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1.
Pharm Biol ; 57(1): 13-20, 2019 Dec.
Artículo en Inglés | MEDLINE | ID: mdl-31199705

RESUMEN

Context: Huoxin formula is a Traditional Chinese Medicine for coronary heart disease (CHD) treatment. Objective: To explore the therapeutic mechanism of the Huoxin formula on arterial functions in CHD patients. Materials and methods: Fifty-eight CHD patients receiving cardiovascular drugs including ß-receptor blocker, statins, and antiplatelet medications or others were randomized into intervention [additionally 13.5 g Huoxin formula granules dissolved in 150 mL warm water per time, twice a day (n = 30)] and control [only cardiovascular drugs (n = 28)] groups. Serum biomarkers (hs-CRP, IL-18, IL-17, TNF-α, MMP-9), and cardiovascular indicators of the common and internal carotid arteries (ICAs) were monitored before and after the treatments. Results: After 3 months of treatment, the increases of intima-media thicknesses (IMT) of the left and right common carotid arteries (CCAs) as well as of the left and right ICAs and the increases of the left and right cardio-ankle vascular index were all significantly (all p < 0.001) less in the intervention than in control group (all p < 0.001). Serum concentrations reductions of hs-CRP, IL-18, IL-17 and MMP9 (all p < 0.001) levels were higher in the intervention compared to the control group, which correlated with the changes of left ICA (hs-CRP: r = 0.581, p = 0.009; IL-18: r = 0.594, p = 0.007; IL-17: r = 0.575, p = 0.006). Discussion and conclusion: Since the Huoxin formula improved arterial functions and reduced inflammatory factor activities in CHD patients, a large-scale clinical trial is warranted.


Asunto(s)
Arterias Carótidas/efectos de los fármacos , Enfermedad Coronaria/tratamiento farmacológico , Citocinas/efectos de los fármacos , Medicamentos Herbarios Chinos/farmacología , Adulto , Anciano , Asarum , Astragalus propinquus , Biomarcadores/sangre , Biomarcadores/metabolismo , Grosor Intima-Media Carotídeo , Citocinas/sangre , Citocinas/metabolismo , Dalbergia , Medicamentos Herbarios Chinos/química , Femenino , Humanos , Masculino , Medicina Tradicional China , Persona de Mediana Edad , Panax notoginseng , Pacientes
2.
Brain Behav Immun ; 51: 56-69, 2016 Jan.
Artículo en Inglés | MEDLINE | ID: mdl-26231971

RESUMEN

Suppression of excessive inflammation can ameliorate blood brain barrier (BBB) injury, which shows therapeutic potential for clinical treatment of brain injury induced by stroke superimposed on systemic inflammatory diseases. In this study, we investigated whether and how clematichinenoside (AR), an anti-inflammatory triterpene saponin, protects brain injury from stroke superimposed on systemic inflammation. Lipopolysaccharide (LPS) was intraperitoneally injected immediately after middle cerebral artery occlusion (MCAO) in rats. Rat microvessel endothelial cells (rBMECs) were exposed to hypoxia/reoxygenation (H/R) coexisting with LPS. The results revealed that AR suppressed the excessive inflammation, restored BBB dysfunction, alleviated brain edema, decreased neutrophil infiltration, lessened neurological dysfunction, and decreased infarct rate. Further study demonstrated that the expression of nucleus nuclear factor kappa B (NF-κB), inducible nitric oxide synthase (iNOS), intercellular adhesion molecule-1 (ICAM-1), tumor necrosis factor-α (TNF-α) and interlukin-1ß (IL-1ß) were suppressed by AR via zinc finger protein A20. Besides, AR increased in vitro BBB integrity through A20. In conclusion, AR alleviated cerebral inflammatory injury through A20-NF-κB signal pathway, offering an alternative medication for stroke associated with systemic inflammatory diseases.


Asunto(s)
Antiinflamatorios/administración & dosificación , Barrera Hematoencefálica/efectos de los fármacos , Isquemia Encefálica/prevención & control , Proteínas de Unión al ADN/metabolismo , Inflamación/prevención & control , Saponinas/administración & dosificación , Accidente Cerebrovascular/prevención & control , Animales , Barrera Hematoencefálica/metabolismo , Barrera Hematoencefálica/ultraestructura , Edema Encefálico/prevención & control , Hipoxia de la Célula/efectos de los fármacos , Células Endoteliales/efectos de los fármacos , Células Endoteliales/metabolismo , Células Endoteliales/ultraestructura , Inflamación/inducido químicamente , Inflamación/metabolismo , Mediadores de Inflamación/metabolismo , Interleucina-1beta/sangre , Lipopolisacáridos , Masculino , Microvasos/efectos de los fármacos , Microvasos/ultraestructura , Infiltración Neutrófila/efectos de los fármacos , Ratas , Ratas Sprague-Dawley , Proteína 3 Inducida por el Factor de Necrosis Tumoral alfa , Factor de Necrosis Tumoral alfa/sangre
3.
Adv Exp Med Biol ; 913: 1-21, 2016.
Artículo en Inglés | MEDLINE | ID: mdl-27796877

RESUMEN

Telocytes (TCs) are identified as a peculiar cell type of interstitial cells in various organs. The typical features of TCs from the other cells are the extending cellular process as telopodes with alternation of podomeres and podoms. Before the year of 2010, TCs were considered as interstitial Cajal-like cells because of the similar morphology and immunohistochemical features with interstitial cells of Cajal which were found more than 100 years ago and considered to be pacemakers for gut motility. Subsequently, it demonstrated that TCs were not Cajal-like cells, and thus the new name "telocyte" was proposed in 2010. With the help of different techniques, e.g., transmission electron microscopy, immunohistochemistry, or omics science, TCs have been detected in various tissues and organs from different species. The pathological role of TCs in different diseases was also studied. According to observation in situ or in vitro, TCs played a vital role in mechanical support, signaling transduction, tissue renewal or repair, immune surveillance, and mechanical sensor via establishing homo- or heterogenous junctions with neighboring cells to form 3D network or release extracellular vesicles to form juxtacrine and paracrine. This review will introduce the origin, distribution, morphology, functions, omics science, methods, and interaction of TCs with other cells and provide a better understanding of the new cell type.


Asunto(s)
Linaje de la Célula/fisiología , Vesículas Extracelulares/metabolismo , Uniones Intercelulares/metabolismo , Telocitos/citología , Animales , Bibliometría , Fenómenos Biomecánicos , Comunicación Celular , Biología Computacional , Vesículas Extracelulares/inmunología , Humanos , Vigilancia Inmunológica/fisiología , Uniones Intercelulares/inmunología , Regeneración/fisiología , Transducción de Señal , Telocitos/inmunología , Telocitos/metabolismo
4.
Eur J Med Chem ; 162: 650-665, 2019 Jan 15.
Artículo en Inglés | MEDLINE | ID: mdl-30481687

RESUMEN

Glucose intolerance is associated with metabolic syndrome and type 2 diabetes mellitus (T2DM) while some new therapeutic drugs, such as rosiglitazone (Rosi), for T2DM can cause severe cardiovascular side effects. Herein we report the synthesis of Rosi-ferulic acid (FA)-nitric oxide (NO) donor trihybrids to improve glucose tolerance and minimize the side effects. In comparison with Rosi, the most active compound 21 exhibited better effects on improving glucose tolerance, which was associated with its NO production, antioxidant and anti-inflammatory activities. Furthermore, 21 displayed relatively high stability in the simulated gastrointestinal environments and human liver microsomes, and released Rosi in plasma. More importantly, 21, unlike Rosi, had little stimulatory effect on the membrane translocation of aquaporin-2 (AQP2) in kidney collecting duct epithelial cells. These, together with a better safety profile, suggest that the trihybrids, like 21, may be promising candidates for intervention of glucose intolerance-related metabolic syndrome and T2DM.


Asunto(s)
Ácidos Cumáricos/química , Intolerancia a la Glucosa/tratamiento farmacológico , Donantes de Óxido Nítrico/química , Rosiglitazona/química , Antiinflamatorios , Antioxidantes , Acuaporina 2/metabolismo , Células Cultivadas , Ácidos Cumáricos/farmacología , Ácidos Cumáricos/uso terapéutico , Diabetes Mellitus Tipo 2/tratamiento farmacológico , Diseño de Fármacos , Humanos , Túbulos Renales Colectores/citología , Túbulos Renales Colectores/metabolismo , Síndrome Metabólico/tratamiento farmacológico , Microsomas Hepáticos , Donantes de Óxido Nítrico/farmacología , Donantes de Óxido Nítrico/uso terapéutico , Rosiglitazona/farmacología , Rosiglitazona/uso terapéutico
5.
Sci Rep ; 6: 35319, 2016 10 12.
Artículo en Inglés | MEDLINE | ID: mdl-27731393

RESUMEN

Hyperlipidemia aggravates myocardial ischemia/reperfusion (MI/R) injury through stimulating excessive inflammatory response. Therefore, blockade of inflammatory signal is a potential therapeutic management for MI/R complicated with hyperlipidemia. Hydroxysafflor yellow A (HSYA, a monomer extracted from Carthamus tinctorius L.), was studied in this article to address that the regulation of inflammatory signal would alleviate MI/R combined with hyperlipidemia injury. High-fat diet induced hyperlipidemia worsened MI/R mediated heart injury (elevation of infarct size, CK-MB and LDH activity), activated TLR4 over-expression in hearts, released inflammatory cytokines (LPS, TNF-α and IL-1ß) excessively. HSYA administration suppressed the over-expression of TLR4 and alleviated heart damage caused by MI/R complicated with hyperlipidemia. Furthermore, HSYA had little influence on MI/R injury in TLR4-knockout mice, which indicated that HSYA protected MI/R through TLR4 inhibition. In vitro, hypoxia/reoxygenation (H/R) coexisting with LPS model in neonatal rat ventricular myocytes (NRVMs) induced serious damage compared with H/R injury to NRVMs. HSYA decreased excessive secretion of inflammatory cytokines, down-regulated over-expression of TLR4 and NF-κB in H/R + LPS injured NRVMs. In conclusion, HSYA alleviated myocardial inflammatory injury through suppressing TLR4, offering an alternative medication for MI/R associated with hyperlipidemia.


Asunto(s)
Antiinflamatorios/farmacología , Chalcona/análogos & derivados , Hiperlipidemias/tratamiento farmacológico , Daño por Reperfusión Miocárdica/tratamiento farmacológico , Quinonas/farmacología , Transducción de Señal/efectos de los fármacos , Receptor Toll-Like 4/antagonistas & inhibidores , Animales , Chalcona/farmacología , Dieta Alta en Grasa/efectos adversos , Regulación de la Expresión Génica , Hiperlipidemias/complicaciones , Hiperlipidemias/etiología , Hiperlipidemias/genética , Interleucina-1beta/antagonistas & inhibidores , Interleucina-1beta/genética , Interleucina-1beta/inmunología , L-Lactato Deshidrogenasa/genética , L-Lactato Deshidrogenasa/inmunología , Lipopolisacáridos/inmunología , Lipopolisacáridos/metabolismo , Masculino , Ratones , Ratones Noqueados , Daño por Reperfusión Miocárdica/complicaciones , Daño por Reperfusión Miocárdica/genética , Miocitos Cardíacos/efectos de los fármacos , Miocitos Cardíacos/inmunología , Miocitos Cardíacos/patología , FN-kappa B/antagonistas & inhibidores , FN-kappa B/genética , FN-kappa B/inmunología , Cultivo Primario de Células , Ratas , Ratas Wistar , Receptor Toll-Like 4/deficiencia , Receptor Toll-Like 4/genética , Receptor Toll-Like 4/inmunología , Factor de Necrosis Tumoral alfa/antagonistas & inhibidores , Factor de Necrosis Tumoral alfa/genética , Factor de Necrosis Tumoral alfa/inmunología
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