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木犀草素通过抑制 NF-κB 信号通路防止 LPS 诱导的心肌细胞 TNF-α 表达。

Luteolin prevents LPS-induced TNF-α expression in cardiac myocytes through inhibiting NF-κB signaling pathway.

机构信息

Department of Pharmacy, Shaoyang Medical College, No.18 West of Baoqing Road, Daxiang District, Shaoyang, 422000, Hunan, China.

出版信息

Inflammation. 2011 Dec;34(6):620-9. doi: 10.1007/s10753-010-9271-7.

DOI:10.1007/s10753-010-9271-7
PMID:21076936
Abstract

Luteolin, a plant flavonoid, has been shown to suppress inflammatory responses; however, the mechanism of luteolin on cardiac myocyte inflammation is still unknown. Because tumor necrosis factor-α (TNF-α), an inflammatory cytokine, is elevated in the failing heart and exerts multiple potentially harmful effects on cardiac myocytes, we therefore sought to examine the effects of luteolin on the expression of TNF-α in neonatal rat cardiac myocytes. In the present study, enzyme-linked immunosorbent assay (ELISA), real-time PCR, immunoblot, immunochemistry staining, and electrophoretic mobility shift assays (EMSA) were performed. ELISA assay showed that luteolin decreased lipopolysaccharide (LPS)-induced production of TNF-α in the medium. Real-time PCR assay confirmed that luteolin also inhibited LPS-induced increase in TNF-α mRNA in myocytes. Furthermore, immunoblot and immunochemistry staining assays represented that luteolin blocked LPS-induced IκB-β degradation and NF-κB p65 subunit nuclear translocation. In addition, EMSA demonstrated that luteolin reduced LPS-induced NF-κB DNA binding activity. Luteolin protects against LPS-induced TNF-α expression via inhibition of the NF-κB signaling pathway, suggesting that luteolin may be a potential therapeutic agent for the treatment of inflammation-related myocardial diseases.

摘要

木犀草素是一种植物类黄酮,已被证明能抑制炎症反应;然而,木犀草素对心肌细胞炎症的作用机制尚不清楚。由于肿瘤坏死因子-α(TNF-α)是一种炎症细胞因子,在衰竭的心脏中升高,并对心肌细胞产生多种潜在的有害影响,因此我们试图研究木犀草素对新生大鼠心肌细胞中 TNF-α表达的影响。在本研究中,进行了酶联免疫吸附测定(ELISA)、实时 PCR、免疫印迹、免疫化学染色和电泳迁移率变动分析(EMSA)。ELISA 检测表明,木犀草素可减少脂多糖(LPS)诱导的心肌细胞培养基中 TNF-α的产生。实时 PCR 检测证实,木犀草素还可抑制 LPS 诱导的心肌细胞 TNF-α mRNA 的增加。此外,免疫印迹和免疫化学染色检测表明,木犀草素可阻止 LPS 诱导的 IκB-β降解和 NF-κB p65 亚基核转位。此外,EMSA 表明,木犀草素可降低 LPS 诱导的 NF-κB DNA 结合活性。木犀草素通过抑制 NF-κB 信号通路来保护 LPS 诱导的 TNF-α表达,提示木犀草素可能是治疗炎症相关心肌疾病的潜在治疗药物。

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