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首页> 外文期刊>Clinica chimica acta: International journal of clinical chemistry and applied molecular biology >Captopril inhibits the production of tumor necrosis factor-alpha by human mononuclear cells in patients with congestive heart failure.
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Captopril inhibits the production of tumor necrosis factor-alpha by human mononuclear cells in patients with congestive heart failure.

机译:卡托普利抑制充血性心力衰竭患者的人单核细胞产生肿瘤坏死因子-α。

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摘要

To study the effects of captopril on tumor necrosis factor-alpha produced by peripheral blood mononuclear cells (PBMC) of patients with congestive heart failure (CHF), we determined the TNF-alpha concentrations of culture supernatants of PBMC with and without catopril in 74 CHF patients with various heart diseases. The results showed that the supernatants concentrations of TNF-alpha in cultured PBMC (PBMC-TNF-alpha) were significantly increased in non-cachetic and cachetic CHF patients, and even higher in cachetic CHF patients, as compared with the controls (i.e., patients with New York Heart Association CHF classification I). The PBMC-TNF-alpha was significantly inhibited by captopril. These results demonstrate that the expression of TNF-alpha in PBMC is increased and can be inhibited by captopril in patients with CHF, especially in those accompanied by cachexia. This suggests that the immunomodulatory effects of captopril may contribute to its beneficial effects in heart failure patients.
机译:为了研究卡托普利对充血性心力衰竭(CHF)患者外周血单个核细胞(PBMC)产生的肿瘤坏死因子-α的影响,我们测定了有或没有卡托普利的PBMC培养上清液的TNF-α浓度在74 CHF患有各种心脏病的患者。结果显示,与对照组(即,患者)相比,在非恶性和恶性CHF患者中,培养的PBMC中的TNF-α上清液浓度(PBMC-TNF-α)显着增加,在恶性CHF患者中甚至更高。纽约心脏协会CHF分类I)。 PBMC-TNF-α被卡托普利明显抑制。这些结果表明,在CHF患者中,特别是在伴随恶病质的患者中,PBMC中TNF-α的表达增加并且可以被卡托普利抑制。这表明卡托普利的免疫调节作用可能有助于其对心力衰竭患者的有益作用。

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