Tianjin Key Laboratory on Technologies Enabling Development of Clinical Therapeutics and Diagnostics, School of Pharmacy, Tianjin Medical University, Tianjin, 300070, China.
Pharmacy Department, Tanggu Hospital of Infectious Diseases of Tianjin Binhai New Area, Tianjin, 300454, China.
Inflammation. 2017 Dec;40(6):1959-1966. doi: 10.1007/s10753-017-0636-z.
In the present study, we investigated the anti-inflammatory effect of roburic acid on production of nitric oxide (NO) and interlukin-6 (IL-6) in lipopolysaccharide (LPS)-stimulated RAW264.7 macrophage cells. We found that roburic acid reduced production of NO and IL-6, and the expression of inducible nitric oxide synthases (iNOS). Meanwhile, phosphorylation of inhibitor of κBα (IκBα) and IκB kinase α/β (IKKα/β), as well as translocation of nuclear factor-κB (NF-κB) to the nucleus, was suppressed by roburic acid treatment. In addition, phosphorylation of mitogen-activated protein kinase (MAPKs) including p38 and c-Jun-NH-terminal kinase (JNK) was inhibited. Roburic acid exhibited inhibitory activities on production of NO and IL-6 via blocking IKK/IκB/NF-κB and MAPKs pathway, suggesting the potential application as a drug candidate for therapy of inflammatory diseases.
在本研究中，我们研究了熊果酸对脂多糖（LPS）刺激的 RAW264.7 巨噬细胞细胞中一氧化氮（NO）和白细胞介素-6（IL-6）产生的抗炎作用。我们发现熊果酸降低了 NO 和 IL-6 的产生，以及诱导型一氧化氮合酶（iNOS）的表达。同时，熊果酸处理抑制了核因子-κB（NF-κB）向核内的易位，以及抑制κB 激酶α/β（IKKα/β）和 IκBα 的磷酸化。此外，丝裂原激活的蛋白激酶（MAPKs）包括 p38 和 c-Jun-NH-末端激酶（JNK）的磷酸化也被抑制。熊果酸通过阻断 IKK/IκB/NF-κB 和 MAPKs 途径来抑制 NO 和 IL-6 的产生，表明其作为治疗炎症性疾病的药物候选物的潜力。
