脂质过氧化反应在大鼠急性酒精性肝损害中的作用

目的观察脂质过氧化反应在酒精导致大鼠急性肝损害中的作用。方法健康雄性Wistar大鼠40只，随机分为4组。A组（空白对照组）灌胃生理氯化钠溶液20mL·kg-1·d-1；其余各组灌胃等剂量白酒；其中C组（阳性药物干预组1）在B组基础上预先1h灌胃茴三硫10mg·kg-1·d-1，D组（阳性药干预组2）在B组基础上预先1h灌胃硫普罗宁100mg·kg-1·d-1；实验共10d。实验第6天、第11天取各组大鼠血液，检测谷胱甘肽过氧化物酶（GSH—Px）、丙二醛（MDA）、谷丙转氨酶（ALT）、谷草转氨酶（AST）；实验结束时处死动物，取肝组织，HE、Masson染色，光镜检查。结果急性酒精中毒可引起大鼠血清MDA升高，GSH—Px降低；ALT、AST升高，提示有显著的脂质过氧化反应和肝功能损害，肝脏病理出现肝细胞脂肪变性，炎症坏死病变。使用两种药物干预后脂质过氧化反应受到抑制，肝功能和肝脏病理学损害均有减轻，各组间差异有统计学意义。结论脂质过氧化反应在大鼠急性酒精性肝损害的发生中起重要作用，抑制该反应可显著减轻肝脏损伤。     

肝再生增强因子对肝星状细胞基因表达谱的影响

目的将pcDNA3．1（-）．ALR（hALR）和pcDNA3．1（-）分别转染人肝星形细胞（HSC）,筛选在人肝星形细胞中存在表达差异的基因,进一步研究hALR的生物学功能及机制。方法以脂质体技术将pcDNA3．1（-）．ALR和pcDNA3．1（-）分别转染人肝星形细胞系,提取总mRNA,逆转录为cDNA,应用基因表达谱芯片方法分析差异表达的基因。结果在所筛选的4096个基因中,有2个基因表达水平显著上调,25个基因表达水平显著下调。结论hALR对于人肝星形细胞基因表达谱有显著影响,为进一步研究hALR的生物学功能和作用机制提供了线索。     

肝细胞生长因子与肝再生增强因子重组表达质粒对大鼠肝纤维化的影响

目的 研究肝细胞生长因子(HGF)与肝再生增强因子(ALR)重组表达质粒对大鼠实验性肝纤维化的治疗作用.方法 建立二甲基亚硝胺肝纤维化模型后的90只S-D大鼠分为空白组、pcDNA3.1治疗组、pcDNA3.1-HGF治疗组、pcDNA3.1-ALR治疗组、pcDNA3.1-HGF与pcDNA3.1-ALR共治疗组、pcDNA3.1-HGF-ALR治疗组,每组15只.各治疗组大鼠每24小时经尾静脉注射1次相应质粒0.1 μmol,连续3次,空白组不接受任何治疗,另取同批次S-D大鼠10只作为对照组.治疗结束后4 d处死大鼠,留取肝组织采用HE染色观察肝脏的病理形态,采用免疫组织化学染色检测增殖细胞核抗原(PCNA)和c-jun的表达.计量资料采用单因素方差分析,两两比较采用SNK检验,计数资料采用Fisher确切概率法分析.结果 空白组和pcDNA3.1治疗组大鼠肝组织有明显的条索状纤维间隔形成,可见假小叶,两组肝纤维化程度差异无统计学意义(x2=0.317,P=1. 000);其他治疗组肝纤维化均有不同程度改善,以pcDNA3.1-HGF-ALR治疗组改善最明显.对照组肝组织PCNA和c-jun表达均较低,其吸光度值分别为8.6±1.9和3.2±1.2;空白组与pcDNA3.1治疗组肝组织PCNA和c-jun表达均增加,其吸光度值分别为24.1±3.0.24.5±4.3与23.8±3.1、24.9±4.2,与对照组比较,差异有统计学意义(均P＜0.01);其他治疗组的PCNA表达显著增加,c-jun表达显著降低,均以pcDNA3.1-HGF-ALR治疗组的变化最明显.结论 重组表达质粒pcDNA3.1-HGF-ALR能较好地改善大鼠实验性肝纤维化,并可能通过促进肝细胞增殖和抑制原癌基因c-jun的表达来发挥其抗肝纤维化作用.     

人肝再生增强因子在肝衰竭患者血清及肝组织中的表达及其意义

目的 探讨人肝再生增强因子(ALR)在肝衰竭患者血清及肝组织中的表达水平及其意义.方法 制备Balb/c小鼠来源的人ALR蛋白多克隆抗体并纯化其IgG组分,以该抗体通过酶联免疫吸附法建立ALR浓度与吸光值的标准曲线.获取18例肝衰竭患者、24例慢性乙型肝炎患者及10名正常人血清,比较其血清ALR水平差异,实时荧光PCR法比较各组患者肝组织ALR mRNA表达水平差异.据资料不同采用Bonferroni或LSD检验进行统计学分析. 结果 Western blot结果发现人ALR蛋白多克隆抗体能特异性结合人ALR蛋白,酶联免疫法检测结果发现其在一定的ALR浓度范围内有良好的线性关系.18例肝衰竭患者中,6例好转出院的患者血清ALR水平为(1613.5±369.6)pmol/ml,高于12例肝功能恶化、死亡或不得不接受肝移植患者的(462.3±235.8)pmol/ml(t=11.21,P<0.05);慢性乙型肝炎患者为(969.2±332.5)pmol/ml,与正常人的(806.9±240.8)pmol/ml差异无统计学意义(t=2.17,P>0.05).5例接受肝移植的患者肝组织ALR mRNA表达水平为(3.45±0.38)log10拷贝/μl,低于慢性乙型肝炎患者的(4.37±0.15)log10拷贝/μl及正常供体的(4.31±0.10)log10拷贝/μl(P<0.05),而后两者差异无统计学意义(P>0.05).结论 血清ALR水平反映了肝脏ALR mRNA表达水平,其在预测慢加急性肝衰竭患者的预后方面有一定意义.     

Protective effects of mild hypothermia against hepatic injury in rats with acute liver failure

Introduction and ObjectivesAcute liver failure (ALF) is a severe disease which is associated with a high mortality rate. As mild hypothermia has been shown to have protective effects on the brain, this study aimed to determine whether it also provides protection to the liver in rats with ALF and to explore its underlying mechanism.Materials and methodsIn total, 72 rats were divided into 3 groups: control group (CG, treated with normal saline), normothermia group (NG, treated with d-galactosamine and lipopolysaccharide; d-GalN/LPS), and mild hypothermia group (MHG, treated with d-GalN/LPS and kept in a state of mild hypothermia, defined as an anal temperature of 32–35 °C). The rats were examined at 4, 8, and 12 h after treatment.ResultsMild hypothermia treatment significantly reduced serum alanine transaminase and aspartate transaminase levels and improved the liver condition of rats with d-GalN/LPS-induced ALF at 12 h. Serum tumor necrosis factor-alpha levels were significantly lower in the MHG than in the NG at 4 h, but no significant differences were observed in the interleukin-10 levels between the NG and MHG at any time. The serum and hepatic levels of high mobility group box 1 were significantly lower in the MHG than in the NG at 8 and 12 h. The protein expression levels of cytochrome C and cleaved-caspase 3 in hepatic tissues were significantly lower in the MHG than in the NG at 8 h.ConclusionMild hypothermia improved the liver conditions of rats with ALF via its anti-inflammatory and anti-apoptotic effects.     

Effects of augmentation of liver regeneration recombinant plasmid on rat hepatic fibrosis

AIM: To investigate the effects of eukaryotic expression of plasmid on augmentation of liver regeneration (ALR) in rat hepatic fibrosis and to explore their mechanisms. METHODS: Ten rats were randomly selected from 50 Wistar rats as normal control group. The rest were administered intraperitoneally with porcine serum twice weekly. After 8 wk, they were randomly divided into: model control group, colchicine group (Col), first ALR group (ALR1), second ALR group (ALR2). Then colchicine ALR recombinant plasmid were used to treat them respectively. At the end of the 4th wk, rats were killed. Serum indicators were detected and histopathological changes were graded. Expression of type Ⅰ, Ⅲ, collagen and TIMP-1 were detected by immunohisto-chemistry and expression of TIMP-1 mRNA was detected by semi-quantified RT-PCR. RESULTS: The histologic examination showed that the degree of the rat hepatic fibrosis in two ALR groups was lower than those in model control group. Compared with model group, ALR significantly reduced the serum levels of ALT, AST, HA, LN, PCIII and IV (P<0.05). Immunohistochemical staining showed that expression of type Ⅰ, Ⅲ, collagen and TIMP-1 in two ALR groups was ameliorated dramatically compared with model group (I collagen: 6.94±1.42,5.80±1.66 and 10.83±3.58 in ALR1, ALR2 and model groups, respectively; Ⅲ collagen: 7.18±1.95, 4.50±1.67 and 10.25±2.61, respectively; TIMP-1: 0.39±0.05,0.20±0.06 and 0.53±0.12, respectively,P<0.05 or P<0.01). The expression level of TIMP-1 mRNA in the liver tissues was markedly decreased in two ALR groups compared with model group (TIMP-1 mRNA/β-actin: 0.89±0.08, 0.65±0.11 and 1.36±0.11 in ALR1, ALR2 and model groups respectively, P<0.01). CONCLUSION: ALR recombinant plasmid has beneficial effects on rat hepatic fibrosis by enhancing regeneration of injured liver cells and inhibiting TIMP-1 expressions.     

大黄对暴发性肝衰竭大鼠肝损伤及肝再生的影响

[目的]探讨大黄对暴发性肝衰竭(FHF)大鼠肝损伤及肝再生的影响.[方法]Wistar大鼠随机分4组:正常对照(对照)组、模型(FHF)组、大黄组、促肝细胞生长素(PHGF)组.FHF、大黄组和PHGF组动物模型采用皮下注射(sc)硫代乙酰胺(TAA)600 mg/kg体重,2次,每次间隔24 h,复制FHF动物模型.大黄组和PHGF组动物除予TAA外,于实验前3天至实验结束分别sc大黄注射液1 ml/100 g和PHGF 1 ml/100g,对照组和FHF组同时sc 0.85%氯化钠液1 ml/100g.FHF组、大黄组和PHGF组,于第2次注射TAA后24 h,随机各取8只,腹主动脉取血测肝功能.迅速取肝组织,用10%甲醛液固定,石蜡切片,检测肝细胞有丝分裂指数(MI)和增殖细胞核抗原(PCNA).[结果]大黄具有降低FHF大鼠丙氨酸氨基转移酶、天冬氨酸转氨酶及总胆红素,并能显著提高MI和PCNA(P＜0.05,＜0.01).[结论]大黄具有改善FHF大鼠肝功能和促进肝细胞增殖及再生的作用.     

基质细胞衍生因子-1对小鼠急性肝损伤修复的实验研究

目的探索基质细胞衍生因子对急性肝损伤修复的影响,并与单纯骨髓单个核细胞移植治疗肝损伤疗效相比较。方法建立小鼠CCl4-AAF肝损伤模型,从小鼠骨髓分离骨髓单个核细胞。实验A组经腹腔向模型小鼠体内注入基质细胞衍生因子,实验B组经尾静脉向模型小鼠体内注入单个核细胞,对照C组经尾静脉向模型小鼠体内注入生理盐水,在第2周、3周、4周,从各组取出相同的小鼠处死,通过测肝功能指标（AST、ALT、TBil）和肝组织病理切片,比较各组小鼠肝损伤修复的差异。结果分别在第2周、3周、4周测得的SDF-1组（A组）和单个核细胞组（B组）的数值比较（U/L）：ALT（第2周：19.0±2.0 vs 19.7±4.7,P〉0.05;第3周：19.0±5.0 vs 14.5±2.5,P〉0.05;第4周：40.0±17.0 vs 15.0±3.0,P〉0.05）;AST（第2周：117.1±18.0 vs 116.7±20.0,P〉0.05;第3周：97.5±5.0 vs 104.5±23.5,P〉0.05;第4周：177.3±61.0 vs 105.0±49.1,P〉0.05）;TBil（第2周：1.8±0.1 vs 1.9±0.3,P〉0.05;第3周：1.75±0.55 vs 1.5±0.4,P〉0.05;第4周：1.8±0.6 vs 1.5±0.3,P〉0.05）。在病理方面第2周、4周时A组及B组肝细胞仍有肿胀,但组织结构较急性损伤时有明显改善。结论基质细胞衍生因子和单个核细胞都能够促进肝损伤的修复,在病理方面骨髓单个核细胞对损伤修复效果更明显一些。     

精氨酸对急性肝衰竭大鼠血清细胞因子水平的影响

目的探讨不同剂量精氨酸对急性肝衰竭大鼠血清细胞因子的影响。方法 60只大鼠被随机分为A组（正常对照组）、B组（肝衰竭组）、C组（精氨酸强化Ⅰ组）、D组（精氨酸强化Ⅱ组）、E组（精氨酸强化Ⅲ组）和F组（精氨酸强化Ⅳ组）。采用D-半乳糖胺诱导法复制大鼠急性肝衰竭模型。结果肝衰竭大鼠血清TNF-α含量升高,其中B、C组与A组比较差别有统计学意义（P〈0.05）;肝衰竭大鼠IL-2含量均低于正常组,其中B、C、D、F组与A组比较差别有统计学意义（P〈0.05）;肝衰竭动物IL-10含量均低于正常组,其中B、C组与A组比较差别有统计学意义（P〈0.05）;肝衰竭大鼠血清IGF-1含量降低,其中B、C组与A组比较差别有统计学意义（P〈0.05）。结论精氨酸可调节肝衰竭大鼠体内细胞因子水平,以0.8g.kg-1.d-1和1.6g.kg-1.d-1剂量比低剂量或高剂量效果更明显。     

糖皮质激素联合生长激素对大鼠急性肝衰竭的保护作用及其机制初步探讨

目的研究糖皮质激素（氢化考的松琥珀酸钠,HCSS）联合生长激素（GH）对大鼠急性肝衰竭的影响.方法采用Wistar大鼠注射脂多糖（LPS）和D氨基半乳糖（D-GalN）制备急性肝衰竭模型,随机分为正常对照组、模型对照组、药物干预组及造模后4 h干预组,各组于末次给药6 h后处死大鼠,常规H-E染色观察大鼠肝脏病理变化,检测肝功能和血清TNF-α,IL-8,IL-6水平;分离培养大鼠库普否细胞（KC）,经LPS（10μg/ml）刺激,于刺激开始（0 h）和4 h后分别给药,并于0、2、4、8和24 h后收集上清,测定TNF-α.结果HCSS或HCSS联合GH预防给药可显著降低急性肝衰竭大鼠血清TBIL、ALT、AST和TNF-α、IL-8、IL-6水平,药物干预组较模型组肝细胞坏死有明显改善.LPS刺激2 h后,KC培养上清中TNF-α浓度开始上升并在4 h达高峰.在培养开始加用HCSS可明显降低TNF-α水平,而培养4 h后加用HCSS不能明显降低TNF-α水平.在培养开始加用GH可进一步升高TNF-α水平,而联合给予HCSS后可降低TNF-α水平.结论预防性给予大鼠药物干预可明显减轻肝损伤,而在造模4 h后使用HCSS则无明显效果.联合使用合理剂量的HCSS和GH仍能较好的减轻肝损伤.     

Hepatic stimulator substance administration ameliorates liver regeneration in an animal model of fulminant hepatic failure and encephalopathy

Abstract: Aims/Background: Hepatic stimulator substance (HSS) is a liver‐specific growth factor implicated in hepatocellular proliferation and hepatoprotection in models of acute liver injury. In the present study, we examined the effect of exogenous HSS administration on liver proliferating capacity and survival outcome in an experimental animal model of fulminant hepatic failure (FHF) and encephalopathy, induced by repeated injections of thioacetamide (TAA) in rats. Methods: Fulminant hepatic failure was induced in adult male Wistar rats by three consecutive intraperitoneal injections of TAA (400 mg/kg of body weight), at 24 h time intervals. The animals received intraperitoneally either a saline solution or HSS (50 mg protein/kg of body weight), 2 h after the second and third TAA injections. The animals were killed at 6, 12 and 18 h post the last injection of TAA. Results: Levels of liver enzymes and urea in serum, blood ammonia values, liver histology, stage of hepatic encephalopathy and survival were statistically significantly improved in TAA‐intoxicated and HSS‐treated rats compared to TAA‐intoxicated and saline‐treated ones. Furthermore, HSS ameliorated liver regenerative indices – DNA biosynthesis, thymidine kinase activity and hepatocyte mitotic activity – in a statistically significant manner. Conclusions: Our data suggest the beneficial effect of HSS administration in this animal model of FHF and encephalopathy, supporting evidence for a possible use of HSS as supportive therapy, by increasing hepatocellular proliferation, in management of FHF.     

大鼠肝细胞生长因子与肝再生增强因子融合基因真核表达质粒的构建及鉴定

目的 构建大鼠肝细胞生长因子(rHGF)与大鼠肝再生增强因子(rALR)融合基因的真核表达质粒并进行鉴定,为新的肝纤维化治疗方法奠定实验基础.方法 分别以重组质粒pUC18-rHGF和pUC18-rALR为模板,进行PCR扩增,获得rHGF和rALR的基因片段;利用重叠延伸PCR方法将获得的基因片段通过一个连接序列(linker)进行连接,构建融合基因rHGF-linker-rALR,将融合基因定向插入pcDNA3.1真核表达质粒的Kpn Ⅰ和Xba Ⅰ酶切位点之间,构建重组真核表达质粒pcDNA3.1-rHGF-linker-rALR,并进行双酶切及测序鉴定.结果 rHGF和rALR的PCR扩增产物电泳后分别观察到2200 bp和400 bp的条带,与理论值相符.重叠延伸PCR获得的融合基因产物电泳后观察到2600 bp的条带,与预期值一致.重组真核表达质粒pcDNA3.1-rHGF-linker-rALR经双酶切,电泳后观察到2600 bp和5400 bp的两条DNA条带,与预期值相符,测序鉴定结果表明序列正确.结论 成功构建了rHGF与rALR融合基因的真核表达质粒,为肝纤维化的基因治疗奠定了实验基础.     

丹参对暴发性肝衰竭大鼠肝损伤及肝再生的影响

目的：探讨丹参对暴发性肝衰竭（FHF）大鼠肝损伤及肝再生的影响。方法：Wistar大鼠随机分为4组：正常对照组、FHF组、丹参组、促肝细胞生长素（PHGF）组。FHF、丹参组和PHGF组动物模型采用TAA皮下注射,剂量按每kg体重600mg,2次,每次间隔24h,复制FHF动物模型。丹参组和PHGF组动物除皮下注射TAA外,于实验前3天至实验结束分别于皮下注射丹参注射液1ml/100g和PHGF1ml/100g,正常对照组和FHF组大鼠同时皮下注射生理盐水1ml/100g。FHF组、丹参组和PHGF组,于第2次注射TAA后24h,随机取大鼠各8只,腹主动脉取血测肝功能。迅速取肝组织,用10%甲醛液固定,制成石蜡切片,检测肝细胞有丝分裂指数（MI）和增殖细胞核抗原（PCNA）。结果：丹参具有降低FHF大鼠ALT、AST及TBil,显著提高肝细胞MI和PCNA的作用（P〈0.05,P〈0.01）。结论：丹参具有改善FHF大鼠肝功能和促进肝细胞增殖及再生的作用。     

急性肝功能哀竭动物模型的建立

目的建立与临床较相近的急性肝功能衰竭动物模型.方法应用中国实验小型猪7头,采用Β期门静脉-下腔静脉吻合、Ⅱ期(48 h后)供肝动脉暂时结扎4 h的方法建立缺血性急性肝功能衰竭动物模型;中国实验小型猪6头给于1.2 g/kg的D-氨基半乳糖诱导肝功能衰竭,建立药物性急性肝功能衰竭动物模型.观察比较每组动物一般状况、生存时间、生理生化指标、颅内压、组织病理等方面的变化.结果在缺血性模型中,1头猪死于术中大出血,1头猪的生存时间超过5 d,其余5头存活时间为18～30h[平均存活时间(22.5±5.6)h];反映肝功能的主要指标(AST,总胆红素、凝血酶原时间、血氨、血糖)均明显异常;组织病理显示肝脏大块坏死.在药物性模型中,动物在给药后12 h各项指标开始变化明显,给药后48 h损伤达高峰,平均存活时间为(67.9±9.4)h,最终死于严重肝功能衰竭.结论应用缺血方法与药物方法均能建立急性肝功能衰谒动物模型,其中D-氨基半乳糖1.2g/kg的给药剂量建立的模型稳定性好且能较好模拟临床急性肝功能衰竭发生发展的病理生理过程,可用于研究机制和评价疗效.     

Intensive liver care and management of acute hepatic failure

In describing acute liver failure, the term fulminant hepatic failure (FHF) is used to denote patients with the most rapid progression, normally defined as the onset of encephalopathy within eight weeks of the onset of symptoms. For patients with a slower onset of encephalopathy, ranging from eight weeks to six months after the onset of symptoms, late-onset hepatic failure is the term used to reflect the overlap in clinical features with some patients with FHF. The importance of accurately determining the type of acute liver failure results from increasing evidence of an inverse relationship between the tempo of disease progression and the chances of recovery. Prognosis is also dependent on the underlying etiology. Principles of management are as follows: (1) an accurate recognition of the tempo of the hepatic failure—fulminant, late onset, acute on chronic—and the establishment of a likely etiology; (2) early detection and treatment of complications, particularly metabolic acidosis (early), renal failure, cerebral edema, and infection (late); (3) optimization of conditions for regeneration by maintenance of a near normal metabolic milieu (with removal of toxins by various methods of artificial liver support if necessary); and (4) early consideration of an orthotopic liver transplant for those patients in the poor prognosis group. Variations in the natural history and clinical features of acute liver failure (ALF) have led to a number of different classifications and subgroupings. Knowledge of these is important in relation to the assessment of prognosis and is even more important now that transplantation is a therapeutic option. Fulminant hepatic failure (FHF) is the term used to denote the subgroup where the tempo is greatest and is variously defined as the onset of encephalopathy within four weeks (1), six weeks (EASL, 1979) and eight weeks [as described by Trey and Davidson (2)] of the onset of symptoms, or within two weeks of the onset of jaundice (3). The patients with a more protracted course are designated by the terms subacute or late-onset hepatic failure (LOHF) (4) or subfulminant hepatic failure (3). The etiology of the hepatic failure also has a major influence on the likely prognosis.Presented at the Proceedings of International Meeting on Normal and Neoplastic Growth in Hepatology, Bari, Italy, June 1989.     

急性肝衰竭大鼠血浆神经降压素和降钙素基因相关肽水平的变化

目的探讨急性肝衰竭(ALF)大鼠血浆神经降压素(NT)和降钙素基因相关肽(CGRP)含量的变化。方法采用硫代乙酰胺制备ALF大鼠模型。采用RIA法测定血浆NT和CGRP含量。结果模型组大鼠血浆NT和CGRP含量明显升高,与正常对照组比,差异有统计学意义(P0.01);模型组大鼠分别于造模后12h、24h、36h和48h,肝性脑病逐渐进展,血浆NT和CGRP含量也呈进行性升高。结论测定血浆NT和CGRP含量可作为判断肝性脑病早期诊断的指标之一,其含量的变化对肝性脑病严重程度的判断有重要的参考价值。     

Roles of hepatic stellate cells in acute liver failure: From the perspective of inflammation and fibrosis

Acute liver failure(ALF) usually results in hepatocellular dysfunction and coagulopathy and carries a high mortality rate. Hepatic stellate cells(HSCs) are famous for their role in liver fibrosis. Although some recent studies revealed that HSCs might participate in the pathogenesis of ALF, the accurate mechanism is still not fully understood. This review focuses on the recent advances in understanding the functions of HSCs in ALF and revealed both protective and promotive roles during the pathogenesis of ALF: HSC activation participates in the maintenance of cell attachment and the architecture of liver tissue via extracellular matrix production and assists liver regeneration by producing growth factors; and HSC inflammation plays a role in relaying inflammation signaling from sinusoids to parenchyma via secretion of inflammatory cytokines.A better understanding of roles of HSCs in the pathogenesis of ALF may lead to improvements and novel strategies for treating ALF patients.     

蓝莓预防大鼠肝损伤实验研究

目的探讨蓝莓对四氯化碳（CCl4）所致大鼠急性肝损伤的预防保护作用。方法SD大鼠随机分为蓝莓汁低、高两个剂量预防组、齐墩果酸阳性药对照组、正常对照组及模型组,采用CCl4致大鼠急性肝损伤模型。测定大鼠血清丙氨酸氨基转移酶（ALT）、天冬氨酸氨基转移酶（AST）以及肝组织匀浆超氧化物歧化酶（SOD）、还原型谷胱甘肽（GSH）、过氧化氢酶（CAT）及丙二醛（MDA）,光镜下观察肝脏病理变化。结果蓝莓各剂量组及阳性对照组血清ALT及AST均明显低于模型组（P〈0．01）。与模型组比较,齐墩果酸组、蓝莓汁高剂量组肝匀浆GSH、SOD、CAT明显升高,MDA明显降低（P〈0．01或P〈0．05）;蓝莓汁低剂量组肝匀浆GSH升高不明显,肝匀浆SOD、CAT升高,MDA降低（P〈0．05）。结论蓝莓对CCl4所致大鼠急性肝损伤具有良好的预防保护作用,其机制可能与抗脂质过氧化作用有关。