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Protective effect of Lactobacillus salivarius Li01 on thioacetamide-induced acute liver injury and hyperammonaemia.
Microbial Biotechnology ( IF 4.8 ) Pub Date : 2020-07-11 , DOI: 10.1111/1751-7915.13629 Liya Yang 1 , Xiaoyuan Bian 1 , Wenrui Wu 1 , Longxian Lv 1 , Yating Li 1 , Jianzhong Ye 2 , Xianwan Jiang 1 , Qing Wang 1 , Ding Shi 1 , Daiqiong Fang 1 , Jingjing Wu 1 , Kaicen Wang 1 , Qiangqiang Wang 1 , Jiafeng Xia 1 , Jiaojiao Xie 1 , Yanmeng Lu 1 , Lanjuan Li 1
Microbial Biotechnology ( IF 4.8 ) Pub Date : 2020-07-11 , DOI: 10.1111/1751-7915.13629 Liya Yang 1 , Xiaoyuan Bian 1 , Wenrui Wu 1 , Longxian Lv 1 , Yating Li 1 , Jianzhong Ye 2 , Xianwan Jiang 1 , Qing Wang 1 , Ding Shi 1 , Daiqiong Fang 1 , Jingjing Wu 1 , Kaicen Wang 1 , Qiangqiang Wang 1 , Jiafeng Xia 1 , Jiaojiao Xie 1 , Yanmeng Lu 1 , Lanjuan Li 1
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The gut microbiota plays pivotal roles in liver disease onset and progression. The protective effects of Lactobacillus salivarius Li01 on liver diseases have been reported. In this study, we aimed to detect the protective effect of L. salivarius Li01 on thioacetamide (TAA)‐induced acute liver injury and hyperammonaemia. C57BL/6 mice were separated into three groups and given a gavage of L. salivarius Li01 or phosphate‐buffered saline for 7 days. Acute liver injury and hyperammonaemia were induced with an intraperitoneal TAA injection. L. salivarius Li01 decreased mortality and serum transaminase levels and improved histological liver damage caused by TAA. Serum inflammatory cytokine and chemokine and lipopolysaccharide‐binding protein (LBP) concentrations, nuclear factor κB (NFκB) pathway activation and macrophage and neutrophil infiltration into the liver were significantly alleviated by L. salivarius Li01. L. salivarius Li01 also reinforced gut barrier and reshaped the perturbed gut microbiota by upregulating Bacteroidetes and Akkermansia richness and downregulating Proteobacteria, Ruminococcaceae_UCG_014 and Helicobacter richness. Plasma and faecal ammonia levels declined noticeably in the Li01 group, accompanied by improvements in cognitive function, neuro‐inflammation and relative brain‐derived neurotrophic factor (BDNF) gene expression. Our results indicated that L. salivarius Li01 could be considered a potential probiotic in acute liver injury and hepatic encephalopathy (HE).
中文翻译：
唾液乳杆菌 Li01 对硫代乙酰胺诱导的急性肝损伤和高氨血症的保护作用。
肠道微生物群在肝脏疾病的发生和进展中发挥着关键作用。唾液乳杆菌Li01 对肝脏疾病的保护作用已有报道。在本研究中，我们旨在检测L. salivarius Li01 对硫代乙酰胺 (TAA) 诱导的急性肝损伤和高氨血症的保护作用。 C57BL/6 小鼠被分为三组，灌胃L. salivarius Li01 或磷酸盐缓冲盐水 7 天。腹腔注射 TAA 诱导急性肝损伤和高氨血症。 L. salivarius Li01 降低了死亡率和血清转氨酶水平，并改善了 TAA 引起的组织学肝损伤。唾液乳杆菌Li01 显着减轻了血清炎症细胞因子、趋化因子和脂多糖结合蛋白 (LBP) 浓度、核因子 κB (NFκB) 通路激活以及巨噬细胞和中性粒细胞向肝脏的浸润。 L. salivarius Li01 还通过上调拟杆菌和阿克曼氏菌的丰富度以及下调变形菌、瘤胃球菌科_UCG_014和螺杆菌的丰富度来增强肠道屏障并重塑受干扰的肠道微生物群。 Li01 组的血浆和粪便氨水平显着下降，同时认知功能、神经炎症和相关脑源性神经营养因子 (BDNF) 基因表达得到改善。我们的结果表明， L. salivarius Li01 可被视为治疗急性肝损伤和肝性脑病 (HE) 的潜在益生菌。
更新日期：2020-07-11
中文翻译：
唾液乳杆菌 Li01 对硫代乙酰胺诱导的急性肝损伤和高氨血症的保护作用。
肠道微生物群在肝脏疾病的发生和进展中发挥着关键作用。唾液乳杆菌Li01 对肝脏疾病的保护作用已有报道。在本研究中，我们旨在检测L. salivarius Li01 对硫代乙酰胺 (TAA) 诱导的急性肝损伤和高氨血症的保护作用。 C57BL/6 小鼠被分为三组，灌胃L. salivarius Li01 或磷酸盐缓冲盐水 7 天。腹腔注射 TAA 诱导急性肝损伤和高氨血症。 L. salivarius Li01 降低了死亡率和血清转氨酶水平，并改善了 TAA 引起的组织学肝损伤。唾液乳杆菌Li01 显着减轻了血清炎症细胞因子、趋化因子和脂多糖结合蛋白 (LBP) 浓度、核因子 κB (NFκB) 通路激活以及巨噬细胞和中性粒细胞向肝脏的浸润。 L. salivarius Li01 还通过上调拟杆菌和阿克曼氏菌的丰富度以及下调变形菌、瘤胃球菌科_UCG_014和螺杆菌的丰富度来增强肠道屏障并重塑受干扰的肠道微生物群。 Li01 组的血浆和粪便氨水平显着下降，同时认知功能、神经炎症和相关脑源性神经营养因子 (BDNF) 基因表达得到改善。我们的结果表明， L. salivarius Li01 可被视为治疗急性肝损伤和肝性脑病 (HE) 的潜在益生菌。
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