Stoyanova Irina Ivanova
Department of Anatomy, Faculty of Medicine, Thracian University, BG-6010 Stara Zagora, Bulgaria.
Rom J Gastroenterol. 2004 Sep;13(3):203-9.
Chronic liver diseases commonly result in liver fibrosis, and eventually liver cirrhosis. In the last decade, a new theory explaining liver fibrosis has been established. Accordingly, the development of liver fibrosis due to chronic liver diseases is thought to be mediated by inflammatory cells. They release fibrogenic mediators such as transforming growth factors (TGF)-beta, which are considered to be responsible for the activation and transformation of fat-storing cells. Recently, the involvement of mast cells and peripheral and autonomic nervous system in the fibrogenesis has been suggested. This study was aimed to establish the presence and distribution of mast cells and nerve fibers in the rat liver in the light of their implication in liver inflammatory and fibrotic disorders. Mast cells and afferent (sensory) fibers were detected immunohistochemically. An immunofluorescent method was applied to demonstrate tryptase and serotonin (SER) in the mast cells, while the primary sensory neuronal processes were identified by using antibodies against their marker calcitonin gene-related peptide (CGRP) and the proinflammatory mediator substance P (SP). The portal tracts and fibrous septa contained numerous mast cells, which exhibited strong immuno-reactivity to tryptase and SER. SER-positive nerve fibers were also found. It is generally accepted that no nerve fibers are present in the hepatic lobules, but the current investigation clearly demonstrates availability of CGRP-, SP, and SER-immunoreactive nerve fibers there. Our results indicate that in the rat liver portal tracts and hepatic lobules there are numerous mast cells, sensory and autonomic nerve fibers, which may be involved in liver injury by the inflammatory mediators they release.
慢性肝病通常会导致肝纤维化，最终发展为肝硬化。在过去十年中，一种解释肝纤维化的新理论得以确立。据此，慢性肝病所致肝纤维化的发展被认为是由炎症细胞介导的。它们释放诸如转化生长因子（TGF）-β等促纤维化介质，这些介质被认为是导致贮脂细胞活化和转化的原因。最近，有人提出肥大细胞以及外周和自主神经系统参与了肝纤维化的形成。本研究旨在根据肥大细胞和神经纤维在肝脏炎症和纤维化疾病中的作用，确定其在大鼠肝脏中的存在情况和分布。采用免疫组织化学方法检测肥大细胞和传入（感觉）纤维。应用免疫荧光法检测肥大细胞中的类胰蛋白酶和5-羟色胺（SER），同时使用抗其标志物降钙素基因相关肽（CGRP）和促炎介质P物质（SP）的抗体来识别初级感觉神经元突起。门管区和纤维间隔含有大量肥大细胞，它们对类胰蛋白酶和SER表现出强烈的免疫反应性。还发现了SER阳性神经纤维。一般认为肝小叶中不存在神经纤维，但当前研究清楚地表明肝小叶中存在CGRP、SP和SER免疫反应性神经纤维。我们的结果表明，在大鼠肝脏的门管区和肝小叶中有大量肥大细胞、感觉神经纤维和自主神经纤维，它们可能通过释放炎症介质参与肝损伤。
