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酸性多糖逆转慢性疾病贫血涉及抑制炎症性hepcidin 和 NF-B 激活。

Acidic Polysaccharide from Reverses Anemia of Chronic Disease Involving the Suppression of Inflammatory Hepcidin and NF-B Activation.

机构信息

Hubei Key Laboratory of Natural Medicinal Chemistry and Resource Evaluation, Tongji Medical College of Huazhong University of Science and Technology, No. 13, Hangkong Road, Wuhan 430030, China.

Union Hospital of Tongji Medical College, Huazhong University of Science and Technology, No. 1277, Jiefang Road, Wuhan 430022, China.

出版信息

Oxid Med Cell Longev. 2017;2017:7601592. doi: 10.1155/2017/7601592. Epub 2017 Sep 24.

Abstract

Anemia of chronic disease (ACD) is the second most prevalent anemia and frequently occurs in patients with acute or chronic immune activation. In the current study, we evaluated the therapeutic efficacy of polysaccharide (ASP) against ACD in rats and the potential mechanisms involved. The results showed that ASP inhibited inflammatory hepcidin in both HepG2 cells and ACD rats by blocking the IL-6/STAT3 and BMP/SMAD pathways. In ACD rats, the administration of ASP increased ferroportin expression, mobilized iron from the liver and spleen, increased serum iron levels, caused an elevation of serum EPO, and effectively relieved the anemia. Furthermore, ASP inhibited NF-B p65 activation via the IB kinases- (IKKs-) IB pathway, thereby reducing the secretion of interleukin-6 (IL-6) and TNF-, which is known to inhibit erythropoiesis. Our findings indicate that ASP is a potential treatment option for patients suffering from ACD.

摘要

慢性病性贫血(ACD)是第二大常见贫血,常发生于急性或慢性免疫激活的患者中。在本研究中,我们评估了多糖(ASP)对大鼠 ACD 的治疗效果及其潜在的作用机制。结果表明,ASP 通过阻断 IL-6/STAT3 和 BMP/SMAD 途径,抑制 HepG2 细胞和 ACD 大鼠中的炎症性铁调素。在 ACD 大鼠中,ASP 的给药增加了铁蛋白的表达,从肝脏和脾脏中动员铁,增加血清铁水平,导致血清 EPO 升高,并有效缓解贫血。此外,ASP 通过 IKKs-IB 途径抑制 NF-B p65 激活,从而减少已知抑制红细胞生成的白细胞介素 6(IL-6)和 TNF-α的分泌。我们的研究结果表明,ASP 是治疗 ACD 患者的一种潜在治疗选择。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/21e8/5632906/34361933c7a4/OMCL2017-7601592.001.jpg

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