Is HMGB1 a New Indirect Marker for Revealing Fibrosis in Chronic Hepatitis and a New Therapeutic Target in Treatment?
Is HMGB1 a New Indirect Marker for Revealing Fibrosis in Chronic Hepatitis and a New Therapeutic Target in Treatment?
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DOI：
10.1089/vim.2010.0080
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发表时间：
2010-12-01
期刊：
影响因子：
2.2
通讯作者：
Uslu, Hakan
中科院分区：
文献类型：
--
作者：
Albayrak, Ayse;Uyanik, Muhammet H.;Uslu, Hakan
在慢性乙型肝炎病毒感染中，包括促炎性细胞因子在内的炎症相关细胞因子参与了肝纤维化的发生发展。肝脏是许多可能影响肝功能的细胞因子的来源。高迁移率族蛋白1(HMGB1)是一种炎性细胞因子。HMGB1存在于所有哺乳动物细胞的细胞核中，通过各种细胞的主动分泌和坏死细胞的被动释放来释放。在这里，我们探讨HMGB1血浆水平与肝纤维化的关系。慢性乙肝患者血清HMGB1水平、HBVDNA和ALT值显著高于对照组。此外，低纤维化患者(纤维化评分1-2)的HMGB1血清水平显著高于高纤维化患者(纤维化评分3-4)。在目前的研究中，我们已经证明HMGB1是一种非侵入性的、可重复的、简便的标记物，用于区分慢性乙肝患者的晚期纤维化和低纤维化。我们认为，抑制HMGB1可能会减少炎症、细胞凋亡和纤维化，并可能阻止慢性肝病的进展。此外，我们认为，抑制HMGB1可以防止慢性肝病患者肝纤维化的进展，这种物质可以作为慢性乙肝治疗的一种新手段。
In chronic hepatitis B virus (HBV) infection, inflammation-associated cytokines including proinflammatory cytokines are involved in the development and progression of liver fibrosis. The liver is a source of many cytokines that may influence liver function. High-mobility group box 1 (HMGB1) was identified as an inflammatory cytokine. HMGB1 is present in nuclei of all mammalian cells and is released both through active secretion from various cells and by passive release from necrotic cells. Here we explore the relationship between HMGB1 plasma levels and liver fibrosis. HMGB1 serum levels, HBV-DNA, and ALT values were significantly higher in patients with chronic HBV than in controls. In addition, HMGB1 serum levels were significantly higher in patients with low fibrosis (fibrosis score 1-2) compared to those with high fibrosis (fibrosis score 3-4). In the present study, we have shown that HMGB1 is a noninvasive, repeatable, and convenient marker for distinguishing advanced fibrosis from low fibrosis in chronic HBV patients. We believe that the inhibition of HMGB1 may reduce inflammation, apoptosis, and fibrosis, and may stop the progression of chronic liver disease. Furthermore, we are of the opinion that fibrotic progression in chronic liver patients may be prevented by the inhibition of HMGB1, and that this substance can be a new means of following chronic HBV treatment.