Global Metabolomic Profiling of Mice Brains following Experimental Infection with the Cyst-Forming Toxoplasma gondii

The interplay between the Apicomplexan parasite Toxoplasma gondii and its host has been largely studied. However, molecular changes at the metabolic level in the host central nervous system and pathogenesis-associated metabolites during brain infection are largely unexplored. We used a global metabolomics strategy to identify differentially regulated metabolites and affected metabolic pathways in BALB/c mice during infection with T. gondii Pru strain at 7, 14 and 21 days post-infection (DPI). The non-targeted Liquid Chromatography-Mass Spectrometry (LC-MS) metabolomics analysis detected approximately 2,755 retention time-exact mass pairs, of which more than 60 had significantly differential profiles at different stages of infection. These include amino acids, organic acids, carbohydrates, fatty acids, and vitamins. The biological significance of these metabolites is discussed. Principal Component Analysis and Orthogonal Partial Least Square-Discriminant Analysis showed the metabolites’ profile to change over time with the most significant changes occurring at 14 DPI. Correlated metabolic pathway imbalances were observed in carbohydrate metabolism, lipid metabolism, energetic metabolism and fatty acid oxidation. Eight metabolites correlated with the physical recovery from infection-caused illness were identified. These findings indicate that global metabolomics adopted in this study is a sensitive approach for detecting metabolic alterations in T. gondii-infected mice and generated a comparative metabolic profile of brain tissue distinguishing infected from non-infected host.     

Bulleyaconitine A inhibits the lung inflammation and airway remodeling through restoring Th1/Th2 balance in asthmatic model mice

ABSTRACT

The current study aimed to study the effects of Bulleyaconitine A (BLA) on asthma. Asthmatic mice model was established by ovalbumin (OVA) stimulation, and the model mice were treated by BLA. After BLA treatment, the changes in lung and airway resistances, total and differential leukocytes in the bronchoalveolar lavage fluid (BALF) were detected, and the changes in lung inflammation and airway remodeling were observed. Moreover, the secretion of IgE, Th1/Th2-type and IL-17A cytokines in BALF and serum of the asthmatic mice were determined. The resuts showed that BLA attenuated OVA-induced lung and airway resistances, inhibited the inflammatory cell recruitment in BALF and the inflammation and airway remodeling of the asthmatic mice. In addition, BLA suppressed the secretion of IgE, Th2-type cytokines, and IL-17A, but enhanced secretions of Th1-type cytokines in BALF and serum. The current study discovered that BLA inhibited the lung inflammation and airway remodeling via restoring the Th1/Th2 balance in asthmatic mice.     

钩藤散改善APP/PS1双转基因小鼠学习记忆功能的代谢组学研究

目的:采用非靶向的高通量尿液代谢组学技术对钩藤散改善淀粉样前体蛋白/早老素蛋白1基因,即APP/PS1双转基因小鼠的作用机制进行研究。方法:5月龄APP/PSI小鼠采用Morris水迷宫实验检测双转基因小鼠的空间学习能力,在确定出现空间记忆能力功能损伤地条件下采用基于非靶向的尿液代谢组学技术研究APP/PSI小鼠的代谢网络,聚焦关键通路,同时观察钩藤散在水迷宫和代谢水平上的治疗作用。结果:Morris水迷宫对比发现APP/PSI小鼠的空间记忆能力明显长于同窝野生小鼠,给予钩藤散后呈现一定程度的回调趋势,经非靶向的代谢轮廓分析和核心代谢通路聚焦后,成功发现正常小鼠(同窝野生小鼠)和APP/PSI双转基因小鼠代谢轮廓间差异最大的信号,经质谱解析和权威数据库检索后鉴定6个与学习记忆相关的潜在生物标记物,分别是牛磺酸(taurine)、叶酸(pteroylglutamic acid)、新蝶呤(neopterin)、磺乙谷酰胺(glutaurine)、戊邻酮二酸盐(2-oxoglutarate)、二氢新蝶呤(dihydroneopterin),他们主要涉及牛磺酸代谢及叶酸代谢等,经钩藤散治疗后能有效回调。结论:钩藤散对APP/PSI双转基因小鼠的学习记忆能力具有一定治疗作用,本次发现的6个生物标记物可能是APP/PSI双转基因小鼠发病的潜在靶点,为钩藤散的相关药效学研究提供实验依据。     

罗汉果皂苷V在人工胃液中的稳定性和体外代谢研究

为了研究罗汉果皂苷V在胃肠道中的稳定性及体外代谢特征,该研究首先考察罗汉果皂苷V在人工胃液中的稳定性,然后在体外模拟人肠内环境,研究人肠内细菌对该成分的代谢作用,并采用LCMS/IT-TOF液质联用仪分析了培养液中的化学成分,考察了罗汉果皂苷V在人工胃液和人肠道菌群培养液中的变化。结果表明:罗汉果皂苷V在人工胃液条件下,迅速发生酸水解反应,分别脱去3个糖苷、4个糖苷、5个糖苷及2个氢转化为二糖苷、一糖苷与脱氢苷元,其脱糖反应随着时间的延长而反应越完全,反应4 h后就只剩下苷元; 该化合物在人的肠道菌群作用下经过脱糖反应转化为四糖苷、三糖苷、二糖苷、一糖苷,经过糖苷化反应转化成六糖苷。通过体外实验,初步了解罗汉果皂苷V在胃液和肠道环境中的降解规律,该研究结果为今后探讨罗汉果皂苷在人体内的代谢与生物转化规律提供了物质和技术基础。     

A UPLC-Q-TOF/MS-based plasma metabolomics approach reveals the mechanism of Compound Kushen Injection-based intervention against non-small cell lung cancer in Lewis tumor-bearing mice

BackgroundCompound Kushen Injection (CKI), a well-known Chinese Medicine preparation, has been used to treat non-small cell lung cancer (NSCLC) for more than 15 years, and its clinical curative effect is considered to be beneficial.Hypothesis/PurposeThis study was designed to evaluate the effects and underlying mechanisms of CKI against NSCLC using an ultra-high-performance liquid chromatography quadrupole time-of-flight mass spectrometry (UPLC-Q-TOF/MS)-based plasma metabolomics approach.Methods4′,6-diamidino-2-phenylindole (DAPI) staining and 3-(4,5-dimethyl-thiazol-2-yl)-2,5-diphenyl-tetrazolium bromide (MTT) dye reduction assay were employed to assess apoptosis and the viability of A549 cells with and without CKI treatment. The weight/volume of Lewis lung carcinoma (LLC) sarcomas and histopathological examinations were used to evaluate the anti-tumor effects of CKI against NSCLC. A UPLC-Q-TOF/MS method combined with multivariate data analysis was developed to characterize metabolomic fingerprinting and to screen functional biomarkers that are linked to the CKI treatment of LLC mice, and then metabolic pathway analysis was used to investigate the therapeutic mechanism of CKI.ResultsDAPI staining and MTT dye reduction assays indicated that CKI-induced apoptosis and inhibited the proliferation of A549 cells, respectively, in a concentration-dependent manner. The sarcoma volumes and weights in LLC tumor-bearing mice in CKI-dosed groups were significantly lower than those in a model group, which was treated with physiological saline. Histopathological analysis of sections of sarcomas and left pulmonary lobes indicated that CKI exerts an ameliorative effect against LLC. Fourteen functional biomarkers that are related to the therapeutic effects of CKI on LLC were screened and identified using a metabolomics study. Analysis of metabolic pathways revealed that the therapeutic effects of CKI on LLC mainly involved glycerophospholipid metabolism, amino acid metabolism and sphingolipid metabolism. As glycerophospholipid metabolism is a crucial feature of cancer-specific metabolism, the enzymes that are involved in 1-acyl-sn-glycero-3-phosphoinositol biosynthesis were further evaluated. Western blotting results indicated that CKI modulated the abnormal biosynthesis pathway of 1-acyl-sn-glycero-3-phosphoinositol by activation of cytidine diphosphate-diacylglycerol-inositol 3-phosphatidyltransferase (CDIPT) and cytosolic phospholipase A2 (cPLA2), and by inhibition of lysophosphatidic acid acyltransferase gamma (AGPAT3).ConclusionThis study demonstrated that CKI has a favorable anti-tumor effect and that a UPLC-Q-TOF/MS-based metabolomics method in conjunction with further verifications at the biochemical level is a promising approach for investigating its underlying mechanisms.     

Asiaticoside might attenuate bleomycin‐induced pulmonary fibrosis by activating cAMP and Rap1 signalling pathway assisted by A2AR

Asiaticoside (AS) has been reported to have protective effect on pulmonary fibrosis (PF). In this study, we aimed to explore the potential mechanism of the therapeutic role of AS and its relationship with A2AR in PF. Adenosine 2A receptor gene knockout (A2AR^?/?) mice and wild‐type (WT) mice were used to establish bleomycin (BLM)‐induced PF models and were then treated with AS (50 mg/kg/d). Pulmonary inflammation and fibrosis were observed in the PF model with much higher severity in A2AR^?/?mice than that in WT mice and AS significantly alleviated lung inflammation and fibrosis; however, it was less effective in A2AR^?/? mice than in WT mice via histopathological analysis. Using RNA sequencing analysis, we found up‐regulated differentially expressed genes (DEGs) in BLM group were enriched in immune and inflammation‐associated pathways compared with control group. There were 242 common DEGs between down‐regulated in BLM vs control group and up‐regulated in BLM + AS vs BLM group, which were enriched in cAMP and Rap1 signalling pathways. Furthermore, the expression of five key factors of these two pathways including adenylate cyclase (ADCY1, ADCY5, ADCY8, cAMP and Rap1) were confirmed up‐regulated by AS with the presence of A2AR. Therefore, AS might attenuate BLM‐induced PF by activating cAMP and Rap1 signalling pathways which is assisted by A2AR, making it a promising therapeutic optional for PF.     

Exploring the protective effects of Danqi Tongmai tablet on acute myocardial ischemia rats by comprehensive metabolomics profiling

BackgroundDanqi Tongmai tablet (DQTM), a combination of salvianolic acids (SA) and panax notoginsenosides (PNS), is now in phase II clinical trial developed for the treatment of cardiovascular diseases. However, the mechanisms of its protective effects through regulating endogenous metabolites remain unclear.PurposeThe purpose of this study was to explore the protective effects of DQTM on acute myocardial ischemia rats by comprehensive metabolomics profiling.Study designThe rats were divided into three groups: sham-operating, acute myocardial ischemia (AMI) and DQTM groups. The plasma and heart were collected and profiled by LC-MS based metabolomics and lipidomics. Based on the identified differential metabolites, the pathway analysis results were obtained and further validated using the network pharmacology approach.MethodsThe AMI model was induced by ligating the left anterior descending coronary artery. The metabolomics and lipidomics profiling were based on two established LC–QTOF/MS analysis methods. The raw data were processed using XCMS Online, then the differential metabolites with nonparametric t-test p value less than 0.05 were selected and identified using HMDB and METLIN. The pathway analysis was conducted using MetaboAnalyst and validated with the predicted network results obtained by BATMAN-TCM.ResultsThe metabolomics and lipidomics profiles of plasma and heart in response to AMI and DQTM were significantly different. The AMI operation had a serious influence on metabolites in heart ischemia region, while DQTM had a greater impact on lipids in heart non-ischemia region. A total of 151 differential metabolites were identified, including mainly amino acids and fatty acids. Multiple metabolic pathways were disturbed after AMI and could be restored by DQTM, of which arachidonic acid metabolism was further validated with the predicted results of network pharmacology.ConclusionThe protective effects of DQTM on acute myocardial ischemia rats could be achieved through the regulation of multiple metabolic pathways.     

Serum and colon metabolomics study reveals the anti-ulcerative colitis effect of Croton crassifolius Geisel

BackgroundCroton crassifolius Geisel (CCG, also known as Ji-Gu-Xiang in Traditional Chinese Medicine), is traditionally prescribed for the therapy of rheumatic arthritis and gastrointestinal ulcer. However, the effect of CCG on ulcerative colitis (UC) has not been investigated.PurposeTo explore the therapeutic potential and underlying mechanism of CCG extract against UC by colonic and serum metabolomics.MethodsIn order to standardize the CCG extract, UPLC-QTOF-MS was used for quantitative and qualitative analysis of the representative terpenoids. C57BL/6J mice were divided into control, Dextran Sulfate Sodium (DSS), mesalazine (100 mg•kg⁻¹), CCG extract (150 and 600 mg•kg⁻¹) groups. The mice were provided 3% DSS dissolved in distilled water ad libitum for 7 days except control group. Weight change, disease activity index (DAI), colon lengths and expression of inflammatory mediators iNOS and COX-2 in colonic tissue were determined. Serum and colon metabolomics using UPLC–QTOF-MS technology coupled with multivariate data analysis were performed to reveal the underlying mechanism.ResultsThirty-five terpenoids in CCG were identified by fingerprint, in which ten representative terpenes were quantified. CCG could relieve the weight loss, the degree of bloody stool and ulcer of colon, as well as significantly lowering the expression level of iNOS and COX-2. Metabolomics analysis showed that 25 biomarkers were obviously interfered by CCG treatment and 16 of them were highly correlated with the efficacy of CCG. The analysis of metabolic pathway showed that the anti-UC effect of CCG was associated with the regulation on linoleic acid metabolism, sphingolipid metabolism, α-linolenic acid metabolism, and glycerophospholipids metabolism.ConclusionsThe oral administration of CCG significantly alleviated DSS-induced UC symptoms by reducing inflammation and rectifying the metabolic disorder. CCG may provide a new strategy for the management of UC.     

Serum metabonomics study of pregnant women with gestational diabetes mellitus based on LC-MS

ObjectiveThrough metabolomics method, the objective of the paper is to differentially screen serum metabolites of GDM patients and healthy pregnant women, to explore potential biomarkers of GDM and analyze related pathways, and to explain the potential mechanism and biological significance of GDM.MethodsThe serum samples from 30 GDM patients and 30 healthy pregnant women were selected to conduct non-targeted metabolomics study by liquid chromatography-mass spectrometry. The differential metabolites between the two groups were searched and the metabolic pathway was analyzed by KEGG database.ResultsMultivariate statistical analysis found that serum metabolism in GDM patients was different significantly from healthy pregnant women, 36 differential metabolites and corresponding metabolic pathways were identified in serum, which involved several metabolic ways like, fatty acid metabolism, butyric acid metabolism, bile secretion, and amino acid metabolism.ConclusionThe discovery of these biomarkers provided a new theoretical basis and experimental basis for further study of the early diagnosis and pathogenesis of GDM. At the same time, LC-MS-based serum metabolomics methods also showed great application values in disease diagnosis and mechanism research.     

Indoleamine 2,3-Dioxygenase Is Not a Pivotal Regulator Responsible for Suppressing Allergic Airway Inflammation through Adipose-Derived Stem Cells

BackgroundAlthough indoleamine 2,3-dioxygenase (IDO)-mediated immune suppression of mesenchymal stem cells (MSCs) has been revealed in septic and tumor microenvironments, the role of IDO in suppressing allergic airway inflammation by MSCs is not well documented. We evaluated the effects of adipose-derived stem cells (ASCs) on allergic inflammation in IDO-knockout (KO) asthmatic mice or asthmatic mice treated with ASCs derived from IDO-KO mice.ConclusionsIDO did not play a pivotal role in the suppression of allergic airway inflammation through ASCs, suggesting that it is not the major regulator responsible for suppressing allergic airway inflammation.     

基于液相色谱串联高分辨质谱技术的小细胞肺癌血浆代谢组学研究

摘要 目的：对小细胞肺癌患者血浆开展质谱代谢组学研究,表征其基线代谢特征,为小细胞肺癌诊疗提供基础代谢数据及线索。方法：基于液相色谱串联四极杆飞行质谱技术,以45例小细胞肺癌患者和53例对照组（健康人群）血浆为研究对象,进行非靶向代谢组学分析及代谢表征。结果：与对照组相比,基线期小细胞肺癌患者血浆代谢发生显著改变,共发现113种差异代谢物,其中2''-deoxyguanosine 5''-monophosphate（FC=9.17）、cyclic adenosine monophosphate（FC=7.72）、inosine（FC=6.38）等59种代谢物水平升高,2-aminobenzoic acid（FC=0.24）、glutathione（FC=0.27）、xanthine（FC=0.29）等54种代谢物水平下降,差异代谢通路主要涉及色氨酸等氨基酸代谢。结论：小细胞肺癌患者基线血浆代谢轮廓与健康人群存在显著差异,相关差异代谢物及通路的挖掘有助于推动小细胞肺癌新型诊断标志物发现和代谢干预靶点的揭示,改善其治疗手段有限等现状。     

淫羊藿苷对RSV感染诱发哮喘小鼠体内PGD2水平的影响

摘要 目的：观察淫羊藿苷对RSV感染诱发哮喘小鼠血清及支气管肺泡灌洗液中前列腺素D2（Prostaglandin D2,PGD2）表达水平的影响,以期为哮喘治疗寻找新的靶点。方法：30只Balb/c小鼠随机均分为三组：即正常组,OVA/RSV-YYH组（即淫羊藿苷治疗组）及OVA/RSV-非YYH组（即未经淫羊藿苷治疗组）。卵蛋白致敏RSV感染诱发小鼠哮喘模型成功建立后,予以淫羊藿苷2.5 mg连续腹腔注射治疗2周,比较治疗前后肺功能检测结果、支气管肺泡灌洗液（bronchoalveolar lavage fluid,BALF）中细胞分类计数、血清及BALF中PGD2表达水平、肺组织病理学变化。结果：淫羊藿苷治疗后,哮喘小鼠肺功能较治疗前明显改善,差异有统计学意义（P<0.05）;PGD2水平较前明显下降,差异有统计学意义（P<0.05）;各分类白细胞计数较前明显减少,差异有统计学意义（P<0.01）,气道管壁增厚及管腔狭窄现象较前明显改善,肺组织炎症细胞浸润较前减少。结论：淫羊藿苷可有效降低RSV感染诱发哮喘小鼠体内炎性介质PGD2水平,从而改善气道重塑,减轻小鼠的哮喘症状,它可能是以后哮喘治疗的一个新的靶点。     

Metabolic changes associated with selenium deficiency in mice

Selenium (Se), which is a central component for the biosynthesis and functionality of selenoproteins, plays an important role in the anti-oxidative response, reproduction, thyroid hormone metabolism and the protection from infection and inflammation. However, dietary Se effects have not well been established to date and the available studies often present contradictory results. To obtain a better understanding of Se intake and its influence on the metabolism of living systems, we have utilized a metabolomics approach to gain insight into the specific metabolic alterations caused by Se deficiency in mice. Serum samples were collected from two groups of C57BL/6 mice: an experimental group which was fed a Se-deficient diet and controls consuming normal chow. The samples were analyzed by ¹H nuclear magnetic resonance spectroscopy and gas chromatography-mass spectrometry. The resulting metabolite data were examined separately for both analytical methods and in a combined manner. By applying multivariate statistical analysis we were able to distinguish the two groups and detect a metabolite pattern associated with Se deficiency. We found that the concentrations of 15 metabolites significantly changed in serum samples collected from Se-deficient mice when compared to the controls. Many of the perturbed biological pathways pointed towards compensatory mechanisms during Se deficiency and were associated with amino acid metabolism. Our findings show that a metabolomics approach may be applied to identify the metabolic impact of Se and reveal the most impaired biological pathways as well as induced regulatory mechanisms during Se deficiency.     

Systematic exploration of Astragalus membranaceus and Panax ginseng as immune regulators: Insights from the comparative biological and computational analysis

BackgroundImmune system plays a decisive role for defending various pathogenic microorganisms. Astragalus membranaceus (AM) and Panax ginseng (PG) are two tonic herbs used in traditional Chinese medicine (TCM) as immune booster and help to control diseases with their healthy synergistic effect on immune system.PurposeThis study was aimed to investigate the promote effect and molecular mechanisms of AM and PG on immune system as booster and to control the target diseases using animal and computational systematic study.MethodsComputational models including absorption, distribution, metabolism, and elimination (ADME) with weighted ensemble similarity (WES) algorithm-based models and ClueGo network analysis were used to find the potential bioactive compounds targets and pathways, which were responsible for immune regulation. Viscera index analysis, proliferation activity of splenic lymphocytes and cytotoxic activity of NK cells assays were performed to validate the effect of AM and PG on immune system of long-term administrated mice. Metabonomic study of mice plasma was conducted to investigate effect of AM and PG on the endogenous metabolic perturbations, together with correlation analysis.ResultsAM and PG simultaneously showed the ability to strengthen the immune system function including enhancement of spleen and thymus index, proliferation of splenic lymphocytes and cytotoxic activity of NK cells. Besides, the different molecular mechanisms of AM and PG on immune regulation were also investigated by analyzing the potential bioactive compounds, enzymes actions and pathways. Quercetin, formononetin and kaempferol were the main immune-related compounds in AM, while ginsenoside Ra1, ginsenoside Rh1 and kaempferol in PG. About 10 target proteins were found close to immune regulation, including acetylcholinesterase (ACHE, common target in AM and PG), sphingosine kinase 1(SPHK1), cytidine deaminase (CDA), and Choline O-acetyltransferase (CHAT). Glycerophospholipid metabolism was regulated in both AM and PG groups. Pyrimidine metabolism and sphingolipid metabolism were considered as the special pathway in AM groups. Energy metabolism and glycerolipid metabolism were the special pathways in PG groups.ConclusionA novel comprehensive molecular mechanism analysis method was established and applied to clarify the scientific connotation of AM and PG as immune regulation, with similar herbal tonic effect provided in clinical practice of TCM, which can provide a new line of research for drug development (immune booster) using AM and PG.     

Vitamin A deficiency in mice alters host and gut microbial metabolism leading to altered energy homeostasis

Vitamin A deficiency (A−) is a worldwide public health problem. To better understand how vitamin A status influences gut microbiota and host metabolism, we systematically analyzed urine, cecum, serum and liver samples from vitamin A sufficient (A+) and deficient (A−) mice using ¹H NMR-based metabolomics, quantitative (q)PCR and 16S rRNA gene sequencing coupled with multivariate data analysis. The microbiota in the cecum of A− mice showed compositional as well as functional shifts compared to the microbiota from A+ mice. Targeted ¹H NMR analyses revealed significant changes in microbial metabolite concentrations including higher butyrate and hippurate and decreased acetate and 4-hydroxyphenylacetate in A+ relative to A− mice. Bacterial butyrate-producing genes including butyryl-CoA:acetate CoA-transferase and butyrate kinase were significantly higher in bacteria from A+ versus bacteria from A− mice. A− mice had disturbances in multiple metabolic pathways including alterations in energy (hyperglycemia, glycogenesis, TCA cycle and lipoprotein biosynthesis), amino acid and nucleic acid metabolism. A− mice had hyperglycemia, liver dysfunction, changes in bacterial metabolism and altered gut microbial communities. Moreover, integrative analyses indicated a strong correlation between gut microbiota and host energy metabolism pathways in the liver. Vitamin A regulates host and bacterial metabolism, and the result includes alterations in energy homeostasis.     

Metabolomics study of the hepatoprotective effect of Phellinus igniarius in chronic ethanol-induced liver injury mice using UPLC-Q/TOF-MS combined with ingenuity pathway analysis

BackgroundPhellinus igniarius (L.) Quèl as a potential medicinal mushroom possesses multiple biological activities including hepatoprotection, but the hepatoprotective mechanism is not clear.PurposeTo elucidate the hepatoprotective effect and potential target of P. igniarius.MethodsThe male C57BL/6 mice were fed with the Lieber–DeCarli diet containing alcohol or isocaloric maltose dextrin as control diet with or without P. igniarius decoction (PID) in the dosage of 0.65 g/kg and 2.6 g/kg. The levels of serum biomarkers were detected by an automatic biochemistry analyser. The histopathological changes of liver were observed by hematoxylin and eosin (H&E) staining. Ultra performance liquid chromatography-quadrupole/time-of-flight mass spectrometry (UPLC-Q/TOF-MS) was applied for investigating the dynamic changes of serum metabolites in chronic ethanol-induced liver injury mice and after treatment with PID. Ingenuity pathway analysis (IPA) was employed to identify the potential target of PID.ResultsPID could significantly reduce the levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST), triglyceride (TG) and total bile acid (TBA) in serum and improved hepatic steatosis and inflammation. In terms of metabolism, a total of 36 serum differential metabolites were identified, and PID intervention regulated 24 of them, involving the key metabolic pathways such as the biosynthesis of unsaturated fatty acids, primary bile acid biosynthesis, glycerophospholipid metabolism, fatty acids biosynthesis, ether lipid metabolism and arachidonic acid metabolism. On the mechanism, IPA showed that farnesol X receptor (FXR) was the major potential target for PID, and PID could improve chronic alcohol intake induced by the inhibition of mRNA expression of FXR in the liver and the activation of mRNA expression of FXR in the intestine in mice.ConclusionThe present study for the first time systematically illustrated the hepatoprotective effect of P. igniarius and preliminarily explored its potential target FXR. P. igniarius might be exploited as a promising therapeutic option for alcoholic liver injury.