Abstract：
The development of amoebic liver abscess (ALA) leads to liver necrosis, accompanied by an exacerbated inflammatory response and the formation of multiple granulomas. Adequate management of the infection through the administration of treatment and the timely response of the organ to the damage allows the injury to heal with optimal regeneration without leaving scar tissue, which does not occur in other types of damage such as viral hepatitis that may conducts to fibrosis or cirrhosis. The Hedgehog signaling pathway (Hh) is crucial in the embryonic stage, while in adults it is usually reactivated in response to acute or chronic injuries, regeneration, and wound healing. In this work, we characterized Hh in experimental hepatic amoebiasis model, with the administration of treatment with metronidazole, as well as a pathway inhibitor (cyclopamine), through histological and immunohistochemical analyses including an ultrastructure analysis through transmission electron microscopy. The results showed an increase in the percentage of lesions obtained, a decrease in the presence of newly formed hepatocytes, a generalized inflammatory response, irregular distribution of type I collagen accompanied by the presence of fibroblast-type cells and a decrease in effector cells of this pathway. These results constitute the first evidence of the association of the activation of Hh with the liver regeneration process in experimental amebiasis.
摘要：
阿米巴肝脓肿（ALA）的发展导致肝坏死，伴随着加剧的炎症反应和多发性肉芽肿的形成。通过治疗和器官对损伤的及时反应来充分管理感染，可以使损伤以最佳的再生方式愈合，而不会留下疤痕组织。这不会发生在其他类型的损害，如病毒性肝炎，可能导致纤维化或肝硬化。Hedgehog信号通路（Hh）在胚胎阶段至关重要，而在成人中，它通常会在急性或慢性损伤时重新激活，再生,伤口愈合。在这项工作中,我们在实验性肝阿米巴病模型中表征了Hh，随着甲硝唑的治疗，以及途径抑制剂（环巴胺），通过组织学和免疫组织化学分析，包括通过透射电子显微镜的超微结构分析。结果显示获得的病变百分比增加，减少新形成的肝细胞的存在，广泛的炎症反应，I型胶原蛋白的不规则分布伴随着成纤维细胞型细胞的存在和该途径的效应细胞的减少。这些结果构成了实验性阿米巴病中Hh活化与肝再生过程相关的第一个证据。
