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Bcl-2 is a negative regulator of interleukin-1β secretion in murine macrophages in pharmacological-induced apoptosis

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Bcl-2 is a negative regulator of interleukin-1β secretion in murine macrophages in pharmacological-induced apoptosis

dc.contributor.author	Escandell, JM	es_ES
dc.contributor.author	Recio Iglesias, María del Carmen	es_ES
dc.contributor.author	Giner Pons, Rosa María	es_ES
dc.contributor.author	Máñez, S.	es_ES
dc.contributor.author	Ríos Cañavate, José Luis	es_ES
dc.date.accessioned	2015-06-29T10:34:09Z
dc.date.available	2015-06-29T10:34:09Z
dc.date.issued	2010	es_ES
dc.identifier.citation	British Journal of Pharmacology Vol. 160 Issue 7: pp. 1844-1856	es_ES
dc.identifier.uri	http://hdl.handle.net/10550/44803
dc.description.abstract	BACKGROUND AND PURPOSECucurbitacin R, a natural anti-inflammatory product, has been shown to exhibit activity against both adjuvant-induced arthritis and delayed-type hypersensitivity reactions induced by various agents. Previous studies have demonstrated that the effects of cucurbitacin R stem from its inhibition of both cytokine production and lymphocyte proliferation.EXPERIMENTAL APPROACHESEffects of cucurbitacin R were investigated on lipopolysaccharide-stimulated RAW 264.7 cells. Cell cycle evolution was analysed by flow cytometry, detection of apoptosis by DNA ladder, Bcl-2, p21, p53, Bax, cleaved caspase-1 (p10), caspase-9, and caspase-3, cleaved caspase (p17) and interleukin-1β detection was followed by Western blot analysis and mRNA expression with quantitative real time reverse transcription-polymerase chain reaction (qRT-PCR).KEY RESULTSCucurbitacin R was found to induce apoptosis in lipopolysaccharide-stimulated RAW 264.7 macrophages through the inhibition of Bcl-2 expression, which regulates pro-inflammatory caspase-1 activation and interleukin-1β release. Also, cucurbitacin R arrested the cell cycle in the G2/M phase and increased the subG0 population in lipopolysaccharide-stimulated RAW 264.7 macrophages. Moreover, it increased the expression of proteins p53 and p21, down-regulated the expression of Bcl-2, activated the activity of caspase-1 and augmented the production of interleukin-1β. Finally, the transfection of RAW 264.7 macrophages with a Bcl-2 expression plasmid produced the inhibition of apoptosis and caspase-1 activation/interleukin-1β release induced by cucurbitacin R in RAW 264.7 cells.CONCLUSIONS AND IMPLICATIONSTaken together, these results point to a new apoptotic process in which interleukin-1β release is directly regulated by Bcl-2 status; this contributes to the evidence that apoptotic processes do not induce inflammation.	es_ES
dc.subject	apoptosis	es_ES
dc.subject	cucurbitacin R	es_ES
dc.subject	interleukin-1β	es_ES
dc.subject	Bcl-2	es_ES
dc.subject	caspase-1	es_ES
dc.subject	RAW 264.7 macrophages	es_ES
dc.title	Bcl-2 is a negative regulator of interleukin-1β secretion in murine macrophages in pharmacological-induced apoptosis	es_ES
dc.type	journal article	es_ES
dc.identifier.doi	10.1111/j.1476-5381.2010.00856.x	es_ES
dc.identifier.idgrec	064920	es_ES