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1.
Complement Ther Med ; 82: 103037, 2024 Jun.
Artículo en Inglés | MEDLINE | ID: mdl-38582376

RESUMEN

BACKGROUND AND PURPOSE: Rheumatoid arthritis (RA) is called "immortal cancer", and it affects the quality of life, disability rate and even the survival of patients. This study aimed to observe the clinical efficacy, and adverse reactions of intradermal acupuncture (IA) in the treatment of RA patients with liver and kidney deficiency syndrome. MATERIALS AND METHODS: 132 RA patients were split into an IA group and a sham IA group at a 1:1 ratio. Both groups were assessed before and after the intervention with the assessments: a traditional Chinese medicine (TCM) syndrome evaluation, the Health Assessment Questionnaire (HAQ), the Disease Activity Score 28 (DAS28) and serum C-reactive protein (CRP). RESULTS: There was a statistically significant difference in TCM syndrome evaluation, HAQ, DAS28, and CRP between both groups before and after treatment (P < 0.01). The improvement of TCM syndrome evaluation (95% CI [1.14(0.38-1.89)]; P = 0.001), HAQ (95% CI [2.00(1.00-3.00)]; P = 0.003), and DAS28 (95% CI [0.11(0.02-0.20)]; P = 0.021) in the IA group was more obvious than that in the sham IA group (P < 0.05), except for CRP (95% CI [0.50(- 2.09 to 7.08)], P = 0.786). The difference in CRP outcome changes between the two groups was not statistically significant (P > 0.05). Both groups had comparable results in the implementation of RA in the upper and lower extremity acupoints and did not differ due to different sites (IA group: P = 0.852; sham IA group: P = 0.861). The comparison of effective rate of the upper limb as well as that of the lower limb was statistically significant (P = 0.001). Besides, patients reported no adverse effects. CONCLUSION: The IA intervention was associated with a promising effect on the decrease in RA disease activity and delayed overall disease progression.


Asunto(s)
Terapia por Acupuntura , Artritis Reumatoide , Medicina Tradicional China , Humanos , Femenino , Masculino , Terapia por Acupuntura/métodos , Persona de Mediana Edad , Artritis Reumatoide/terapia , Artritis Reumatoide/complicaciones , Adulto , Medicina Tradicional China/métodos , Proteína C-Reactiva/análisis , Calidad de Vida , Hígado , Riñón/fisiopatología , Resultado del Tratamiento , Anciano
2.
J Sci Food Agric ; 99(8): 3967-3975, 2019 Jun.
Artículo en Inglés | MEDLINE | ID: mdl-30719705

RESUMEN

BACKGROUND: As a result of a low bioavailability, the majority of Cyclocarya paliurus flavonoids (CPF) remain in the large intestine where they accumulate to exert a modulatory effect on the intestinal micro-ecology. Therefore, the present study investigated the modulatory effect of CPF on intestinal microbiota. RESULTS: CPF dramatically ameliorated the obesity-induced gut dysbiosis. A significant decrease (P < 0.05) was observed in the ratio of Firmicutes/Bacteroidetes after CPF treatment for 8 weeks. Moreover, Kyoto Encyclopedia of Genes and Genomes pathways of biosynthesis of amino acids, the two-component system and ATP-binding cassette transporters enriched the most differentially expressed genes after CPF intervention. CONCLUSION: The results of the present study indicate that CPF might have prebiotic-like activity and could be used as a functional food component with potential therapeutic utility to prevent obesity-related metabolic disorders by manipulating the gut flora and affecting certain metabolic pathways, thus contributing to the improvement of human health. © 2019 Society of Chemical Industry.


Asunto(s)
Bacterias/genética , Flavonoides/administración & dosificación , Microbioma Gastrointestinal/efectos de los fármacos , Intestinos/microbiología , Juglandaceae/química , Obesidad/tratamiento farmacológico , Extractos Vegetales/administración & dosificación , Adulto , Animales , Bacterias/clasificación , Bacterias/efectos de los fármacos , Bacterias/aislamiento & purificación , Dieta Alta en Grasa/efectos adversos , Modelos Animales de Enfermedad , Disbiosis/tratamiento farmacológico , Disbiosis/metabolismo , Disbiosis/microbiología , Femenino , Flavonoides/análisis , Humanos , Masculino , Metagenómica , Ratones , Ratones Endogámicos C57BL , Obesidad/microbiología , Extractos Vegetales/análisis
3.
Medicine (Baltimore) ; 97(51): e13526, 2018 Dec.
Artículo en Inglés | MEDLINE | ID: mdl-30572452

RESUMEN

BACKGROUND: Influenza, measles, and mumps are common viral infectious diseases in Mongolia. The traditional Mongolian medicine (TMM) classified them as warm disease, and still plays a major role in the diagnoses and treatments. METHODS: To interpret the connotation of the complex theoretical system in TMM with scientific technique, in this study, a high throughput mass spectrometry was used to identify potential protein markers of TMM symptom types. Fifty venous blood samples were drawn from influenza, measles and mumps patients. Differential proteins between samples of patients diagnosed as immature and mature heat in TMM were detected by mass spectrometry. RESULTS: After proteomics analysis, 1500 proteins and 7619 polypeptides were identified and 1323 in total showed differential expression between those 2 symptom types; then enrichment analysis of the differentially expressed proteins revealed the significant biological functions related to the differentially expressed proteins, including cardiomyopathy, several bacterial and parasitic infections, bacterial invasion of epithelial cells, insulin signaling pathway, and regulation of actin cytoskeleton. The network analysis showed that FBP2 and Talin-1 were critical points and might determine the evolution directions of TMM warm disease symptom. CONCLUSIONS: This study suggests that the identified core differential proteins may be regarded as potential biomarkers, and benefit to evaluate the evolutionary tendency of TMM warm disease symptoms.


Asunto(s)
Fructosa-Bifosfatasa/sangre , Gripe Humana/diagnóstico , Sarampión/diagnóstico , Medicina Tradicional Mongoliana/métodos , Paperas/diagnóstico , Talina/sangre , Adolescente , Adulto , Anciano , Biomarcadores/sangre , Ensayos Analíticos de Alto Rendimiento , Humanos , Espectrometría de Masas , Persona de Mediana Edad , Proteómica , Adulto Joven
4.
Planta Med ; 83(1-02): 51-56, 2017 Jan.
Artículo en Inglés | MEDLINE | ID: mdl-27224270

RESUMEN

Arctigenin is a phenylpropanoid dibenzylbutyrolactone lignan compound possessing antitumor, anti-inflammatory, anti-influenza, antioxidant, antibacterial, and hypoglycaemic activities. Our previous study demonstrated that arctigenin exerts neuroprotective effects both in vitro and in vivo in a Parkinson's disease model. However, the exact mechanism through which arctigenin improves amyloid beta-induced memory impairment by inhibiting the production of the hyperphosphorylated tau protein is unknown. Amyloid ß1-42 was slowly administered via the intracerebroventricular route in a volume of 3 µL (≈ 410 pmmol/mouse) to mice. The mice were administered arctigenin (10, 40, or 150 mg/kg) or vehicle starting from the second day after amyloid ß1-42 injection to the end of the experiment. Behavioural tests were performed from days 9 to 15. On day 16 after the intracerebroventricular administration of amyloid ß1-42, the mice were sacrificed for biochemical analysis. Arctigenin (10-150 mg/kg) significantly attenuated the impairment of spontaneous alternation behaviours in the Y-maze task, decreased the escape latency in the Morris water maze test, and increased the swimming times and swimming distances to the platform located in the probe test. Arctigenin attenuated the level of phosphorylated tau at the Thr-181, Thr-231, and Ser-404 sites in the hippocampus, and increased the phosphorylation levels of phosphatidylinositol-3-kinase, threonine/serine protein kinase B, and glycogen synthase kinase-3ß. Arctigenin effectively provides protection against learning and memory deficits and in inhibits hyperphosphorylated tau protein expression in the hippocampus. The possible mechanism may occur via the phosphatidylinositol-3-kinase/protein kinase B-dependent glycogen synthase kinase-3ß signalling pathway.


Asunto(s)
Enfermedad de Alzheimer/tratamiento farmacológico , Furanos/farmacología , Lignanos/farmacología , Trastornos de la Memoria/tratamiento farmacológico , Fármacos Neuroprotectores/farmacología , Enfermedad de Alzheimer/inducido químicamente , Péptidos beta-Amiloides/efectos adversos , Animales , Modelos Animales de Enfermedad , Femenino , Furanos/química , Glucógeno Sintasa Quinasa 3 beta/metabolismo , Hipocampo/efectos de los fármacos , Hipocampo/metabolismo , Lignanos/química , Masculino , Aprendizaje por Laberinto/efectos de los fármacos , Trastornos de la Memoria/inducido químicamente , Ratones , Fármacos Neuroprotectores/química , Fosfatidilinositol 3-Quinasa/metabolismo , Fosforilación/efectos de los fármacos , Transducción de Señal/efectos de los fármacos , Proteínas tau/metabolismo
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