干扰素α抗肝纤维化的实验研究

我们研究ＩＦＮα对肝纤维化ＥＣＭ、ＴＧＦβ及肝脏病理的影响，探讨ＩＦＮα抗肝纤维化的作用机理。 一、材料与方法 １．动物模型的建立：ＳＤ大鼠６３只，体重２００ｇ左右，随机分为正常对照组（ａ组）、模型对照组（ｂ组）、干扰素治疗组（ｃ组），各２１只。其中ｂ组及ｃ组采用皮下注射４０％ＣＣｌ４（用精制橄榄油配制）３ｍｌ／ｋｇ，每３日１次，首剂加倍，共１２周，诱导肝纤维化［１］。ａ组注射等剂量的精制橄榄油，ｃ组隔日１次皮下注射ＩＦＮα（沈阳三生药业有限公司提供）５万单位。ａ、ｂ、ｃ三组分别于早期（３周），中…     

激活素A、TGF β 1在实验性肝纤维化中的表达比较

激活素（ａｃｔｉｖｉｎ,ＡＣＴ）与肝纤维化形成有关,本实验以四氯化碳（ＣＣ１４）制备大鼠肝纤维化模型,分析了肝纤维化时ＡＣＴ Ａ、转化生长因子β１（ＴＧＦβ１）的表达变化。 １．材料与方祛：（１）模型的建立：雄性ＳＤ大鼠２４只,体重１８０－２１０ｇ,随机被分为正常对照组（ｎ＝１２）和模型组（ｎ＝１２）,模型组动物皮下注射４０％ＣＣ１４（精制橄榄油配制）０．４ ｍｌ／１００ｇ体重,首次剂量加倍,每周２次,正常对照组皮下注射等体积生理盐水,７周后处死各组动物,处死时距最后一次ＣＣ１４往射时间为７２ｈ。…     

丹参伍用牛磺酸对大鼠CCl_4中毒性肝纤维化的防治作用

本实验在大鼠ＣＣｌ４中毒性肝纤维化模型上，观察丹参和牛磺酸联合应用对肝纤维化的影响，以为临床应用提供依据。 一、材料和方祛 １．主要试剂：丹参注射液（上海生化制药厂）；牛磺酸（湖州市生物化学试剂厂）；羟脯氨酸（上海生化研究所）层粘连素（ＬＮ）ＥＬＩＳＡ测定试剂盒（本院临床免疫中心）；透明质酸（ＨＡ）放射免疫测定试剂盒（海军医学研究所）；其它试剂均系国产分析纯。 ２．动物分组及检测指标：取体重１３５～１７５ ｇ雌性 ＳＤ大鼠 ４０只（本校实验动物中心提供），随机分成４组；正常组（１０只）、ＣＣｌ４组（１…     

依那普利对大鼠肝纤维化治疗作用的实验研究

背景:血管紧张素转化酶抑制剂(ACEI)能预防肝纤维化的形成,但有关其能否有效治疗肝纤维化的报道尚较少.目的:探讨ACEI依那普利(Ena)对大鼠实验性肝纤维化的治疗作用.方法:以CCl4诱导大鼠肝实质损伤性肝纤维化模型.将大鼠随机分为4组,分别为Ena高、低剂量治疗组、模型组和对照组.Ena治疗组和模型组大鼠皮下注射40?l4橄榄油混合液,每3天1次,共10周;对照组注射等体积精制橄榄油.治疗组于造模第5周起(纤维隔初步形成时)予Ena灌胃,每天1次,直至造模结束.实验结束后称量大鼠体重,处死大鼠,计算肝、脾指数;HE和Masson三色染色评价肝组织炎症和纤维化程度;透射电镜观察肝细胞超微结构的变化.结果:Ena治疗组和模型组大鼠的体重均显著低于对照组(P<0.01).与模型组相比,Ena治疗组的肝、脾指数均显著降低(P<0.01);Ena高剂量治疗组的肝组织炎症和纤维化程度显著减轻(P<0.01),肝细胞超微结构明显改善.结论:Ena能延缓已形成的肝纤维化的进展,有明显的肝细胞保护作用,对CCl4诱导的大鼠实验性肝纤维化有良好的治疗作用.     

依那普利对肝组织bax和bcl-2基因表达的影响

目的探讨血管紧张素转化酶抑制剂（ACEI）依那普利（Ena）对大鼠肝纤维化的防治作用及其部分机制，及对肝组织bax和bcl-2基因表达的影响。方法以四氯化碳（CCl4）诱导形成大鼠肝实质损伤性肝纤维化模型。大鼠分为空白对照组、模型对照组、预防组及治疗组。除空白对照组外，其余各组大鼠均皮下注射40％CCl4橄榄油混合液，每3日1次，共10周。预防组同时给予Ena灌胃。治疗组则在造模第5周给予Ena灌胃。对肝组织标本炎症及纤维化程度进行评价，并用RT—PCR技术观察Ena对肝组织bax和bcl-2基因表达的影响。结果Ena高剂量预防及高剂量治疗组肝组织炎症和纤维化程度较模型对照组显著减轻（P〈0．01）。Ena高剂量预防及高剂量治疗组肝组织bax基因表达显著弱于模型对照组（P〈0．01），bcl-2基因表达显著强于模型对照组（P〈0．01），bax／bcl-2基因表达比值和肝纤维化程度呈显著直线正相关（P〈0．01）。结论Ena能有效防治大鼠肝纤维化，抑制促凋亡基因bax的表达，促进抑凋亡基因bcl-2的表达，是其可能机制之一。bax／bcl-2基因表达比值与肝纤维化程度正相关。     

川芎嗪对大鼠肝纤维化脂质过氧化的影响

研究从中药川芎中分离提取的生物碱单体川芎嗪对ＣＣｌ４大鼠肝纤维化脂质过氧化及肝组织中贮脂细胞的影响。 １．材料与方法：（１）动物处置：ＳＤ大鼠３２只,雌雄各１６只,体重（１５ ±１５）ｇ,随机分为正常对照组（ｎ＝８）,ＣＣｌ４。组（ｎ＝１２）和川芎嗪组（ｎ＝１２）。正常对照组仅腹腔注射生理盐水尽两组均给予体积分数５０％ ＣＣＬ４石蜡油溶液,按 １ｍｌ／ｋｇ腹腔注射,每周 ２次,川芎嗪组在 Ｃ Ｃｌ４等处理同时予以川芎嗪注射液 ２０ ｍｇ／ｋｇ腹腔注射,每日 １次,每周６次。实验共６周,于第４５天乙醚麻醉大…     

激活素和卵泡抑素mRNA在肝纤维化形成过程中的作用

目的 观察四氯化碳（ＣＣｌ４）诱导实验性肝纤维化模型大鼠肝纤维化形成过程中激活素（ＡＣＴ）βＡ、βＣ、βＥ及卵泡抑素（ＦＳ）ｍＲＮＡ的表达。方法 ４０％ＣＣｌ４皮下注射制备大鼠实验性肝纤维化模型，注射 ＣＣｌ４后１、２、３、４、５、６、７周分批处死动物，每次 ６～１２只，采用半定量 ＲＴ—ＰＣＲ检测 ＡＣＴ βＡ、βＣ、βＥ亚基及 ＦＳｍＲＮＡ的表达。结果 正常肝脏可检测到ＡＣＴ βＡ、βＣ、βＥ及ＦＳ亚基ｍＲＮＡ，往射ＣＣｌ４２～３周后，βＡ水平下降至检测不到的水平，４周以后，又逐渐升高，注射 ６～７周时其表达水平明显高于正常对照组（Ｐ＜０．０１）；注射ＣＣｌ４１～４周可检测到βＣ亚基ｍＲＮＡ，５～７周后其表达水平明显高于正常对照组（Ｐ＜０．０５）。βＥ亚基ｍＲＮＡ在 ＣＣｌ４注射１～５周后水平下降至检测下到的水平，注射 ６～７周后其表达水平则明显高于正常对照组（Ｐ＜０．０５）。ＣＣｌ４注射后的各个时期均未检测到ＦＳ ｍＲＮＡ表达。结论 肝纤维化形成过程中ＡＣＴ、ＦＳ表达发生了不同的变化，ＡＣＴ—ＦＳ系统失衡可能参与了肝纤维化的形成。     

褐藻胶对大鼠实验性肝纤维化的防治作用

目的研究褐藻胶对大鼠实验性肝纤维化的防治作用．方法用４０％四氯化碳（ＣＣｌ４）制备大鼠肝纤维化模型，实验分组为正常对照组（ｎ＝８），ＣＣｌ４组（ｎ＝８），秋水仙硷（ＣＯＬ）组（ｎ＝６）和褐藻胶组（ｎ＝６）（２００ｍｇ／ｋｇ，ｉｇ，３次／周×４）．观察肝脏组织学和血清Ⅲ型前胶原（ＰＣⅢ）及透明质酸（ＨＡ）水平的变化．结果褐藻胶组ＰＣⅢ（１４２８μｇ／Ｌ±７６１μｇ／Ｌ）和ＨＡ水平（２６５５μｇ／Ｌ±９３１μｇ／Ｌ）显著低于ＣＣｌ４组（２９３５μｇ／Ｌ±７８３μｇ／Ｌ，５１９８μｇ／Ｌ±１１８３μｇ／Ｌ，Ｐ＜００１），而褐藻胶组与ＣＯＬ组间无显著差异．病理学观察显示，ＣＣｌ４组肝纤维化程度重于褐藻胶组和ＣＯＬ组．结论褐藻胶对实验性肝纤维化有防治作用．     

贝那普利对肝纤维化大鼠胰岛素样生长因子-Ⅰ受体的影响

目的研究血管紧张素转换酶抑制剂贝那普利对大鼠肝纤维化模型的疗效,以及对其肝组织胰岛素样生长因子-Ⅰ受体(IGF-ⅠR)的影响.方法取Wistar雄性大鼠42只随机分为3组,正常对照组12只,模型组15只,贝那普利治疗组15只.制备四氯化碳诱导的大鼠肝纤维化模型,同时应用贝那普利灌胃,共8周.对肝组织进行苏木精-伊红染色...     

肝细胞色素P450 2E1在实验性肝纤维化组织中的表达

目的 研究肝细胞色素Ｐ４５０ ２Ｅ１在实验性肝纤维化组织中的表达。方法 ８只Ｗｉｓｔａｒ大鼠,建立四氯化碳（ＣＣｌ４）肝纤维化模型,用免疫组织化学方法观察肝纤维化模型肝组织中肝细胞色素Ｐ４５０ ２Ｅ１。结果 正常肝组织内,ＣＹＰ ２Ｅ１表达仅见于中央静脉周围区,主要表达于肝腺泡Ⅲ区,２～３层细胞厚,肝细胞浆和细胞膜可见ＣＹＰ ２Ｅ１表达。在ＣＣｌ４模型肝组织中,ＣＹＰ ２Ｅ１表达的强度增加,分布的     

奥曲肽抗肝纤维化的实验研究

目的 观察奥曲肽(Oct)对大鼠实验性肝纤维化的治疗效果,并探讨其作用机制。方法 用四氯化碳诱导大鼠肝纤维化模型,将实验动物随机分为正常对照组、治疗前模型组、治疗后模型组和Oct治疗组。Oct治疗组给予Oct(50ng/100g)皮下注射,每日2次,连续用药30d,分别用放射免疫法检测血清层黏连蛋白(LN)、Ⅲ型前胶原(PC Ⅲ)及透明质酸(HA)。VG染色法组织切片观察组织病理变化,免疫组织化学法检测肝组织平滑肌肌动蛋白(α-SMA)和转化生长因子β_1(TGFβ_1)表达及逆转录聚合酶链反应法检测Ⅰ型和Ⅲ型前胶原mRNA表达。结果 治疗前和治疗后模型组大鼠血清HA(ng/L)为121.8±9.5和110.3±13.4,正常对照组为33.1±3.7、LN(μg/L)为85.7±12.1和78.2±7.9,正常对照组为37.1±6.3、PC Ⅲ(ng/L)为35.9±3.5和33.7±2.6,正常对照组为15.6±2.8。Oct组大鼠血清HA为55.8±7.2、LN为43.1±3.4、PC Ⅲ为27.8±3.4,与模型组大鼠比较,差异有显著性,t=2.76～11.07,P<0.05。Oct能显著降低纤维化大鼠肝组织纤维化积分,下调α—SMA和TGFβ_1蛋白质及I型和III前胶原mRNA表达水平。结论 Oct抑制肝星状细胞激活和转化、下调TGFβ_1蛋白质及I型和III型前胶mRNA表达而发挥抗肝纤维化作用。     

姜黄素治疗肝纤维化及其作用机制的初步研究

目的观察姜黄素治疗肝纤维化的效果,初步探讨其作用机制。方法四氯化碳腹腔注射制作大鼠肝纤维化模型,以丹参治疗作为阳性对照,检测血清ALT、AST、HA、LN、Ⅲ型前胶原（PCⅢ）、一氧化氮（NO）含量;检测肝组织超氧化物歧化酶（SOD）、羟脯氨酸（Hyp）、丙二醛（MDA）含量;肝组织行HE和Masson胶原染色,光镜下观察病理学改变,并按肝纤维化半定量计分系统进行评分。结果与模型组比较,姜黄素治疗组能明显降低肝纤维化时异常升高的ALT、AST、NO、HA、LN、PCⅢ、MDA、Hyp,模型对照组分别为（693.75±117.57）U/L、（892.50±105.69）U/L、（70.95±10.23）μmol/L、（468.22±93.45）mg/L、（346.44±75.08）mg/L、（279.82±54.00）μg/L、（402.25±39.16）nmol/g、（752.50±77.62）μg/g,姜黄素（每100g体重40mg）治疗组分别为（218.50±48.89）U/L、（376.60±79.13）U/L、（47.96±6.53）μmol/L、（289.96±60.43）mg/L、（107.35±27.24）mg/L、（148.95±28.63）μg/L、（236.10±30.54）nmol/g、（478.40±75.74）μg/g,P值均〈0.05;提升肝纤维化时异常降低的肝组织SOD水平,姜黄素（每100g体重40 mg）治疗组和对照组分别为（90.39±21.23）U/mg、（46.52±20.01）U/mg,P〈0.05;明显改善四氯化碳所致大鼠肝纤维化的病理学改变,肝纤维化评分明显降低（P〈0.05）,接近正常对照组,且该作用随着姜黄素剂量增大而加强。结论姜黄素具有治疗大鼠肝纤维化作用;抗脂质过氧化损伤、直接影响胶原代谢可能是其重要的作用机制。     

Effects of PPARg agonist pioglitazone on rat hepatic fibrosis

AIM: To investigate effects of pioglitazone on rat hepatic fibrosis and to explore its mechanism. METHODS: Rat hepatic fibrosis was induced by carbontet. achloride (CCI4). Forty Sprague-Dawley rats were divided randomly into 4 groups: control, model, and two treatment (PⅠ, PⅡ) groups. Except for rats in control group, all rats were given subcutaneous injection of 400 mL/L CCI4, twice a wk for 8 wk. Rats in PⅠ and PⅡ groups were also treated with pioglitazone of 3 mg/kg, daily via gastrogavage beginning on the 1^st day and at the end of the 2^nd week, administration of CCI4 respectively. Liver functions (ALT, AST), serum fibrotic markers (HA, LN, PCIII) and hepatic hydroxyproline (HP) concentration were determined respectively. Histochemical staining of formalin-fixed liver sections with HE, Masson-Trichrome, and immunohistochemical staining for m-smooth muscle actin (α-SMA) were performed. Modified Knodell and Chevallier semi-quantitative scoring system (SSS) was used to evaluate necroinflammatory activity and fibrosis degree. RESULTS: Compared with model group, pioglitazone significantly reduced the serum levels of ALT, AST, HA, LN and PCⅢ (P&lt;0.05 or &lt;0.01). The HP concentrations in PⅠ(210.90&#177;24.07 μg/g), and PⅡ (257.36&#177;30.55 μg/g) groups were also lower than those in model group (317.80&#177;36.44) μg/g) (P&lt;0.01). Histologic examination showed that PⅠ and PⅡ groups had milder hepatocellular degeneration, necrosis and infiltration of inflammatory cells, and thinner or less fibrotic septa than did model group. The scores for necroinflammation in P (2.80&#177;1.03), and PⅡ (3.00&#177;1.05) groups were significantly reduced as compared with model group (4.88&#177;2.30) (P&lt;0.05 or &lt;0.01); the fibrosis scores in PⅠ (3.40&#177;1.65), and PⅡ (4.60&#177;1.35) groups were also markedly lower than those in model group (7.00&#177;3.21) (P&lt;0.05 or &lt;0.01). Immunohistochemical staining showed that expression of α-SMA in PⅠ and PⅡ groups was ameliorated dramatically compared with model group. CONCLUSION: PPARγ, agonist pioglitazone greatly retards the progression of rat hepatic fibrosis induced by CCI4 through inhibition of HSC activation and amelioration of hepatocyte necroinflammation in rats.     

肝硬化患者血浆中尿激酶型纤溶酶激活物的检测及其意义

目的 探讨肝硬化患者血浆尿激酶型纤溶酶激活物(uPA)、尿激酶型纤溶酶激活物受体(uPAR)、纤溶酶原激活物抑制剂-1(PAI-1)的变化及其意义。 方法 确诊的72例乙型肝炎后肝硬化患者,Child-pugh分级A级23例(A组),B级29例(B组),C级20例(C组)。6例健康志愿献血者为正常对照组。酶联免疫吸附实验测定血浆uPA、uPAR、PAI-1的变化。并同时检测血透明质酸(HA)、Ⅳ型胶原(C Ⅳ)、Ⅲ型前胶原(PC Ⅲ)、血浆白蛋白、胆红素、凝血酶原时间及其活动度改变。 结果 随着肝硬化的进展,血浆uPA、uPAR、PAI-1逐渐增加,HA、PC Ⅲ也明显增加。Child C组患者血浆uPA、uPAR、PAI-1水平(μg/L)分别为1.88±0.64、4.82±2.02和52.60±16.87,A组分别为1.36±0.43、3.03±1.48和24.09±7.14,B组分别为1.79±0.62、4.80±2.22和41.40±17.52,C组与A、B组比较,t值为2.81～7.38,P值均<0.01。A组血浆uPA与PC Ⅲ呈负相关(r=-0.4785,P<0.05);C组PAI-1与HA呈正相关(r=0.5447,P<0.01)。 结论 肝硬化晚期,虽然血浆uPA、PAI-1增加,但总的效应表现为uPA相对不足,肝基质纤维降解受抑制,血浆uPA、PAI-1与肝硬化发展密切相关。     

Effect of emodin on pancreatic fibrosis in rats

AIM： To establish the rats model of chronic fibrosing pancreatitis and to prove the anti-fibrotic effect of emodin in chronic pancreatitis with fibrosis.
METHODS： Fifty rats were randomly divided into five groups, 10 rats in each group. Trinitrobenzene sulfonic acid （TNBS） was infused into the pancreatic duct to induce chronic pancreatitis in rats （except for normal group）. Emodin-treated rats were fed with different doses of emodin （20, 40 and 80 mg/kg body weight） for 28 d, while normal group and control group received 0.9% sodium chloride solution. Serum levels of hyaluronic acid （HA） and laminin （LN） were determined by radioimmunoassay. Histopathological alterations were studied by optical microscopy. Expression of collagen was also examined while transforming growth factor- beta-1 （TGF-131） was localized by immunochemistry. RESULTS： In emodin-treated rats, the serum levels of HA and LN were decreased significantly （HA, 62.2 ± 19.3 μg/L vs 112.7 ± 26.5μg/L, P 〈 0.05; LN 44.3 ± 10.4 μg/L vs 86.2 ± 16.5 μg/L, P 〈 0.05）; the degree of fibrosis was ameliorated observably; the expression of collagen in pancreatic tissue was reduced especially in high-dose emodin-treated group （36% ± 5% vs 42% ± 6%, P 〈 0.05）; with the increased doses of emodin, the expression of TGF-β1 was declined, compared with those in control group.
CONCLUSION： Emodin has an anti-fibrotic effect on pancreatic fibrosis in rats. Because of its anti-fibrotic effect, it could be a potential herb for the treatment of chronic pancreatitis.     

Morphological and serum hyaluronic acid, laminin and type IV collagen changes in dimethylnitrosamine-induced hepatic fibrosis of rats

AIM: To study the morphological and serum hyaluronic acid (HA), laminin (LN), and type IV collagen changes in hepatic fibrosis of rats induced by dimethylnitrosamine (DMN). METHODS: The rat model of liver fibrosis was induced by DMN. Serum HA, type IV collagen, and LN were measured by ELISA. The liver/weight index and morphological changes were examined under electron microscope on d 7, 14, 21, and 28 by immunohistochemical alpha smooth muscle actin alpha-SMA staining as well as Sirius-red and HE staining. RESULTS: The levels of serum HA, type IV collagen and LN significantly increased from d 7 to d 28 (P = 0.043). The liver/weight index increased on d 7 and decreased on d 28. In the model group, the rat liver stained with HE and Sirius-red showed evident hemorrhage and necrosis in the central vein of hepatic 10 lobules on d 7. Thin fibrotic septa were formed joining central areas of the liver on d 14. The number of alpha-SMA positive cells was markedly increased in the model group. Transitional hepatic stellate cells were observed under electron microscope. All rats in the model group showed micronodular fibrosis in the hepatic parenchyma and a network of alpha-SMA positive cells. Typical myofibroblasts were embedded in the core of a fibrous septum. Compared to the control group, the area-density percentage of collagen fibrosis and pathologic grading were significantly different in the model group (P<0.05) on different d (7, 14, and 28). The area-density percentage of collagen fibrosis in hepatic tissue had a positive correlation with the levels of serum HA, LN, and type IV collagen. CONCLUSION: The morphological and serum HA, type IV collagen, and LN are changed in DMN-induced liver fibrosis in rats.     

代偿性肝硬化无创性诊断指标的筛选及评价

目的：比较肝纤维化血清标志物对慢性乙型肝炎（CHB）代偿性肝硬化的诊断评价，筛选可行的无创性诊断标志物。方法：350例CHB患者经皮肝脏穿刺活检术行病理组织学检查，B型超声波检查肝硬化图像，检测血清透明质酸（HA）、Ⅲ型前胶原肽（PCⅢ）、层黏连蛋白（LN）及Ⅳ型胶原（CⅣ）等肝纤维化标志物。用临床流行病学方法确定诊断截断值，并对各项指标作诊断评价分析，比较不同标志物的诊断评价指标。结果：85例CHB患者经肝脏活检术确认为代偿性肝硬化，81例经B型超声波检查有肝硬化图像，ROC曲线下面积以HA最高；血清HA、PCⅢ、LN及CⅣ对代偿期肝硬化的诊断截断值分别为154．35μg/L、198．44μg/L，137．58μg/L和100．80μg/L，对其应诊断灵敏度分别为82．4％，63．5％，57．3％及70．6％，特异度为79．3％，54．0％，56．8％及68．3％，准确度为80．0％，56．3％，56．9％及68．9％，并联试验诊断虽可提高灵敏度，但相应降低特异度及准确度，与其他无创性诊断方法比较，HA有较高水平的诊断评价指标（u≥1．814，P＜0．05），血清HA诊断代偿性肝硬化的截断值以119．17μg/L较恰当，其相应诊断灵敏度，特异性度，准确度，阳性预告值及阴性预选值分别为87．1％、67．6％、72．3％、46．25％，94．7％。结论：在现有肝脏纤维化血清标志物及超声波检查等无创性诊断指标中，血清HA是代偿性肝硬化最好的诊断标志物。     

Inhibitory effect of Huangqi Zhechong decoction on liver fibrosis in rat

AIM: To assess the inhibitory effect of Huangqi Zhechong decoction on hepatic fibrosis in rats induced by CCl(4) plus alcohol and high fat low protein diet. METHODS: Male SD rats were randomly divided into hepatic fibrosis model group, control group and 3 treatment groups consisting of 12 rats in each group. Except for the normal control group, all the rats were subcutaneously injected with CCl(4) at a dosage of 3 mL/kg. In 3 treated groups, either high-dose group (9 mL/kg), or medium-dose group (6 mL/kg), or low-dose group (3 mL/kg) was daily gavaged with Huangqi Zhechong decoction, and saline vehicle was given to model and normal control rats. Enzyme-linked immunosorbent assay (ELISA) and biochemical examinations were used to determine the changes of alanine aminotransferase (ALT), aspartate aminotransferase (AST), hyaluronic acid (HA), laminin (LN), type-III-procollagen-N-peptide (PIIIP), and type IV collagen content in serum, and hydroxyproline (Hyp) content in liver after sacrificing the rats. Pathologic changes, particularly fibrosis were examined by hematoxylin and eosin (HE) and Van Gieson staining. RESULTS: Compared with the model control group, serum ALT, AST, HA, LN, PIIIP and type IV collagen levels dropped markedly in Huangqi Zhechong decoction groups, especially in the medium-dose Huangqi Zhechong decoction group (1 954+/-576 U/L vs 759+/-380 U/L, 2 735+/-786 U/L vs 1 259+/-829 U/L, 42.74+/-7.04 ng/mL vs 20.68+/-5.85 ng/mL, 31.62+/-5.84 ng/mL vs 14.87+/-1.45 ng/mL, 3.26+/-0.69 ng/mL vs 1.47+/-0.46 ng/mL, 77.68+/-20.23 ng/mL vs 25.64+/-4.68 ng/mL, respectively) (P<0.05). The Hyp content in liver tissue was also markedly decreased (26.47+/-11.24 mg/mgprot vs 9.89+/-3.74 mg/mgprot) (P<0.01). Moreover, the stage of the rat liver fibrosis in Huangqi Zhechong decoction groups was lower than that in model group, and more dramatic drop was observed in medium-dose Huangqi Zhechong decoction group (P<0.01). CONCLUSION: Huangqi Zhechong decoction can inhibit hepatic fibrosis resulted from chronic liver injure, retard the development of cirrhosis, and notably ameliorate the liver function. It may be a safe and effective therapeutic drug for patients with fibrosis.     

ROC curves in evaluation of serum fibrosis indices for hepatic fibrosis

AIM:Use Receiver operating characteristic(ROC) curves to find out the relationship between serum level of hyaluronic acid(HA),typeⅢ procollagen (PCⅢ）,N-terminal procollagen Ⅲ peptied(PⅢNP),iaminin(LN),type Ⅳ collagen(C-Ⅳ）and hepatic fibrosis,as well as to determined their value in clinical practice.     

肝病患者纤维化不同分期时肝左叶上下径和前后径的测定及意义

目的研究慢性肝炎患者纤维化不同分期时肝左叶上下径、前后径的变化规律及其联合血清纤维化指标对无创诊断中晚期肝纤维化或早期肝硬化的价值。方法经肝活检确定72例慢性肝炎患者肝纤维化分期。肝穿前一日,B超测定肝左叶上下径、前后径等及肝穿刺点定位。放射免疫法测定血清HA、LN、CⅣ和PCⅢ含量。结果随纤维化程度增加,肝左叶上下径呈缩短趋势,其S4期测值为（5.7±1.5）cm明显短于S0期测值（7.7±1.4）cm;肝左叶前后径呈增长趋势,其S4期测值长于S0期分别为（6.5±1.1）cm和（5.3±0.7）cm。血清HA、LN、CⅣ和PCⅢ含量亦随纤维化增加而升高,HA、PCⅢ在S3期开始显著升高,均高于同组S0期［（273.4±131.3）μg/L对（66.2±35.0）μg/L、（167.4±48.1）μg/L对（103.4±23.8）μg/L］。结论肝左叶上下径、前后径及血清HA、PCⅢ含量变化可能间接反映了活动性肝纤维化中晚期或早期肝硬化。