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1.
Zhongguo Zhong Yao Za Zhi ; 40(2): 180-4, 2015 Jan.
Artículo en Zh | MEDLINE | ID: mdl-26080541

RESUMEN

Macrophages are heterogeneous and diversified, and can be polarized into different phenotypes in various microenvironments and physiological or pathological conditions. Major macrophage subpopulations including classically activated(M1) and alternatively activated(M2) macrophages, which represent different surface receptors, secret different cytokines and chemokines, are regulated by different signal paths of transcriptions and epigenetic levels, and play distinctive roles in tumor progress. TCMs may improve the microenvironment by regulating phenotype polarization of macrophages. So far, specific biomarkers and polarized molecules mechanisms generated through the macrophage polarization approach are still unclear. In this article, we merely summarize the advance in domestic and foreign studies on phenotype polarization of macrophages and regulatory mechanisms and look into the future of intervention with TCMs.


Asunto(s)
Macrófagos/fisiología , Medicina Tradicional China , Neoplasias/tratamiento farmacológico , Neoplasias/inmunología , Animales , Polaridad Celular , Humanos , Fenotipo
2.
Zhongguo Zhong Yao Za Zhi ; 40(22): 4475-81, 2015 Nov.
Artículo en Zh | MEDLINE | ID: mdl-27097427

RESUMEN

To study the mechanisms of total flavonoid from Glycyrrhizae Radix et Rhizoma (TFGR) and its ingredient isoliquiritigenin (ISL) on their regulation of M2 phenotype polarization of macrophages. IL-4 (60 µg x L(-1)) induced RAW264.7 cells for 6 h to establish the M2 macrophage model. TFGR and ISL restrained breast cancer cells migration with the aid of M2 macrophages in vitro. TFGR and ISL inhibited gene and protein expression of Arg-1, up-regulated gene of HO-1 and protein expression of iNOS, enhanced the expression of microRNA 155 and its target gene SHIP1, meanwhile down-regulated.the phosphorylation of STAT3 and STAT6. So TFGR and ISL were the bioactive fraction and ingredient in Glycyrrhizae Radix et Rhizoma to reverse M2 phenotype macrophages polarization. TFGR and ISL inhibited the promotion of M2 macrophages to breast cancer cells migration in vitro, STAT signal pathways and miR155 were partly involved.


Asunto(s)
Chalconas/farmacología , Flavonoides/farmacología , Glycyrrhiza/química , Macrófagos/efectos de los fármacos , Animales , Línea Celular Tumoral , Movimiento Celular/efectos de los fármacos , Polaridad Celular/efectos de los fármacos , Interleucina-4/genética , Interleucina-4/metabolismo , Macrófagos/citología , Macrófagos/metabolismo , Ratones , Células RAW 264.7 , Rizoma/química
3.
Artículo en Inglés | MEDLINE | ID: mdl-24744815

RESUMEN

Artemisia anomala S. Moore has been widely used in China to treat inflammatory diseases for hundreds of years. However, mechanisms associated with its anti-inflammatory effect are not clear. In this study, we prepared ethyl acetate, petroleum ether, n-BuOH, and aqueous extracts from ethanol extract of Artemisia anomala S. Moore. Comparing anti-inflammatory effects of these extracts, we found that ethyl acetate extract of this herb (EAFA) exhibited the strongest inhibitory effect on nitric oxide (NO) production in LPS/IFN γ -stimulated RAW264.7 cells. EAFA suppressed the production of NO in a time- and dose-dependent manner without eliciting cytotoxicity to RAW264.7 cells. To understand the molecular mechanism underlying EAFA's anti-inflammatory effect, we showed that EAFA increased total cellular anti-oxidant capacity while reducing the amount of inducible nitric oxide synthase (iNOS) in stimulated RAW264.7 cells. EAFA also suppressed the expression of IL-1 ß and IL-6, whereas it elevates the level of heme oxygenase-1. These EAFA-induced events were apparently associated with NF- κ B and MAPK signaling pathways because the DNA binding activity of p50/p65 was impaired and the activities of both ERK and JNK were decreased in EFEA-treated cells comparing to untreated cells. Our findings suggest that EAFA exerts its anti-inflammatory effect by inhibiting the expression of iNOS.

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