Acute Toxicity of Jinchuan Formula Plum Wine Extract and Its Protective Effect on Mice with Liver Injury

[Objectives]To investigate the acute toxicity and hepatoprotective effect of Jinchuan formula plum wine extract on mice,determine its safety range,and evaluate its hepatoprotective effect.[Methods]The median lethal dose(LD_(50))was determined by acute toxicity test with the toxic reaction and mortality of mice as indexes.Sixty Kunming mice were randomly divided into 6 groups:normal control group,model group(ConA-induced liver injury model),Jinchuan formula plum wine high,medium and low dose groups(1.0,0.5,0.25 g/kg)and silybin group(0.1 g/kg).The levels of ALT,AST,LDH in serum and TG,VLDL in liver were measured.After HE staining,the pathological changes of liver tissue in mice were observed,and the liver protective effect of Jinchuan formula plum wine extract was analyzed and evaluated.[Results]LD_(50)was 11.18 g/kg,and the 95%confidence limit of LD_(50)was 10.31-12.05 g/kg.The high-dose group of Jinchuan formula plum wine extract could significantly reduce the serum ALT and AST activities of ConA-induced liver injury mice(P<0.05).[Conclusions]Jinchuan formula plum wine extract is relatively safe,and also has a protective effect on liver injury.

The Extraction of Eucommia Ulmoides Oliv Polysaccharides and Its Protective Effect on Liver of Clophasphamidecy Injured Mice

Objective:To study the influenceof eucommia polysaccharide on the mice' liver damaged by clophasphamidecy (CY).Methods:Injecting CY build mice liver damage model,eucommia polysaccharide given different doses, measured blood serum ALT,AST and the liver's SOD,MDA. Results:After the injection CY,blood serum ALT,AST and the MDA of liver rise and the SOD of liver reduce comparedwith the blank group. The eucommia polysaccharide can improve these index.Conclusion:The Eucommia polysaccharide may protect the mice' liver damaged by CY.

Cerebral protective effect of nicorandil premedication on patients undergoing liver transplantation

BACKGROUND:Neurological injury is a common complication in the early period after liver transplantation,posing an enormous obstacle to treatment efficiency and patient survival.Nicorandil is a mitochondrial ATP-sensitive potassium channel(mitoK ATP) opener.It has been reported to be effective in reducing brain injury in recent studies.However,it is still unclear whether nicorandil has cerebral protective effect in patients undergoing liver transplantation.METHODS:Fifty patients scheduled for liver transplantation were randomly divided into a nicorandil group(group N)(n=25),in which patients received 10 mg nicorandil through a nasogastric tube 30 minutes before induction of anesthesia,and a control group(group C)(n=25) who received 10 mL normal saline.The Mini-Mental State Examination(MMSE) was performed before anesthesia(day 0),and on days 3 and 7 after surgery.Blood samples were obtained before induction of anesthesia(T1),and at 12(T2) and 36 hours(T3) after surgery for determination of serum neuron-specific enolase(NSE) and S100β protein(S100β) concentrations.RESULTS:During surgery,5 patients in each group were eliminated due to severe reperfusion or renal insufficiency.Therefore,20 patients remained in each group.The MMSE scores after operation were significantly lower than those before operation in group C.However,there was no difference at days 3 and 7 compared with day 0 in group N.Serum NSE concentrations after surgery were significantly higher than baseline(at T1) in both groups,except at T3 in group N.Serum S100β concentration after surgery was significantly higher than baseline(at T1) in both groups.The MMSE scores at days 3 and 7 in group N were significantly higher than those in group C.The concentrations of serum NSE and S100β at T2 and T3 in group N were significantly lower than those in group C.CONCLUSIONS:Oral nicorandil,as a premedication before liver transplantation,improves postoperative MMSE scores.It also attenuates the increase of NSE and S100β in blood,indicating its cerebral protective effect.

Cyclosporin A protects Balb/c mice from liver damage induced by superantigen SEB and D-GaIN

AIM To investigate the pathogenic effect ofSEB and D-GalN on liver and the protection ofcyclosporin A, the relationship between hepaticapoptosis and necrosis and the possiblemechanism of acute hepatic necrosis.METHODS After staphylococcal enterotoxin B(SEB ) mixed with D--galactosamine (D-GaiN )were injected intraperitoneally into Balb/c miceand those previously treated with cyclosporin A,blood samples were collected and livers wereisolated at 2, 6, 12 and 24 h. Patterns othepatocellular death were studiedmorphologically and biochemically, circulatingcytokines (TNF-a, IFN--y ) and mice mortalitywithin 24h was assessed.RESU’LTS The SEB could induce the typicalapoptotic changes of hepatocytes, the D-GaiNcould induce hepatocytes apoptosis anddegeneration at the same time, and the micehaving received the SEB + D-GaiN injectionsdeveloped apoptosis at 2 and 6 h, but after 12 hhepatocytes were characterized by severein jury, whereas all the examinations in thecyclosporin A treated mice were normal.CONCLUSION Hepatic cell apoptosis might berelated to necrosis, and massive hepatocyteapoptosis is likely the initiating step of acutehepatic necrosis in mice. The effects induced bySEB and D--GaiN on hepatocytes might bemediated by T cells, and could be prevented bycyclosporin A.

Liver protection strategies in liver transplantation

BACKGROUND： Liver transplantation is the therapy of choice for patients with end-stage liver diseases. However, the gap between the low availability of organs and high demand is continuously increasing. Innovative strategies for organ protection are necessary to expand donor pool and to achieve better outcomes for liver transplantation. The present review analyzed and compared various strategies of liver protection.DATA SOURCES： Databases such as PubM ed, Embase and Ovid were searched for the literature related to donor liver protection strategies using following key words： ＂ischemia reperfusion injury＂, ＂graft preservation＂, ＂liver transplantation＂, ＂machine perfusion＂ and ＂conditioning＂. Of the 146 studies identified,only those with cutting edge strategies were analyzed.RESULTS： A variety of therapeutic approaches were proposed to alleviate graft ischemia/reperfusion injury, which included static cold storage, machine perfusion （hypothermic, normothermic and subnormothermic）, manual conditioning （pre,post and remote）, and pharmacological conditioning. Evidences from animal experiments and clinical trials suggested that all these strategies could potentially protect liver graft; however, their clinical applications are limited partially due to their own disadvantages.CONCLUSIONS： There are a plenty of methods suggested to decrease the degree of donor liver transplantation-related injury. However, none of these approaches is perfect in clinical practice. More translational researches （molecular and clinical studies） are needed to improve the techniques in liver graft protection.

Screening on the Pharmacodynemic Active Parts of Protecting Liver of Peristrope japonica (thunb.)Bremek

The pharmacodynamic active parts of protecting liver of Peristrope japonica (thunb.)Bremek were identified. Rat acute liver injury model was induced by D-galactosamine (D-GlaN). The active parts were identified on the whole extraction and 4 fractions. The results showed that the pharmacodynamic active parts of Peristrope japonica were the n-BuOH fraction.

Immune protection of auxiliary liver to other allograft: report of 3 cases

OBJECTIVE: To assess the immune status of auxiliary liver transplantation and to clarify the immune protection of auxiliary liver to other allograft. METHODS: Immunological markers and pathological changes in 3 patients undergoing auxiliary liver transplantation were analysed. RESULTS: The lower the concentration of immunosuppressive agent, the less the rejection and the milder the intensity in the 3 patients. The function of allograft after auxiliary liver transplantation was excellent. CONCLUSIONS: Patients are in a low immune reaction state after auxiliary liver transplantation. Auxiliary liver can protect other allografts by related immunological mechanisms. The side-effects of low-concentration immunosuppressive agents on auxiliary liver and other allografts are mild.

Bitter Melon Powder Protects against Obesity-associated Fatty Liver Disease by Improving Colonic Microenvironment in Rats with High-fat Diet-induced Obesity

This study explored how bitter melon powder （BMP） alters the colonic microenvironment during the development of obesity-associated fatty liver in rats. We observed that BMP effectively inhibited the body weight gain and lipid accumulation in the liver, ameliorated glucose intolerance, and increased the colon weight after an 8-week treatment compared to that in the high-fat diet （HFD） group. BMP significantly decreased fecal water toxicity towards HT-29 cells, as revealed by the cell counting kit （CCK）-8 assay results, and the mRNA expression of Toll-like receptor 4 （TLR4） in colon mucosa. Additionally, gut permeability in the BMP group was restored to normal levels. Finally, BMP alleviated the inflammatory state of the rat colon mucosa and liver tissues as well as the systemic inflammation.

Experimental study on the protective effect of propofol on liver injury in rats with sepsis

Objective:To observe the protective effect of propofol on liver injury in rats with sepsis and explore its protective mechanism.Methods:24 Wister rats were randomly divided into 3 groups,with 8 rats in each group:the sham operation group,the saline group and the propofol group.An intraperitoneal injection of LPS 8 mg/kg was used in the saline group,with continuous infusion of normal saline.An intraperitoneal injection of LPS 8 mg/kg and continuous infusion of propofol saline solution were also performed in the propofol group.Results:Compared with the saline group,the levels of ALT,AST,IL-6 and TNF-αin the sham operation group and the propofol group were significantly lower than those in the saline group.Conclusions:Propofol has a certain protective effect on liver injury in rats with sepsis.

Pharmacological effects and mechanisms of polyphenols in Radix Puerariae on liver protection and anti-diabetes

In recent years,the incidence of liver diseases and diabetes is increasing year by year,and the patients are younger than before.Although the clinical medicine treatment is eff ective,but it would produce side eff ects.Radix Puerariae is the dried root of the Pueraria lobata(Willd.)Ohwi.Puerarin is an isofl avone compound with polyphenol structure.It is one of the main bioactive components of Radix Puerariae.Studies have found that the application of puerarin off ers beatifical act on liver protection,hypoglycemia,blood lipid,antioxidant,anti-osteoporosis,anti-cancer,anti-inflammatory and cardiovascular protection.Puerarin has been used in the treatment of liver disease and diabetes.In this study,the eff ect of puerarin on liver protection,diabetes treatment and the relationship between the two diseases were reviewed.The therapeutic mechanism and molecular targets of puerarin were explored in order to further improve the development of puerarin and increase its clinical application in protection against liver disease and diabetes.

Anti-tumor,Anti-allergy,Anti-angiogenesis and Hepatoprotective Effects of Deoxypodophyllotoxin and Its Molecular Mechanism

Deoxypodophyllotoxin not only has pharmacological effects such as anti-allergy,anti-angiogenesis and liver protection,but also has good anti-tumor activity.It can play an anti-tumor role by inhibiting cell viability,inducing apoptosis,blocking cell cycle and inhibiting cell migration.In this paper,the related research on pharmacological effect and mechanism of deoxypodophyllotoxin is reviewed,to lay a foundation for the follow-up study of deoxypodophyllotoxin and drug development.

Protective Effect of Vitamin E on Liver Damage Induced by 2-Chloro-1, 3-butadiene

The present study was performed to determine the influence of lipid peroxidation and perturbance of Ca2+ homeostasis on liver damage induced by 2-chloro-1, 3-butadiene (CBD) and the protective effects of vitamin E in Wistar rats. Animals were given intraperitoneally different doses (8,40 or 200 mg·kg-1 daily) of CBD for 21 days, and the following dose-dependent events were observed: liver damage, significant increase in liver lipid peroxides, and decreases in activities of erythrocytic glutathione peroxidase (GSH-Px) and superoxide dismutase (SOD). The pretreatment of rats with vitamin E (po 150 mg·kg-1) before administering CBD (iP 60 mg·kg-1 ) daily for 21 days prevented the following CBD-induced changes, the increase in serum cholylglycine (CG), hepatic LP, hepatic mitochondrion LP, hepatic oxidized glutathione (GSSG) (while the significant increase of reduced glutathione (GSH) was not affected) and the decrease in activities of erythrocytic SOD and hepatic mitochondrial calcium sequestration. These results suggest that lipid peroxidation and perturbance of Ca2+ homeostasis appear to contribute to the hepatotoxicity of CBD, and vitamin E might prevent the liver damage induced by CBD. The decrease in activities of GSH-Px and SOD in erythrocytes might be used as biomarkers for adverse effects of CBD on defense system against lipid peroxidation.

Late Protective Effects of the Anticalmodulin Drug Fluphenazine on Carbon Tetrachloride-induced Liver Necrosis

Fluphenazine (FP) treatment (50mg/kg bw, ip in saline) 30 min before or 6 or 10 h after CCl4 administration (1 ml/kg ip in olive oil) significantly prevented the liver necrosis produced by the hepatotoxin at 24 h. FP had enhancing effects on the covalent binding of CCl4 reactive metabolites to cellular constituents and on CCl4 induced lipid peroaldation.FP lowered bOdy temperature of the CCl4-poisoned animals during the 24 h observation period. The obtained results are compatible but do not prove the hypothesis that calmodulin (CaM) had participation in late occurring events preceding necrosis. FP lowering action on body temperature, however, might also play a role in the effects of this drug on the onset of CCl4 induced liver necrosis. FP levels in liver tissue as determined by gas chromatography-mass spectrometry evidenced the presence of the drug in amounts suffi cient to inhibit CaM and that suggests that not all preventive effects of FP are due to its indirect actions on the central nervous system via decreased body temperature

Study on Protection Mechanism of Viscum coloratum (Kom.) Nakai f. lutescens kitag Fruit Polysaccharides on Mice with Acute Alcoholic Liver Injury

This study was conducted to investigate the protective mechanism of V. coloratum fruit polysaccharides（ VCFP） on mice with acute alcoholic liver injury. Acute liver injury model was built by one-time alcohol gavage. The mice were randomly divided into VCFP-treated groups（ low-,medium-,and highdose）,alcohol model group and normal control group at the same time. VCFP-treated groups were administrated polysaccharide intragastrically continuously for4 weeks; and the alcohol model group and normal control group were administrated intragastrically the same amount of normal saline. The general situation and liver tissue morphological structure changes were observed. The results showed that the levels of ALT,AST,TC,TG,MDA contents,and CAT and GSH-Px activity of mice in the model group increased significantly（ P 〈 0. 01）,while the activity of SOD and weight and liver index decreased significantly（ P 〈 0. 01） compared with the normal control group. After 4 weeks of gavage,VCFP could significantly improve weight,liver index and SOD activity,and significantly reduce ALT,AST,TC and TG levels,MDA content and CAT and GSH-Px activity. These results suggest that VCFP can improve antioxidant enzyme activity,remove oxygen free radical and reduce membrane lipid peroxidation reaction,thereby protecting liver cells.

Protective effect of hydrogen-rich saline on liver ischemia-reperfusion injury in mice

Objective To explore protective effect of hydrogen - rich saline on liver ischemia reperfusion ( IR) in mice and possible mechanisms. Methods Twenty - four C57BL /6 mice were randomly divided into 3 groups: sham - operated group,control group ( mice were injec-

基于京尼平结构的衍生物设计与合成及其对HepG2细胞毒性的研究

目的:设计并合成一系列基于京尼平结构的环烯醚萜类衍生物,并探讨其对HepG2细胞的毒性作用,为寻找具有肝保护作用的药物提供一定的理论指导。方法:以京尼平为起始物,以三氟化硼乙醚为催化剂,在低温无水无氧体系下与低碳醇(甲醇、乙醇、正丙醇、异丙醇、正丁醇、叔丁醇)进行S_(N)1取代反应,获得的产物经^(1)H-NMR进行结构表征;采用CCK-8法评价化合物对HepG2细胞的细胞毒性,并以谷胱甘肽为阳性对照,以IC_(50)值表示其毒性强弱。结果:设计并合成了6个京尼平衍生物,分别是1-O-甲基京尼平、1-O-乙基京尼平、1-O-正丙基京尼平、1-O-异丙基京尼平、1-O-正丁基京尼平、1-O-叔丁基京尼平,经^(1)H-NMR表征其结构正确。细胞实验显示,谷胱甘肽的IC_(50)值>1 000μmol/L,京尼平的IC_(50)值为(558.70±22.81)μmol/L,1-O-正丙基京尼平、1-O-正丁基京尼平的IC_(50)值分别为(537.40±188.10)μmol/L、(586.10±42.41)μmol/L,细胞毒性均低于谷胱甘肽,但与京尼平相近;1-O-异丙基京尼平的IC_(50)值为(628.30±38.72)μmol/L,低于谷胱甘肽,但高于京尼平;1-O-甲基京尼平、1-O-乙基京尼平、1-O-叔丁基京尼平的IC_(50)值分别为(324.30±55.67)μmol/L、(111.95±18.06)μmol/L、(91.10±15.20)μmol/L,均低于谷胱甘肽和京尼平。结论:合成了6个京尼平衍生物,获得了一条简单的、可控的京尼平衍生物的合成方法;其中京尼平衍生物1-O-正丙基京尼平、1-O-异丙基京尼平、1-O-正丁基京尼平对HepG2细胞毒性较小。

驱动压导向呼气末正压通气对原位肝移植患者术中氧合和术后并发症的影响

目的评价驱动压导向呼气末正压(PEEP)通气对原位肝移植术(OLT)患者术中氧合和术后并发症的影响。方法选择2020年1月至2023年9月行OLT患者118例,男89例,女29例,年龄18~70岁,BMI<28 kg/m^(2),ASAⅢ或Ⅳ级。采用随机数字表法将患者分为两组:驱动压组(D组)和固定PEEP组(P组),每组59例。两组全麻期间均采用容量控制通气,I∶E 1∶2,V_(T)6 ml/kg(理想体重),RR 10~15次/分。D组在机械通气5 min后开始PEEP滴定试验,将PEEP从2 cmH_(2)O逐渐递增到10 cmH_(2)O,选择能产生最低驱动压的PEEP,维持该PEEP直至手术结束。P组术中维持PEEP 5 cmH_(2)O。记录术中出入量、血管活性药物使用情况。记录插管后5 min(T_(1))、无肝期(T_(2))、新肝期(T_(3))、手术结束即刻(T_(4))的HR、SBP、DBP、气道峰压(Ppeak)、气道平台压(Pplat)、PEEP、血气分析结果,并计算驱动压、动态肺顺应性(Cdyn)、氧合指数(OI)、死腔率(V_(D)/V_(T))。记录术后7 d内术后肺部并发症(PPCs)的发生情况。结果与P组比较,D组晶体液输注量明显增加,去甲肾上腺素、去氧肾上腺素及肾上腺素使用率明显升高(P<0.05)。与T_(2)时比较,两组T_(1)、T_(3)、T_(4)时HR明显减慢,SBP、DBP明显升高(P<0.05)。与T_(1)时比较,两组T_(2)—T_(4)时Ppeak、Pplat、驱动压、OI明显升高,T_(3)、T_(4)时Cdyn明显降低(P<0.05)。与P组比较,D组术后7 d内PPCs发生率明显降低(P<0.05)。两组其余指标差异无统计学意义。结论驱动压导向PEEP通气可改善原位肝移植患者术中氧合,降低PPCs发生率,但术中血管活性药物的使用率升高。

枸杞多糖对肝内胆汁淤积模型大鼠肝脏预防保护作用的研究

目的 探讨枸杞多糖(LBP)对肝内胆汁淤积模型大鼠肝脏损伤的预防保护作用。方法 SPF级雄性SD幼龄大鼠,设阴性对照组、模型组、LBP 50、150、450 mg/kg剂量组,以及阳性对照组,每组各10只。构建大鼠肝内胆汁淤积模型,模型组、LBP各剂量组及阳性对照组,予60mg/kg α-萘异硫氰酸酯,每隔1天给药一次,第2周开始改为每隔3天给药一次,持续6周。第2周起,各剂量组每天予不同剂量的LBP,阳性对照组予熊去氧胆酸,模型组大鼠予蒸馏水。6周后采集血液及肝组织样本,测定血清生化指标、凝血功能指标及白细胞分类计数指标,检测肝组织中的炎症因子含量以及Toll样受体4(TLR4)、核因子κB(NF-κB)、核转录因子(pNF-κB)及髓分化因子88(MyD88)蛋白的表达量,观察大鼠肝脏的病变情况。结果 与阴性对照比较,模型组大鼠血清γ-谷氨酰转移酶(γ-GGT)、碱性磷酸酶(ALP)、总胆汁酸(TBA)、总血红素(TBiL)、胆固醇(CHOL)、丙氨酸氨基转移酶(ALT)及天冬氨酸氨基转移酶(AST)水平,血液白细胞(WBC)、淋巴细胞(LYMP)、中性粒细胞(NEUT)、单核细胞(MONO)及嗜酸性粒细胞(EO)计数,纤维蛋白原(FIB)含量均升高(均P <0.05),肝组织中炎症因子肿瘤坏死因子(TNF-α)、白介素1β(IL-1β)、白介素6及巨噬细胞炎性蛋白2(MIP-2)含量增加,TLR4、pNF-κB、MyD88蛋白表达水平上调(均P <0.05)。肝脏可见多量炎症细胞浸润、胆管增生、纤维组织增生等病理性改变,组织形态学观察评分上升(均P <0.05);与模型组比较,LBP450mg/kg组大鼠血清γ-GGT、TBA、TBiL、ALT水平,血液WBC、LYMP、NEUT计数,FIB含量均下降(均P<0.05),肝组织中炎症因子TNF-α、IL-1β、MIP-2含量降低,TLR4、pNF-κB、MyD88蛋白的表达水平下调(均P<0.05),肝脏组织形态学观察评分下降(均P <0.05),肝脏损伤减轻,LBP 150 mg/kg组大鼠血液FIB含量均下降,TLR4蛋白的表达水平下调(均P<0.05)。结论 LBP对肝内胆汁淤积模型大鼠肝脏损伤有缓解和保护功效,其作用机制可能与下调TLR4/MyD88/NF-κB信号通路相关蛋白的表达,抑制过度炎症反应有关。

陈皮复合固体饮料制备工艺及其对急性酒精性肝损伤小鼠的保护作用

[目的]以药食同源的陈皮、山楂、葛根为主要原料,开发一种具有解酒功能的固体饮料,并探究其对急性酒精性肝损伤小鼠的保护作用。[方法]以浸膏得率和总黄酮含量为标准,采用正交试验选取最佳提取工艺;以感官评价、成型率、溶化性的综合评分为指标,采用单因素试验优化成型工艺。采用52%酒精灌胃的方法建立急性酒精性肝损伤小鼠模型,检测陈皮复合固体饮料对模型小鼠肝脏指数,血清中谷草转氨酶(AST)、谷丙转氨酶(ALT),肝组织中总胆固醇(TC)、甘油三酯(TG)、超氧化物歧化酶(SOD)、丙二醛(MDA)、谷胱甘肽(GSH)及炎症因子白细胞介素-1β(IL-1β)、白细胞介素6(IL-6)、肿瘤坏死因子-α(TNF-α)的影响,苏木素—伊红(HE)染色分析各组肝脏病理变化。[结果]陈皮复合固体饮料最佳制备工艺:3味药材浸泡30 min后提取2次,第一次料液比1∶12(g/mL)、提取时间2.0 h,第二次料液比1∶10(g/mL)、提取时间1.5 h;经浓缩、干燥、粉碎后得到干膏粉;干膏粉与麦芽糊精1∶1混合,加入1.0%的罗汉果甜苷,并以90%乙醇作为润湿剂进行湿法制粒。动物试验表明:与模型组相比,陈皮复合固体饮料组的AST、ALT、TG、TC、MDA、IL-1β、IL-6、TNF-α水平降低(P<0.01或P<0.05),GSH、SOD含量增加(P<0.01或P<0.05),且肝组织病理切片显示给药组小鼠肝损伤程度均有显著改善。[结论]陈皮复合固体饮料色泽均匀、溶解性好、甜度适中、口感细腻,对急性酒精性肝损伤具有良好的保护作用。

双歧杆菌三联活菌散联合保肝治疗对乙型肝炎肝硬化患者肠道菌群及炎性因子水平的影响

目的探讨双歧杆菌三联活菌散联合保肝治疗对乙型肝炎肝硬化患者肠道菌群及炎性因子水平的影响。方法选取2019年3月至2022年5月我院收治的124例乙型肝炎肝硬化患者作为研究对象,根据投掷硬币法将其分为参照组和研究组,每组62例。参照组给予常规保肝及对症治疗,研究组在参照组基础上给予双歧杆菌三联活菌散治疗。比较两组的治疗效果。结果治疗后,研究组的层粘连蛋白(LN)、透明质酸(HA)、Ⅲ型前胶原(PC-Ⅲ)及Ⅳ型胶原(Ⅳ-C)水平低于参照组(P<0.05)。治疗后,研究组的白细胞介素-1β(IL-1β)、肿瘤坏死因子-α(TNF-α)、白细胞介素-8(IL-8)及白细胞介素-6(IL-6)水平低于参照组(P<0.05)。治疗后,研究组的D-乳酸(DLC)、内毒素(ET)及降钙素原(PCT)水平低于参照组(P<0.05)。治疗后,研究组的双歧杆菌、肠球菌、乳酸杆菌及拟杆菌数量多于参照组,酵母样真菌数量少于参照组(P<0.05)。结论双歧杆菌三联活菌散联合保肝治疗乙型肝炎肝硬化患者的效果显著,不仅能够有效调节肝纤维化指标、炎性因子以及肠道通透性指标水平,还能促进肠道菌群平衡。