Delgado-Venegas Catalina Soledad, Martínez-Hernández Sandra Luz, Cervantes-García Daniel, Montes de Oca-Luna Roberto, de Jesús Loera-Arias María, Mata-Martínez María Guadalupe, Ventura-Juárez Javier, Muñoz-Ortega Martín Humberto
Center for Basic Sciences, Department of Morphology, Autonomous University of Aguascalientes, Aguascalientes 20131, Mexico.
National Council of Science and Technology, Center for Basic Sciences, Department of Microbiology, Autonomous University of Aguascalientes, Aguascalientes 20131, Mexico.
Exp Ther Med. 2021 Apr;21(4):339. doi: 10.3892/etm.2021.9770. Epub 2021 Feb 10.
Hepatic cirrhosis is a chronic disease that affects one fifth of the World's population and is the third leading cause of death in Mexico. Attempts have been made to develop treatments for this hepatic cirrhosis, which include manipulating the intestinal microbiota and thus decreasing the early inflammatory response. The microbiota is reportedly altered in patients with cirrhosis. Due to its immunomodulatory properties and its ability to survive in the gastrointestinal tract, () has been used as a therapeutic measure in inflammatory disorders of the colon. The objective of the present study was to evaluate the efficacy of the probiotic NZ9000 in preventing tetrachloromethane (CCl)-induced experimental hepatic fibrosis. The following 4 groups were included in the experimental stage (n=5): i) Control group; ii) group; iii) CCl group; and iv) -CCl group. For the first 2 weeks, was orally administered to the and -CCl groups; CCl was then peritoneally administered to the lactis-CCl group for a further 4 weeks (in addition to the probiotic), while the group received the probiotic only. For the CCl group, CCl was administered for 4 weeks. The experimental groups were all compared with the control group and the + CCl group. Tissue samples were analyzed histologically and biochemically, and the gene expression levels of interleukin (IL)-1, IL-10 and forkhead box protein P3 (FoxP3) were determined. decreased hepatic cirrhosis by preventing steatosis and fibrosis, and by reducing the levels of AST and ALT. Subchronic CCl injury induced upregulation of the IL-1β gene in the liver, which was decreased by . It was also found that the group treated with showed increased expression of Foxp3 in the liver and IL-10 in the gut. These results suggested that oral administration of may be a potential probiotic to prevent or protect against CCl-induced liver injury.
肝硬化是一种影响全球五分之一人口的慢性疾病，是墨西哥第三大死因。人们一直在尝试开发针对这种肝硬化的治疗方法，其中包括操纵肠道微生物群，从而减少早期炎症反应。据报道，肝硬化患者的微生物群会发生改变。由于其免疫调节特性及其在胃肠道中存活的能力，（）已被用作结肠炎症性疾病的一种治疗措施。本研究的目的是评估益生菌NZ9000在预防四氯化碳（CCl）诱导的实验性肝纤维化方面的疗效。实验阶段包括以下4组（n = 5）：i）对照组；ii）（组名缺失）组；iii）CCl组；iv）（组名缺失）-CCl组。在前2周，（相关药物或处理缺失）被口服给予（组名缺失）组和（组名缺失）-CCl组；然后在接下来的4周内，CCl被腹膜内给予乳酸乳球菌-CCl组（除了益生菌），而（组名缺失）组仅接受益生菌（处理）。对于CCl组，CCl给药4周。所有实验组均与对照组和（组名缺失）+ CCl组进行比较。对组织样本进行组织学和生化分析，并测定白细胞介素（IL）-1、IL-10和叉头框蛋白P3（FoxP3）的基因表达水平。（相关药物或处理缺失）通过预防脂肪变性和纤维化以及降低AST和ALT水平减轻了肝硬化。亚慢性CCl损伤诱导肝脏中IL-1β基因上调，而（相关药物或处理缺失）使其降低。还发现用（相关药物或处理缺失）治疗的组肝脏中Foxp3表达增加，肠道中IL-10表达增加。这些结果表明，口服（相关药物或处理缺失）可能是预防或抵御CCl诱导的肝损伤的一种潜在益生菌。
需注意，原文中存在部分信息缺失（如部分组名、部分给药或处理信息等），可能会对准确理解和完整翻译造成一定影响。
