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Role of gut microbiota in the pathogenesis and therapeutics of minimal hepatic encephalopathy via the gut-liver-brain axis

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World Journal of Gastroenterology 2023年第1期29卷 144-156页

作者： Ming Luo Rui-Juan Xin Fang-Rui Hu Li Yao Sheng-Juan Hu Fei-Hu Bai Department of Gastroenterology People’s Hospital of Ningxia Hui Autonomous RegionYinchuan 750021Ningxia Hui Autonomous RegionChina

Minimal hepatic encephalopathy(MHE) is a frequent neurological and psychiatric complication of liver cirrhosis. The precise pathogenesis of MHE is complicated and has yet to be fully elucidated. Studies in cirrhotic patients and experimental animals with MHE have indicated that gut microbiota dysbiosis induces systemic inflammation, hyperammonemia, and endotoxemia, subsequently leading to neuroinflammation in the brain via the gut-liver-brain axis. Related mechanisms initiated by gut microbiota dysbiosis have significant roles in MHE pathogenesis. The currently available therapeutic strategies for MHE in clinical practice, including lactulose, rifaximin, probiotics, synbiotics, and fecal microbiota transplantation, exert their effects mainly by modulating gut microbiota dysbiosis. Microbiome therapies for MHE have shown promised efficacy and safety;however, several controversies and challenges regarding their clinical use deserve to be intensively discussed. We have summarized the latest research findings concerning the roles of gut microbiota dysbiosis in the pathogenesis of MHE via the gut-liver-brain axis as well as the potential mechanisms by which microbiome therapies regulate gut microbiota dysbiosis in MHE patients.

关键词： gut microbiota Minimal hepatic encephalopathy gut-liver-brain axis Pathogenesis Therapeutics

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The contributions of bacteria metabolites to the development of hepatic encephalopathy

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liver Research 2023年第4期7卷 296-303页

作者： Miranda Claire Gilbert Tahereh Setayesh Yu-Jui Yvonne Wan Department of Pathology and Laboratory Medicine University of CaliforniaDavisSacramentoCAUSA

Over 20%of mortality during acute liver failure is associated with the development of hepatic encephalopathy(HE).Thus,HE is a complication of acute liver failure with a broad spectrum of neuropsychiatric abnormalities ranging from subclinical alterations to coma.HE is caused by the diversion of portal blood into systemic circulation through portosystemic collateral vessels.Thus,the brain is exposed to intestinal-derived toxic substances.Moreover,the strategies to prevent advancement and improve the prognosis of such a liver-brain disease rely on intestinal microbial modulation.This is supported by the findings that antibiotics such as rifaximin and laxative lactulose can alleviate hepatic cirrhosis and/or prevent HE.Together,the significance of the gut-liver-brain axis in human health warrants attention.This review paper focuses on the roles of bacteria metabolites,mainly ammonia and bile acids(BAs)as well as BA receptors in HE.The literature search conducted for this review included searches for phrases such as BA receptors,BAs,ammonia,farnesoid X receptor(FXR),G protein-coupled bile acid receptor 1(GPBAR1 or TGR5),sphingosine-1-phosphate receptor 2(S1PR2),and cirrhosis in conjunction with the phrase hepatic encephalopathy and portosystemic encephalopathy.PubMed,as well as Google Scholar,was the search engines used to find relevant publications.

关键词： liver gut-liver-brain axis Bile acids(BAs) Bile acid(BA)receptors Farnesoid X receptor(FXR) Takeda G protein-coupled receptor 5(TGR5) Sphingosine-1-phosphate receptor 2 (S1PR2) brain

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FSS ameliorates behavioral and pathological deterioration via adjust the gut-liver-brain axis in APP/PS1 transgenic mice

FSS ameliorates behavioral and pathological deterioration vi...

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第十四届中国实验动物科学年会

作者： YongBin Zhang XiaoQiuLiu Experimental Animal Center Guangzhou University of Chinese Medicine Spleen and stomach research institute Guangzhou University of Chinese Medicine

Background: Accumulating evidence implicates gut-liver-brain axis are closely related with nervous system diseases,included Alzheimer’s disease(AD),although the specific mechanism is not clear. Due to the failure of various clinical trials of novel drugs for AD, effective drugs for AD treatment are urgently required. Methods:In this study, we used the classic APP/PS1 mouse model to explore the neuroprotective effects of a Classic formula,namely FoshouSan(FSS),and the mechanisms involved.After FSS treatment, Behavioral tests were performed to assess the cognitive of mice. Hematoxylin–Eosin(HE) were used to assess neuronal damage in the Hippocampus, The Aβ level and LPS level in brain were analyzed using immunohistochemistry, the Alkaline phosphatase(AP) activity in brain were tested by Western blotting, Bacteria quantification by real-time PCR(qPCR), The lipopolysaccharides(LPS) in liver, serum and feces were assessed by a quantitative Chromogenic End-point Tachypleusamebocyte lysate(TAL) assay kit,The levels of MDA in liver,serum,Small intestine and fecal were measured by Malondialdehyde(MDA) assay kit,and the levels of alkaline phosphatase(AP) enzyme in liver,serum and Small intestine were assessed by Alkaline Phosphatase Assay Kit.Data between two groups were compared using a Student’s t test. Comparison of the data from multiple groups against one group was performed using a one-way analysis of variance(ANOVA) followed by a Dunnett’s post hoc test or a two-way repeated-measures analysis of variance with a Tukey multiple comparisons test. Results:The medium and high dose treatment mice(FSS-H,6.4 g/kg/d and FSS-M,3.2 g/kg/d) obviously ameliorated the cognitive impairment observed in APP/PS1 mice, including the impairment of object recognition memory, spatial learning and memory. In addition, FSS alleviated the neuron loss in the hippocampus, suppressed the level of Aβ and LPS in the brain, and reduced the concentration of AP in brain and serum, increased in Small intestine and liver of AD mice. FSS treatment als

关键词： FSS Alzheimer’s disease PrP-hAβPPswe/PS1ΔE9 transgenic mouse cognitive behavior AP LPS MDA gut-liver-brain axis

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佛手散通过调节的肠-肝-脑轴来改善阿尔茨海默病小鼠的认知行为和病理变化

佛手散通过调节的肠-肝-脑轴来改善阿尔茨海默病小鼠的认知行为和...

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第十四届中国实验动物科学年会

作者：鲁佳郭鹏飞陈苑高欣郭学军伍军军刘晓秋张永斌广州中医药大学脾胃研究所广州中医药大学实动物中心

目的:越来越多的证据表明,肠-肝-脑轴与神经系统疾病密切相关,包括阿尔茨海默病(AD),但具体机制尚不清楚。由于AD新药的各种临床试验失败,迫切需要有效的治疗AD药物。方法:在本研究中,我们使用经典的APP/PS1双转基因AD小鼠模型来探索经... 详细信息

目的:越来越多的证据表明,肠-肝-脑轴与神经系统疾病密切相关,包括阿尔茨海默病(AD),但具体机制尚不清楚。由于AD新药的各种临床试验失败,迫切需要有效的治疗AD药物。方法:在本研究中,我们使用经典的APP/PS1双转基因AD小鼠模型来探索经典配方即佛手散(FSS)的神经保护作用及其相关机制。经过8周口服FSS治疗,行为学测试评估小鼠的认知能力。苏木精-伊红(HE)染色用于观察海马神经元损伤,通过免疫组织化学来分析脑中Aβ1-42和脂多糖(LPS)的水平,通过Western印迹测试脑中的碱性磷酸酶(AP)活性,通过实时定量PCR(q PCR)定量检测细菌,通过显色基质法鲎试剂盒评估肝脏,血清和粪便中的LPS水平,通过丙二醛(MDA)测定试剂盒测量肝脏,血清,肠道和脑组织中的MDA水平,并通过碱性磷酸酶测定试剂盒评估肝,血清和肠中碱性磷酸酶(AP)的水平。结果:中,高剂量FSS(FSS-H,6.4g/kg/d,FSS-M,3.2g/kg/d)显然改善了AD小鼠的认知障碍,包括情节识别记忆,空间学习和记忆。FSS还减轻了海马神经元的损伤,抑制了大脑中Aβ1-42和LPS的水平,降低了肝脏,血清,粪便中的LPS水平。此外,FSS降低了AD小鼠大脑和血清中的AP活性,增加了AD小鼠肠道和肝脏中的AP活性,并且显着降低了脑,肝,血清,肠中的MDA水平。此外,FSS可以增加乳杆菌的数量,并减少AD小鼠肠道中大肠杆菌的数量。结论:我们发现APP/PS1双转基因AD小鼠模型中肠道微生物组失调,脂多糖(LPS)水平,氧化应激水平和碱性磷酸酶(AP)活性水平都发生了变化;并指出FSS通过调节APP/PS1双转基因AD小鼠的微生物组平衡,降低LPS水平,降低氧化应激水平和调节AP的活性水平来调节肠-肝-脑轴机制,因此FSS对AD小鼠的药效作用机制可能与调节肠-肝-脑轴机制有关。FSS很可能是未来临床上治疗阿尔茨海默病有效方剂。

关键词： FSS Alzheimer's disease PrP-hAβPPswe/PS1ΔE9 transgenic mouse cognitive behavior AP LPS MDA gut-liver-brain axis

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