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| 1 | 肝纤维化的逆转策略及研究现状显示文摘肝硬化是严重危害人类健康的常见病之一,目前我国的发生率仍保持在较高水平.肝硬化的病理学基础是肝纤维化,后者是各种损肝因素(如病毒性肝炎、酒精性肝病、某些代谢性疾病、药物及化学毒物损伤及肝寄生虫病等)引起的肝脏损害和炎症,进而导致慢性肝病发展为肝硬化的必经病理过程.目前认为,肝纤维化时肝组织中细胞外基质(ECM)的病理性改变是由于控制ECM形成及降解的稳态机制失调所致,任何原因使得ECM形成过多或降解减少均可导致ECM过度沉积.近十多年来,我们对肝纤维化的分子生物学及细胞学机制有了较为深入的认识,其诊断与治疗也有了一定进展.但是,迄今为止HBV、HCV和HBV/HDV感染人体后导致肝硬化的机制还未完全阐明,尚存在许多问题,说明病毒性肝纤维化形成机制的复杂性.肝星形细胞(HSC)已公认为肝内ECM堆积的关键因素.随着HSC生物特性的深入了解,更多新的抗纤维化治疗方法被设计出来.当前的治疗主要针对病因,其次是抑制ECM生成、促进纤维降解、抑制HSC活化等.随着分子生物学的发展,肝纤维化的分子机制逐渐得以阐明,从而使肝纤维化的基因治疗成为可能.肝纤维化的基因治疗主要起到阻止纤维化发展、刺激肝细胞分裂和肝组织结构重建三方面的作用.目前,常用的方法一般是通过缺陷病毒(如腺病毒)转入特定的细胞因子和酶的基因,通过靶细胞表达这些因子作用于受损的肝脏,达到延缓和治愈肝纤维化之目的.中国传统的中医药对治疗肝纤维化大有希望,但其长期效果有待观察. 将来,不仅病因可以祛除,其他的目标也可以达到. 但是目前还存在不少问题,尚有许多工作需要进行. | 聂青和 | 2005 | 世界华人消化杂志2005，13，10： | 63 |
| 2 | Methodologic research on TIMP-1,TIMP-2 detection as a new diagnostic index for hepatic fibrosis and its significance显示文摘AIM: To set up a new method to detect tissue inhibitors ofmetalloproteinase1 and -2(TIMP-1 and TIMP-2) in sero ofpatients with hepatic cirrhosis, and to investigate theexpression and location of TIMP-1 and TIMP-2 in liver tissueof patients with hepatic cirrhosis, and the correlationbetween TIMPs in liver and those in sera so as to discusswhether TIMPs can be used ss a diagnosis index of hepaticfibrosisMETHODS: The monoclonal antibodies (McAbs) of TIMP-1and TIMP-2 were used to sensitize erythrocytes, and solid-phase absorption to sensitized erythrocytes (SPASE) wasused to detect TIMP-1 and TIMP-2 in the sera of patients withhepatic cirrhosis. Meanwhile, with the method of in situhybridization and immunohistochemistry, we studied themRNA expression and antigen location of TIMP-1 and TIMP-2in the livers of 40 hepatic cirrhosis patients with pathologicdiagnosis.RESULTS: With SPASE, they were 16.4 % higher in theacute hepatitis group, 33.3 % higher in the chronic hepatitisgroup, and the positive rates were 73.6 % and 61. 2 %respectively in sero of hepatic cirrhosis patients, which wereremarkably higher than those in chronic hepatitis and acutehepatitis group ( P < 0. 001 ). In 40 samples of hepaticcirrhosis tissues, all of them showed positive expression ofTIMP-1 and TIMP-2 mRNA detected withimmunohistochemistry or in situ hybridization (positive ratewas 100 % ). Expression of TIMPs in different degrees couldbe found in liver tissue with cirrhosis. TIMPs were located incytoplasm of liver cells of patients with hepatic cirrhosis.There was a significant correlation between serum TIMPslevel and liver TIMPs level.CONCLUSION: SPASE is a useful method to detect the TIMP-1 and TIMP-2 in sera of patients with hepatic cirrhosis, andTIMP-1 and TIMP-2 can be considered as a useful diagnosticindex of hepatic fibrosis, especially TIMP-1. | Oing-He Nie Yong-Oian Cheng Yu-Mei Xie Yong-Xing Zhou Bai-Xian Guang Yi-Zhan Cao,The Centre of Diagnosis and Treatment for Infectious Disease of Chinese PLA,Tangdu Hospital,Fourth Military Medical University,Xi’an 710038,Shanxi Province,China | 2002 | World Journal of Gastroenterology2002，8，2： | 51 |
| 3 | Hepatoprotective role of ganoderma lucidum polysaccharide against BCG-induced immune liver injury in mice显示文摘AIM: To examine the effect of ganoderma lucidumpolysaccharide (GLP) on the immune liver injuryinduced by BCG infection, and investigate therelationship between degrees of hepatic damage andNO production in mice.METHODS: Immune hepatic injury was markedlyinduced by BCG-pretreatment (125 mg.kg-1, 2-week, iv)or by BCG-pretreatment plus lipopolysaccharide (LPS,125 μg.kg-1, 12-hour, iv) in mice in vivo.Hepatocellulardamage induced by BCG-pretreated plus inflammatorycytokines mixture (CM), which was included TNF-α, IL1β, IFN-γ and LPS in culture medium in vitro.Administration of GLP was performed by oral orincubating with culture medium at immune stimulisimultaneity. Liver damage was determined by activityof alanine aminotransferase (ALT) in serum and inhepatocytes cultured supernatant, by liver weightchanges and histopathological examination. NOproduction in the cultured supematant was determinedby the Griess reaction. Moreover, inducible nitric oxidesynthase (iNOS) protein expression was alsoexaminated by immunohistochemi1cal method.RESULTS: Immune hepatic injury was markedly inducedby BCG or BCG plus inflammatory cytokines in BALB/cmice in vivoand in vitro. Under BCG-stimulated condition,augment of the liver weight and increase of the serum/supernatant ALT level were observed, as well asgranuloma forming and inflammatory cells soakage wereobserved by microscopic analysis within liver tissues.Moreover, NO production was also increased by BCG or/and CH stimuli in the culture supernatant, and a lot ofiNOS positive staining was observed in BCG-prestimulated hepatic sections. Application of GLPsignificantly mitigated hepatic tumefaction, decreasedALT enzyme release and NO production in serum/supernatant, improved the pathological changes ofchronic and acute inflammation induced by BCG-stimuliin mice. Moreover, the immunohistochemical resultshowed that GLP inhibited iNOS protein expression inBCG-immune hepatic damage model.CONCLUSION: The present study indicates that NOparticipates in immune liver injury induced byMycobacterium bovis BCG infection. The mechanismsof protective roles by GLP for BCG-induced immune liverinjury may be due to influence NO production in mice. | Guo-Liang Zhang Ye-Hong Wang Wei Ni Hui-Ling Teng Zhi-Bin Lin Department of Pharmacology,School of Basic Medical Sciences,Beijing University,Beijing 100083,China | 2002 | World Journal of Gastroenterology2002，8，4： | 47 |
| 4 | Expression of TIMP-1 and TIMP-2 in rats with hepatic fibrosis显示文摘AIM: To investigate the location and expression of TIMP-1 and TIMP-2 in the liver of normal and experimental hepatic fibrosis in rats. METHODS: The rat models of experimental immunity hepatic fibrosis (n=20) were prepared by the means of immunologic attacking with human serum albumin (HSA),and normal rats (n=10) served as control group. Both immunohistochemistry and in situ hybridization methods were respectively used to detect the TIMP-1 and TIMP-2 mRNA and related antigens in liver. The liver tissue was detected to find out the gene expression of TIMP-1 and TIMP-2 with RT-PCR. RESULTS: The TIMP-1 and TIMP-2 related antigens in livers of experimental group were expressed in myofibroblasts and fibroblasts (TIMP-1: 482±65 vs 60±20; TIMP-2:336±48 vs 50±19, P<0.001). This was the most obvious in portal area and fibrous septum. The positive signals were located in cytoplasm, not in nucleus. Such distribution and location were confirmed bysitu hybridization (TIMP-1/β-actin: 1.86±0.47 vs 0.36±0.08; TIMP-2/β-actin: 1.06±0.22 vs 0.36±0.08,P<0.001). The expression of TIMP-1 and TIMP-2 was seen in the liver of normal rats, but the expression level was very low. However, the expression of TIMP-1 and TIMP-2 in the liver of experimental group was obviously high. CONCLUSION: In the process of hepatic fibrosis, fibroblasts and myofibroblasts are the major cells that express TIMPs.The more serious the hepatic fibrosis is in the injured liver,the higher the level of TIMP-1 and TIMP-2 gene expression. | Qing-HeNie Guo-RongDuan Xin-DongLuo Yu-MeiXie HongLuo Yong-XingZhou Bo-RongPan | 2004 | World Journal of Gastroenterology2004，10，1： | 43 |
| 5 | Inhibition on the production of collagen type Ⅰ, Ⅲ of activated hepatic stellate cells by antisense TIMP-1 recombinant plasmid显示文摘AIM: To investigate the inhibition effects on the productionof collagen type I, Ⅲ secreted by activated rat hepatic stellatecells (rHSCs) by antisense tissue inhibitors of metalloproteinase1 (TIMP-1) recombinant plasmid through elevating interstitialcollagenase activity.METHODS: rHSCs were extracted from normal rat liverby pronase and collagenase digestion and purified bycentrifugal elutriation, and were cultured on plastic dishesuntil they were activated to a myofibroblastic phenotypeafter 7-10 days. RT-Nest-PCR and gene recombinanttechniques were used to construct the rat antisense TIMP-1 recombinant plasmids which can express in eucaryoticcells. The recombinant plasmid and the pcDNA3 emptyplasmid were transfected in rHSCs by Effectene (QIAGEN)separately. Cells were selected after growing in DMEMcontaining 400 μg/ml G418 for 2-3 weeks. Expression ofexogenous gene was assessed by Northern blot, andexpression oflIMP-1 in rHSCs was determined by Northernblot and Western blot. We tested the interstitial collagenaseactivity with FITC-labled type I collagen as substrate.Ultimately, we quantified the type Ⅰ, Ⅲ collagen byWestern blot.RESULTS: The exogenous antisense TIMP-1 recombinantplasmid could be expressed in rHSCs well, which couldblock the expression of TIMP-1 greatly, the ratio of TIMP-1/GAPDH was 0.67, 2.41, and 2.97 separately at mRNAlevel (P<0.05); the ratio of TIMP-1/β-actin was 0.31, 0.98and 1.32 separately at protein level (P<0.05); It mightelevate active and latent interstitial collagenase activity,the collagenase activity was 0.3049, 0.1411 and 0.1196respectively. (P<0.05), which led to promotion thedegradation of type Ⅰ, Ⅲ collagen, the ratio of collagen I/β-actin was 0.63, 1.78 and 1.92 separately (P<0.05); andthe ratio of collagen Ⅲ/β-actin was 0.59, 1.81 and 1.98separately (P<0.05).CONCLUSION: These data shows that the antisense TIMP-1 recombinant plasmid has the inhibitory effects on theproduction of type Ⅰ, Ⅲ collagens secreted by activatedrHSCs in vitro. It could be a novel method to reverse hepaticfibrosis in the future. | Wen-Bin Liu Chang-Qing Yang Wei Jiang Yi-Qing Wang Jing-Sheng Guo Bo-Ming He Ji-Yao Wang Division of Gastroenterology, Zhongshan Hospital, Fudan University, Shanghai 200032, China | 2003 | World Journal of Gastroenterology2003，9，2： | 42 |
| 6 | Effects of transmitters and interleukin-10 on rat hepatic fibrosis induced by CCl_4显示文摘AIM: To study the effects of transmitters ET, AgII, PGI2,CGRP and GG on experimental rat hepatic fibrosis and the antifibrogenic effects of IL-10.METHODS: One hundred SD rats were randomly divided into 3 groups: control group (N): intraperitoneal injection a week; IL-10 treated group (E): besides same dosage of the third week. In the fifth, the seventh and the ninth week,rats in three groups were selected randomly to collect plasma and liver tissues. The levels of ET, AgII, PGI2, CGRP and GG were assayed by radioimmunoassay (RIA). The liver fibrosis was observed with silver staining.RESULTS: The hepatic fibrosis was developed with the increase of the injection frequency of CCl4. The ET, AgII, PGI2, CGRP The histological examination showed that the degrees of the rats liver fibrosis in group E were lower than those in group C.CONCLUSION: The transmitters ET, AgII, PGI2, CGRP and GG play a significant role in the rat hepatic fibrosis induced by CCl4. IL-10 has the antagonistic action on these transmitters and can relieve the degree of the liver fibrosis. | Xiao-Zhong Wang Li-Juan Zhang Dan Li Yue-Hong Huang Zhi-Xin Chen BinLi Department of Gastroenterology, The Affiliated Union Hospital, Fujian Medical University, Fuzhou, 350001, Fujian Province, China | 2003 | World Journal of Gastroenterology2003，9，3： | 33 |
| 7 | 基质金属蛋白酶组织抑制剂(TIMPs)的基础及临床研究现状显示文摘 | 邵彬 聂青和 | 2005 | 实用肝脏病杂志2005，8，3： | 29 |
| 8 | Expression of insulin-like growth factor 1 and insulin-like growth factor 1 receptor and its intervention by interleukin-10 in experimental hepatic fibrosis显示文摘AIM: To study the expression of IGF-1 and IGF-1R and its intervention by interleuldn-10 in the course of experimental hepatic fibrosis.METHODS: Hepatic fibrosis was induced in rats by carbon tetrachloride intoxication and liver specimens were taken from the rats administered CCl4 with or without IL-10 treatment and the animals of the control group.Immunoreactivities for insulin-like growth factor-1 (IGF-1)and IGF-1 receptor(IGF-1R) were demonstrated by immunohistochemistry, and their intensities were evaluated in different animal groups.RESULTS: The positive levels for IGF-1 and IGF-1R were increased with the development of hepatic fibrosis, with the positive signals localized in cytoplasm and/or at the plasmic membrane of hepatocytes. The positive signals of IGF-1 and IGF-1R were observed more frequently (P<0.01) in the CCl4-treated group (92.0 % and 90.0 %) compared to those in the control group. The positive signals decreased significantly (P<0.05) in IL-10-treated group. The responses in IGF-1 and IGF-1R expression correlated with the time of IL-10 treatment.CONCLUSION: The expression of IGF-1 and IGF-1R immunoreactivities in liver tissue seems to be up-regulated during development of hepatic fibrosis induced by CC14, and exogenic IL-10 inhibits the responses. | Xiao-Zhong Wang Zhi-Xin Chen Li-Juan Zhang Yun-Xin Chen Dan Li Feng-Lin Chen Yue-Hong Huang Department of Gastroenterology,Affiliated Union Hospital,Fujian Medical University,Fuzhou,350001,Fujian Province,China | 2003 | World Journal of Gastroenterology2003，9，6： | 27 |
| 9 | Electroporative interleukin-10 gene transfer ameliorates carbon tetrachlo-ride-induced murine liver fibrosis by MMP and TIMP modulation显示文摘瞄准:肝纤维变性代表响应长期的肝损伤愈合并且结疤的一个过程。为肝纤维变性的有效治疗正在缺乏。Interleukin-10 (IL-10 ) 是 cytokine 下面调整支持 inflammatory 回答并且在肝的纤维发生上有调节效果。这研究的目的是调查 electroporative IL-10 基因治疗是否在老鼠上有肝的 fibrolytic 效果。方法:肝的纤维变性被在老鼠管理四氯化碳(CCl4 ) 10 个星期导致。在肝的纤维变性被建立以后,人的 IL-10 表示原生质标志经由 electroporation 被交付。组织病理学说,反向的抄写聚合酶链反应(RT-PCR ) ,弄污的免疫,和明胶 zymography 被用来调查 IL-10 的行动的可能的机制。结果:人的 IL-10 基因治疗在老鼠颠倒了导致 CCl4 的肝纤维变性。RT-PCR 表明那 IL-10 基因治疗稀释了肝 TGF-beta1,骨胶原 alpha1, fibronectin,和房间粘附分子在规定上面的 mRNA。后面的基因转移,两个都, alpha 光滑的肌肉肌动朊和 cyclooxygenase-2 的激活显著地被稀释。而且, IL-10 显著地禁止了矩阵 metalloproteinase-2 (MMP-2 ) 和矩阵 metalloproteinase (TIMP ) 的织物禁止者在 CCl4 沉醉以后的激活。结论:我们证明那 IL-10 基因治疗在老鼠稀释了导致 CCl4 的肝纤维变性。在调整 fibrogenic 和支持 inflammatory 基因回答上面阻止的 IL-10。它的溶胶原效果可以被归因于 MMP 和 TIMP 调整。IL-10 基因治疗可以是对有潜在的临床的使用的肝纤维变性的一种有效治疗学的形式。 | Wen-ying CHOU Cheng-nan LU Tsung-hsing LEE Chia-ling WU Kung-sheng HUNG Allan M CONCEJERO Bruno JAWAN Cheng-haung WANG | 2006 | Acta Pharmacologica Sinica2006，27，4： | 25 |
| 10 | 金属蛋白酶组织抑制因子在肝纤维化研究中的价值显示文摘 | 罗新栋 聂青和 | 2003 | 肝脏2003，8，2： | 25 |
| 11 | 多脏器纤维化的络病机制探讨显示文摘中医络病的病理机制中血行不畅、络脉失养、气血瘀滞、津凝痰结、络毒蕴结等病理变化涉及了血管活性物质调控异常、血管内皮细胞、血管平滑肌细胞的损伤机制、细胞外基质 (ECM)代谢异常、细胞因子及信号传导通路调控异常等生物学内容。津凝标志着正常分布的ECM的积聚增多 ,痰结则代表了ECM的异常分布。细胞、组织形态学的不可逆转的变化是络毒蕴结积聚的结果 ,也是络病发展的晚期阶段。因此 ,纤维化的发展在中医中应属络病的范畴。若发生肺纤维化 ,则属肺络病 ;肝纤维化 ,则属肝络病 ;肾脏纤维化 ,则属肾络病。从“络病”角度进一步寻求中医药防治多脏器纤维化的特异性规律 ,对指导基础研究与临床治疗有重要意义。 | 牛建昭 姜术霞 李彧 | 2004 | 北京中医药大学学报2004，27，6： | 22 |
| 12 | 木犀草素降低CCl_4诱导的大鼠肝纤维化显示文摘目的:研究黄酮类化合物木犀草素(luteolin,Lu)治疗肝纤维化的作用。方法:30只Wistar大鼠随机分成正常对照组,实验对照组和Lu实验组,实验对照组和Lu实验组给予8wk CCl_4和酒精饮料制备肝纤维化动物模型,Lu实验组从实验开始就用20mg.Kg^(-1).day^(-1)LU灌胃。实验结束后,进行病理学检测和测定肝组织羟脯氨酸含量,用Northern Blot检测Ⅰ型前胶原mRNA表达,并测定了肝组织MDA含量和基质金属蛋白酶(MMPs)的活性。结果:经Lu治疗后,肝脏纤维化程度降低,羟脯氨酸含量减少;同时观察到Lu使肝脏Ⅰ型前胶原mRNA表达降低(5.2±1.4 vs 3.8±1.1,P<0.05)和MDA含量显著减少(12.7±2.6 vs 8.2±2.0μmmol/g,P<0.05),但MMPs的活性没有改变。结论:Lu通过清除自由基,抑制胶原基因表达,在动物体内具有防治肝纤维化作用。 | 赵稳兴 陈忠明 候辉 梁崇礼 庞荣清 赵彬 陈志龙 | 2002 | 世界华人消化杂志2002，10，7： | 22 |
| 13 | Ginkgo biloba extract reverses CCI4-induced liver fibrosis in rats显示文摘AIM: To study the reversing effect of Ginkgo biloba extract (GbE) on established liver fibrosis in rats. METHODS: Following confirmation of CCI4-induced liver fibrosis, GbE or saline was administrated to the rats for 4 weeks. The remaining rats received neither CCI 4 norGbE as normal control. The four groups were compared in terms of serum enzymes, tissue damage, expression of αSMA and tissue inhibitor-1 of metalloproteinase (TIMP-1) and metalloproteinase-1 (MMP-1). RESULTS: Compared with saline-treated group, liver fibrosis rats treated with GbE had decreased serum total bilirubin (P<0.01) and aminotransferase levels (P<0.01) and increased levels of serum albumin (P<0.01). Microscopic studies revealed that the livers of rats receiving GbE showed allieviation in fibrosis (P<0.05) as well as expression of αSMA (P<0.01). The liver collagen and reticulum contents were lower in rats treated with GbE than saline-treated group (P<0.01). RT-PCR revealed that the level of TIMP-1 decreased while the level of MMP-1 increased in GbE group. CONCLUSION: Administration of GbE improved CCI4-induced liver fibrosis. It is possibly attributed to its effect of inhibiting the expression of TIMP-1 and promoting the apoptosis of hepatic stellate cells. | Yan-JunLuo Jie-PingYu Zhao-HongShi LiWang | 2004 | World Journal of Gastroenterology2004，10，7： | 20 |
| 14 | Pathomorphological study on location and distribution of Kupffer cells in hepatocellular carcinoma显示文摘AIM: To clarify the location and distribution of Kupffer cells in hepatocellular carcinoma (HCC), and to investigate their role in hepatocarcinogenesis.METHODS: Kupffer cells were immunohistochemically stained by streptavadin-peroxidase conjugated method (S-P). The numbers of Kupffer cells in cancerous, para-cancerous and adjacent normal liver tissues of 48 HCCs were comparatively examined.RESULTS: The mean number of Kupffer cells in cancerous,para-cancerous and adjacent normal liver tissues was 12.7±6.8, 18.1±8.2 and 18.9±7.9 respectively. The number of Kuppfer cells in cancerous tissues was significantly lower than that in para-cancerous tissues (t=2.423, P<0.05) and adjacent normal liver tissues (t=2.52t, P<0.05). As tumor size increased, the number of Kupffer cells in cancerous tissues significantly decreased (F=4.61, P<0.05). Moreover,there was also a significant difference in the number of Kupffer cells among well-differentiated, moderately-differentiated and poorly-differentiated cases(F=4.49, P<0.05).CONCLUSION: This study suggests that decrease of Kupffer cells in HCCs may play an important role in the carcinogenesis of HCC, the number of Kupffer cells in HCC is closely related to the size and differentiation grade of the tumor. | Kai Liu Xu He Xue-Zhong Lei Lian-San Zhao Hong Tang Li Liu Bing-Jun Lei Division of Molecular Biology of Infectious Disease Key Laboratory of Biotherapy of Human Disease,Ministry of Education,West China Hospital of Sichuan University,Chengdu 610041,Sichuan Province,China | 2003 | World Journal of Gastroenterology2003，9，9： | 19 |
| 15 | 中药小柴胡汤对肝纤维化大鼠MMPs与TIMPs mRNA的影响显示文摘目的探讨中药小柴胡汤对大鼠肝纤维化过程中MMP-2、MMP-9、TIMP-1 mRNA表达的影响。方法用40%的四氯化碳制备大鼠肝纤维化模型,并用不同剂量的小柴胡汤进行干预。应用HE常规染色法对肝组织切片行组织病理学检查;应用逆转录聚合酶链反应法(RT-PCR)半定量测定大鼠肝组织中MMP-2、MMP-9、TIMP-1 mRNA的表达。结果(1)肝组织病理学检查结果显示:小柴胡汤治疗组与模型组相比,肝纤维化程度显著减轻。(2)小柴胡汤治疗组TIMP-1 mRNA与模型组比显著降低(P<0.01),而MMP-2、MMP-9 mRNA与模型组无差异(P>0.05)。结论小柴胡汤能显著减轻大鼠肝纤维化程度,其作用机理可能是通过下调TIMP-1 mRNA的表达而发挥作用,对MMP-2、MMP-9 mRNA表达无影响。 | 帅峰 | 2009 | 安徽医药2009，13，2： | 17 |
| 16 | Apoptosis of rat hepatic stellate cells induced by anti-focal adhesion kinase antibody显示文摘AIM: To explore the role of focal adhesion kinase (FAI)in the apoptosis in culture-activated rat hepatic stellatecells (HSCs) using a specific anti-FAK antibody.METHODS: Rat HSCs were prepared from Wistar rats byin situ perfusion of collagenase and pronase and single-step density Nycodenze gradient. Culture-activatedHSCs were serum-starved and treated with the anti-FAK antibodies for 24, 48 or 72 h. The apoptosis of HSCwas detected by DNA-fragment assay, flow cytometryand caspase-3 activity determination. The expressionof tissue inhibitor of metalloproteinase-1 (TIMP-1)mRNA was assessed by reverse transcriptionpolymerase chain reaction (RT-PCR).RESULTS: The experiment showed that anti-FAKantibodies induced apoptosis of culture-activated ratHSCs. This phenomenon displayed the classical featuresof apoptotic cell death (DNA fragmentation, cell cycleanalysis) after treated with 30 mg@L-1 FAK antibody for72 h, and accompanied by a significant increase ofcespase-3 activity(1208±76) vs (309±28) nmol@min-1@ g-1, t=-208.5, P<0.05. Meanwhile, treatment with theFAK antibody in HSCs could markedly decrease theTIMP-1 mRNA expression (0.07±0.01 vs 0.38±0.03, t=2.72, P<0.05).CONCLUSION: FAK plays an important role in the survivalof HSCs and the specific anti-FAK antibody could inducethe apoptosis in rat HSCs. | Xiao-Jing Liu Ou Qiang Ming-Hui Huang Laboratory of Department of Internal Medicine,West China Hospital,Sichuan University,Chengdu 610041,Sichuan Province,China Li Yang Yi-Ping Wang Department of Gastroenterology of West China Hospital,Sichuan University,Chengdu 610041,Sichuan Province,China Hong-Bin Wu Laboratory of Department of Surgery,West China Hospital,Sichuan University,Chengdu 610041,Sichuan Province,China | 2002 | World Journal of Gastroenterology2002，8，4： | 17 |
| 17 | COPD患者基质金属蛋白酶-9及其抑制物的表达和调控显示文摘基质金属蛋白酶(matrix metalloproteinases,MMPs)及其组织型金属蛋白酶抑制物(tissue inhibitor of metalloproteinases,TIMPs)是调节细胞外基质降解合成的主要酶类,共同作用于呼吸道的细胞外基质和基底膜,与COPD的发生、发展密切相关。该文就近年来基质金属蛋白酶-9及其抑制物与COPD关系的研究作一综述,以供参考。 | 郭瑞霞 张红梅 袁雅冬 | 2008 | 新医学2008，39，2： | 16 |
| 18 | 活血化淤中药益肝浓缩煎剂对大鼠肝纤维化的作用显示文摘目的:研究益肝浓缩煎剂、强肝胶囊、丹参复方(丹参+当归+水蛭)、当归、水蛭对大鼠肝纤维化降解作用,并对其机制进行初步探讨。 方法:将120只(?)SD大鼠随机分成8组,即正常对照组(A组)、模型组(B组)、模型自然恢复组(C组)、中药治疗组(D-C组)。采用400mL·L^(-1)四氯化碳(CCl_4)_(sc)诱导大鼠肝纤维化模型,造模结束后分别给予相应药物进行治疗,持续10wk。测定肝组织羟脯氨酸(Hyp)、丙二醛(MDA)含量,光镜观察肝脏病理形态变化。 结果:益肝浓缩煎剂、强肝胶囊及丹参复方治疗组Hyp、MDA显著降低(Hyp 124±20μg·g^(-1)肝粉,130±18μg·g^(-1)肝粉,149±16μg·g^(-1)肝粉 vs 190±29μg·g^(-1)肝粉P<0.05;MDA13.8±1.6umol·L^(-1),14.1±2.5 umol·L^(-1),15.4±1.5 umol·L^(-1) us 23.1±2.4 umol·L^(_1)P<0.05),胶原沉积明显减轻(P<0.05);当归治疗组Hyp、MDA显著下降(Hyp 163±16μg·g^(-1)肝粉vs 190±29μg·g^(-1)肝粉P<0.05,MDA18.7±2.4umol·L^(-1) vs 23.1±2.4umol·L^(-1)P<0.05),胶原沉积无减轻(P>0.05);水蛭治疗组各项指标均无好转(Hyp179:25μg·g^(-1)肝粉 vs 190±29μg·g^(-1)肝粉P>0.05,MDA21.9±2.6umol·L^(-1)。vs 3.1±2.4umol·L^(-1)P>0.05)。 结论:益肝浓缩煎剂、强肝胶囊? | 姚欣 姚希贤 修贺明 高君萍 张玉琢 | 2002 | 世界华人消化杂志2002，10，5： | 16 |
| 19 | Estrogen reduces CCL_4-induced liver fibrosis in rats显示文摘AIM: Chronic liver diseases, such as fibrosis or cirrhosis,are more common in men than in women. This genderdifference may be related to the effects of sex hormones onthe liver. The aim of the present work was to investigatethe effects of estrogen on CCL4-induced fibrosis of the liverin rats.METHODS: Liver fibrosis was induced in male, female andovariectomized rats by CCL4 administration. All the groupswere treated with estradiol(1 mg/kg) twice weekly. Andtamoxifen wasgiven to male fibrosis model. At the end of 8weeks, all therats were killed to study serum indicators andthe livers.RESULTS: Estradiol treatment reduced aspartateaminotransferase(AST), alanine aminotransferase (ALT),hyaluronic acid(HA) and type IV collagen(CIV) in sera,suppressed hepatic collagen content, decreased the areas ofhepatic stellate cells (HSC) positive for α-smooth muscle actin(α-SMA), and lowered the synthesis of hepatic type I collagensignificantly in both sexes and ovariectomy fibrotic rats inducedby CCL4 administration. Whereas, tamoxifen had the oppositeeffect. The fibrotic response of the female liver to CCL4treatment was significantly weaker than that of male liver.CONCLUSION: Estradiol reduces CCL4-induced hepaticfibrosis in rats. The antifibrogenic role of estrogen in theliver may be one reason for the sex associated differencesin the progression from hepatic fibrosis to cirrhosis. | Jun-Wang Xu Jun Gong Xin-Ming Chang Jin-Yan Luo Lei Dong Zhi-Ming Hao Ai Jia Gui-Ping Xu | 2002 | World Journal of Gastroenterology2002，8，5： | 14 |
| 20 | 小柴胡汤对实验性肝纤维化大鼠TIMP-1 mRNA表达的影响显示文摘①目的 探讨肝纤维化过程中组织金属蛋白酶抑制因子 1 (TIMP 1 )mRNA的表达及小柴胡汤对其表达的影响。②方法 用体积分数 0 .4 0的四氯化碳花生油制备大鼠肝纤维化模型 ,并用不同剂量的小柴胡汤进行干预。应用苏木精 伊红常规染色法进行组织病理学检查 ;采用逆转录聚合酶链反应 (RT PCR)半定量法测定大鼠肝组织中TIMP 1mRNA的表达。③结果 小柴胡汤干预治疗 (6周、1 2周 )可明显减轻四氯化碳所致的大鼠肝纤维化程度。TIMP 1mRNA在肝纤维化模型早期 (6周 )表达上调 ,随纤维化发展进程表达逐渐增强 ,至肝纤维化晚期 (1 2周 )TIMP 1mRNA表达明显升高 (F =1 9.6 2、2 2 .71 ,q =7.0 1、8.71 ,P <0 .0 1 ) ;小柴胡汤不同剂量干预治疗均可抑制肝纤维化早、晚期TIMP 1mRNA表达 (q =4 .2 3~ 7.83,P <0 .0 1 )。④结论 小柴胡汤能显著减轻大鼠肝纤维化程度 ,其可能通过抑制TIMP | 田字彬 帅峰 孙桂荣 张民生 | 2004 | 青岛大学医学院学报2004，40，3： | 13 |
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