Xue Meilan, Liu Ying, Lyu Rui, Ge Na, Liu Man, Ma Yan, Liang Hui
Qingdao University of Medicine, Qingdao, PR China.
Baotou Medical College, Inner Mongolia University of Science and Technology, Baotou, PR China.
PLoS One. 2017 Jun 16;12(6):e0178684. doi: 10.1371/journal.pone.0178684. eCollection 2017.
This study investigated the protective effect of aplysin on the liver and its influence on inflammation and the gut microbiota in rats with ethanol-induced liver injury.
Male Sprague-Dawley rats were randomly assigned to an alcohol-containing liquid diet, control liquid diet or treatment with aplysin for 8 weeks. Hepatic and intestinal histopathological analysis was performed, and cytokine levels and the intestinal mucosal barrier were assessed. Enterobacterial repetitive intergenic consensus polymerase chain reaction (ERIC-PCR) and 16S rDNA high-throughput sequencing were performed to provide an overview of the gut microbiota composition.
Chronic alcohol exposure caused liver damage in rats. Serum aspartate aminotransferase (AST), aminotransferase (ALT), alkaline phosphatase (ALP) and triglyceride (TG) activities in liver tissue were higher than in the control group. Alcohol administration elevated the levels of serum transforming growth factor-β (TGF-β) and tumor necrosis factor-α (TNF-α) and reduced interleukin-10 (IL-10) levels compared with those of control rats. In addition, the levels of plasma endotoxin, diamine oxidase (DAO), and fatty acid-binding protein 2 (FABP2) in the alcohol group were higher than in the control group. The results of ERIC-PCR indicated that aplysin treatment shifted the overall structure of the ethanol-disrupted gut microbiota toward that of the control group. One hundred twenty to 190 genera of bacteria were detected by high throughput sequencing. Alcohol-induced changes in the gut microbial composition were detected at the genus level. These alcohol-induced effects could be reversed with aplysin treatment.
These results suggest that aplysin exerts a protective effect on ethanol-induced hepatic injury in rats by normalizing fecal microbiota composition and repairing intestinal barrier function.
本研究调查了海兔素对乙醇诱导肝损伤大鼠肝脏的保护作用及其对炎症和肠道微生物群的影响。
将雄性Sprague-Dawley大鼠随机分为含酒精液体饮食组、对照液体饮食组或海兔素处理组,持续8周。进行肝脏和肠道组织病理学分析,并评估细胞因子水平和肠道黏膜屏障。采用肠杆菌基因间重复一致序列聚合酶链反应(ERIC-PCR)和16S rDNA高通量测序来概述肠道微生物群组成。
慢性酒精暴露导致大鼠肝脏损伤。肝组织中血清天冬氨酸氨基转移酶(AST)、氨基转移酶(ALT)、碱性磷酸酶(ALP)和甘油三酯(TG)活性高于对照组。与对照大鼠相比,给予酒精使血清转化生长因子-β(TGF-β)和肿瘤坏死因子-α(TNF-α)水平升高,白细胞介素-10(IL-10)水平降低。此外,酒精组血浆内毒素、二胺氧化酶(DAO)和脂肪酸结合蛋白2(FABP2)水平高于对照组。ERIC-PCR结果表明,海兔素处理使乙醇破坏的肠道微生物群的整体结构向对照组转变。通过高通量测序检测到120至190个细菌属。在属水平上检测到酒精诱导的肠道微生物组成变化。这些酒精诱导的效应可通过海兔素处理逆转。
这些结果表明,海兔素通过使粪便微生物群组成正常化和修复肠道屏障功能,对乙醇诱导的大鼠肝损伤发挥保护作用。