapidly. Considering all these aspects, this review provides a comprehensive overview of the recent understanding of exosomes and ncRNAs in CVDs. We provide a great deal of discussion regarding their role in the cardiovascular system, together with providing a glimpse of ideas regarding strategies exploited to harness their potential as a therapeutic intervention and prospective biomarker against CVDs. Thus, it could be envisaged that a thorough understanding of the intricacies related to exosomes and ncRNA would seemingly allow their full exploration and may lead clinical settings to become a reality in near future.
Asunto(s)
Enfermedades Cardiovasculares , Sistema Cardiovascular , Exosomas , Humanos , Exosomas/genética , Enfermedades Cardiovasculares/genética , Enfermedades Cardiovasculares/terapia , ARN no Traducido/genética , BiomarcadoresRESUMEN
Chronic inflammation can extensively burden a healthcare system. Several synthetic anti-inflammatory drugs are currently available in clinical practice, but each has its own side effect profile. The planet is gifted with vast and diverse oceans, which provide a treasure of bioactive compounds, the chemical structures of which may provide valuable pharmaceutical agents. Marine organisms contain a variety of bioactive compounds, some of which have anti-inflammatory activity and have received considerable attention from the scientific community for the development of anti-inflammatory drugs. This review describes such bioactive compounds, as well as crude extracts (published during 2010-2022) from echinoderms: namely, sea cucumbers, sea urchins, and starfish. Moreover, we also include their chemical structures, evaluation models, and anti-inflammatory activities, including the molecular mechanism(s) of these compounds. This paper also highlights the potential applications of those marine-derived compounds in the pharmaceutical industry to develop leads for the clinical pipeline. In conclusion, this review can serve as a well-documented reference for the research progress on the development of potential anti-inflammatory drugs from echinoderms against various chronic inflammatory conditions.
Asunto(s)
Equinodermos , Pepinos de Mar , Animales , Erizos de Mar , Estrellas de Mar , Antiinflamatorios/farmacologíaRESUMEN
OBJECTIVE: Diabetic subjects are at higher risk of ischemic peripheral vascular disease. We tested the hypothesis that advanced glycation end products (AGEs) and their receptor (RAGE) block angiogenesis and blood flow recovery after hindlimb ischemia induced by femoral artery ligation through modulation of immune/inflammatory mechanisms. APPROACH AND RESULTS: Wild-type mice rendered diabetic with streptozotocin and subjected to unilateral femoral artery ligation displayed increased accumulation and expression of AGEs and RAGE in ischemic muscle. In diabetic wild-type mice, femoral artery ligation attenuated angiogenesis and impaired blood flow recovery, in parallel with reduced macrophage content in ischemic muscle and suppression of early inflammatory gene expression, including Ccl2 (chemokine [C-C motif] ligand-2) and Egr1 (early growth response gene-1) versus nondiabetic mice. Deletion of Ager (gene encoding RAGE) or transgenic expression of Glo1 (reduces AGEs) restored adaptive inflammation, angiogenesis, and blood flow recovery in diabetic mice. In diabetes mellitus, deletion of Ager increased circulating Ly6Chi monocytes and augmented macrophage infiltration into ischemic muscle tissue after femoral artery ligation. In vitro, macrophages grown in high glucose display inflammation that is skewed to expression of tissue damage versus tissue repair gene expression. Further, macrophages grown in high versus low glucose demonstrate blunted macrophage-endothelial cell interactions. In both settings, these adverse effects of high glucose were reversed by Ager deletion in macrophages. CONCLUSIONS: These findings indicate that RAGE attenuates adaptive inflammation in hindlimb ischemia; underscore microenvironment-specific functions for RAGE in inflammation in tissue repair versus damage; and illustrate that AGE/RAGE antagonism may fill a critical gap in diabetic peripheral vascular disease.
Asunto(s)
Diabetes Mellitus Experimental/metabolismo , Angiopatías Diabéticas/metabolismo , Eliminación de Gen , Inflamación/metabolismo , Isquemia/metabolismo , Músculo Esquelético/irrigación sanguínea , Neovascularización Fisiológica , Enfermedad Arterial Periférica/metabolismo , Receptor para Productos Finales de Glicación Avanzada/deficiencia , Oxidorreductasas de Alcohol/genética , Oxidorreductasas de Alcohol/metabolismo , Animales , Antígenos Ly/metabolismo , Velocidad del Flujo Sanguíneo , Glucemia/metabolismo , Comunicación Celular , Células Cultivadas , Microambiente Celular , Quimiocina CCL2/genética , Quimiocina CCL2/metabolismo , Diabetes Mellitus Experimental/inducido químicamente , Diabetes Mellitus Experimental/genética , Diabetes Mellitus Experimental/fisiopatología , Angiopatías Diabéticas/genética , Angiopatías Diabéticas/fisiopatología , Proteína 1 de la Respuesta de Crecimiento Precoz/genética , Proteína 1 de la Respuesta de Crecimiento Precoz/metabolismo , Células Endoteliales/metabolismo , Regulación de la Expresión Génica , Predisposición Genética a la Enfermedad , Productos Finales de Glicación Avanzada/metabolismo , Inflamación/genética , Inflamación/fisiopatología , Isquemia/genética , Isquemia/fisiopatología , Macrófagos/metabolismo , Ratones Noqueados , Ratones Transgénicos , Monocitos/metabolismo , Músculo Esquelético/metabolismo , Enfermedad Arterial Periférica/genética , Enfermedad Arterial Periférica/fisiopatología , Fenotipo , Receptor para Productos Finales de Glicación Avanzada/genética , Recuperación de la Función , Flujo Sanguíneo Regional , Transducción de Señal , Estreptozocina , Factores de TiempoRESUMEN
The presence of occult metastases at the time of diagnosis together with the lack of effective chemotherapies pose a dire need for designing new and targeted therapeutics for pancreatic cancer. Fucoidans from brown algae can be regarded as potential candidates in view of their antioxidant, anti-cancer and anti-angiogenic potential. Herein, we investigated the antioxidant and anti-cancer effects of fucoidans, sulfated polysaccharides from Turbinaria conoides (TCFE) in pancreatic cancer cell lines. TCFE exerted significant antioxidant activities against various free radicals. Significant inhibition of cell proliferation and, induction of apoptotic cell death were observed in pancreatic cancer cells in response to TCFE. Also, TCFE exhibited significant anti-angiogenic potential. Evidently, gelatin zymography revealed that TCFE inhibited matrix metalloproteases -2 and -9 activities in pancreatic cancer cells. These results clearly indicate that TCFE could serve as a potential 'deliverable' to alleviate pancreatic cancer progression by inhibiting tumor cell proliferation and angiogenesis.