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| 1 | Effects of cytokines on carbon tetrachloride-induced hepatic fibrogenesis in rats显示文摘AIM: To observe the possible effects of transforming growth factor (TGF) β1, interleukin (IL)-6, tumor-necrosis factor (TNF) α and IL-10 on experimental rat hepatic fibrosis. METHODS: One hundred SD rats were divided randomly into the three groups. Control group received intraperitoneal injection of saline (2 ml-kg^-1), twice a week. Fibrogenesis group was injected intraperitoneally with 50% carbon tetrachloride (CCI4) (2 ml-kg^-1) twice a week. Fibrosisintervention group was given IL-10 at a dose of 4 μg-kg^-1 20 minutes before CCI4 administration from the third week.At the fifth, seventh, and ninth weeks, 7 to 10 rats in each group were sacrificed to collect serum. Levels of TGF-β1,TNF-α, IL-6 and IL-10 were determined by enzyme-linkedimmunosorbent assay (ELISA). The liver tissues were taken for routine histological examination. RESULTS: Hepatic fibrosis was developed with the injection of CCI4. Values of the circulating TGFβ, TNFα, IL-6 and IL-10 in the control group were 25.495.56 ng.L^-1, 15.18±3.83ng.L^-1, 63.64±13.03 ng.L-^1 and 132.90±12.13 ng.L^-1,respectively. Their levels in the CCI4-intoxication group were 31.13±6.41 ng.L^-1, 18.91±5.31 ng.L^-1, 89.08±25.39 ng.L^-1 and 57.63±18.88 ng.L^-1, respectively, and those in the IL-10-intervention group were 26.11±5.32 ng.L^-1,13.99±1.86 ng.L^-1,74.71±21.15 ng.L^-1 and 88.19±20.81 ng.L^-1, respectively. A gradual increase was observed in the levels of TGFβ1, TNFα and IL-6 during hepatic fibrogenesis. These changes were pardally reversed by simultaneous administration of IL-10. The histological parameters, characterized by CCl4-intoxificatJon,also seemed to be improved with IL-10 treatment, the collagen production was reduced at the ninth week and the histological activity index was decreased from 7.9±1.2 to 4.7±0.9. CONCLUSION: TGFβ1, TNFα and IL-6 may play important roles during CCI4-induced hepatic fibrogenesis, and IL-10 may counterbalance their effects. | Li-JuanZhang Jie-PingYu DanLi Yue-HongHuang Zhi-XinChen Xiao-ZhongWang | 2004 | World Journal of Gastroenterology2004，10，1： | 67 |
| 2 | Therapeutic effect of interleukin-10 on CCI_4-induced hepatic fibrosis in rats显示文摘瞄准:在老鼠和它的可能的机制在导致 CCl4 的肝的纤维变性上学习外长的 interleukin-10 的治疗学的效果。方法:四十 -- 七只 SD 老鼠随机被划分成控制组(组 N ) 和导致 CCl4 的肝的纤维变性模型组(组 C ) 。在 CCl4 为 9 wk 被给以后,模型组被划分成三个组。在组 M 的老鼠立即被放到死亡,在组 T 的老鼠为另一三 wk 与 IL-10 被对待然后放了到死亡,在组 R 的老鼠在三个星期以后恢复了并且然后被打死。肝的纤维变性的度被测量由他染色并且组织学的活动索引(HAI ) 。组织学的活动索引(HAI ) ,骨胶原类型的变化我和 III 被染色的 Picrosirius 测量。在肝织物的 TNF-alpha, MMP-2 和 TIMP-1 的表示被 S-P 免疫组织化学测量。结果:CCl4- 导致了试验性的老鼠肝的纤维变性模型成功地被建立。肝的纤维变性的度比在组 M 和 R 在组 T 是显著地更低的,并且二个组之间没有差别。骨胶原类型的表示我和 III 显著地在组 T 被镇压并且稍微在组 M 和 R 被压制。在组 M 的 TNF-alpha, MMP-2 和 TIMP-1 的积极层次在组 N (P<0.01 ) 与那些相比显著地增加了。积极信号在组 T 和 R (P<0.01 ) 显著地减少了,但是积极分数比在组 R (P<0.01 ) 在组 T 是显著地更低的。结论:外长的 IL-10 能在老鼠颠倒导致 CCl4 的肝的纤维变性。IL-10 可以由堵住导致 CCl4 的发炎在肝的纤维变性上施加它的可逆效果,禁止 MMP-2 和 TIMP-1 的表示并且支持骨胶原类型的分辨率我和 III。 | Yue-Hong Huang Hei-Na Shi Wei-Da Zheng Li-Juan Zhang Zhi-Xin Chen Xiao-Zhong Wang | 2006 | World Journal of Gastroenterology2006，12，9： | 27 |
| 3 | 肝纤维化的治疗研究进展显示文摘肝纤维化是慢性肝炎发展至肝硬化的必经病理过程,肝纤维化在一定程度上可以逆转,从而使'慢性肝炎-肝纤维化-肝硬化-肝癌'这条慢性进展过程得以终止。重视肝纤维化的及早治疗,可以极为有效地救治慢性肝病患者,减少社会经济损失。本文将近十年来肝纤维化的治疗研究作以综述。 | 张莎莎 吕文良 张旭 陈兰羽 杨广栋 徐晨光 李川 李娟梅 | 2012 | 浙江中医药大学学报2012，36，4： | 28 |
| 4 | 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 |
| 5 | 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 |
| 6 | Effects of pentoxifylline on the hepatic content of TGF-β1 and collagen in Schistosomiasis japonica mice with liver fibrosis显示文摘AIM: To study the effects of pentoxifylline (PTX) on thecontent of hepatic TGF-β1, type Ⅰ and type Ⅲ collagen inschistosomiasis japonica mice with liver fibrosis and itsmechanism of anti-fibrosis.METHODS: Forty mice with schistosomiasis were dividedinto four groups: one group as control without anytreatment, other three were treated with Praziquantel 500mg/(kg.d)for 2 d, high dose PTX 360 mg/(kg.d) for 8 wk,and low dose PTX 180 mg/(kg.d) for 8 wk respectively.Immunohistochemical technique and multimedia colorpathographic analysis system were applied to observe thecontent change of hepatic TGF-β1, type Ⅰ and type Ⅲcollagen in schistosomiasis japonica mice with liver fibrosisbefore and after PTX treatment.RESULTS: Effects of PTX on the content change of hepaticTGF-β1, type Ⅰ and type Ⅲ collagen in schistosomiasis japonicamice with liver fibrosis were related to the dosage of PTX,high dose PTX treated group could significantly reduce thecontent of TGF-β1 (0.709±0.111), type Ⅰ (0.644±0.108) andtype Ⅲ (0.654±0.152) collagen compared with those ofcontrol group (0.883±0.140, 0.771±0.156, 0.822±0.129)with statistical significance (P<0.05). Low dose PTX couldalso reduce the hepatic content of TGF-β1 (0.752±0.152),type Ⅰ (0.733±0.117) and type Ⅲ (0.788±0.147) collagen,but without statistical significance (P>0.05). Both high doseand low dose PTX groups have significant differences onthe content of TGF-β1, type Ⅰ and type Ⅲ collagen (P<0.05,P<0.05, P< 0.01,respectively).CONCLUSION: High dose of PTX treatment could reducethe content of hepatic TGF-β1, type Ⅰ and type Ⅲ collagensignificantly in schistosomiasis japonica mice with liverfibrosis, and thus plays its role of antifibrosis. | Li-JuanXiong jian-FangZhu Duan-DeLuo Lin-LanZen Shu-QingCai | 2003 | World Journal of Gastroenterology2003，9，1： | 18 |
| 7 | BMP-7防治实验性肝纤维化的研究显示文摘目的观察骨形态发生蛋白-7(bone morphogenetic protein-7,BMP-7)对实验性肝纤维化的影响。方法运用猪血清腹腔注射法,诱导免疫性大鼠肝纤维化模型。实验动物分为5组:肝纤维化模型组、早期治疗组、后期治疗组、预防组、对照组。预防组从实验开始、早期治疗组从实验第2周、晚期治疗组从实验第4周腹腔注射外源性BMP-7,每周3次;对照组注射等剂量生理盐水。采用免疫组化和Western印迹法检测BMP-7对实验性肝纤维化大鼠肝组织中转移生长因子-β_1(transforming growth factor-β_1,TGF-β_1)表达的影响。结果实验性肝纤维化大鼠的早期治疗组、后期治疗组和预防组的肝纤维化级别与模型组之间的差异均有统计学意义(P<0.05);预防组和治疗组中BMP-7可以抑制纤维化肝组织中TGF-β_1的表达,治疗组中的TGF-β_1的表达较模型组中明显减少(P<0.05)。结论 BMP-7有效预防和治疗实验性肝纤维化,其机制可能与抑制纤维化肝组织中的TGF-β_1的表达有关。 | 王胜兰 杨长青 杨丽 常义忠 袁敏 郜恒俊 | 2010 | 同济大学学报(医学版)2010，31，2： | 7 |
| 8 | 三七总皂甙对大鼠肝纤维化防治机制显示文摘目的:观察三七总皂甙对实验性肝纤维化的防治作用,并探讨其可能的机制. 方法:以CCl4、乙醇及胆固醇诱导大鼠肝纤维化模型,同时给予三七总皂甙干预组三七总皂甙腹腔注射.设立模型对照组和正常组.于造模6 wk后大鼠全部处死,取血清及肝组织标本.应用放射免疫法检测血清PCⅢ、LN含量,HE 染色观察肝组织形态学改变,VG染色测定肝组织纤维表达情况,免疫组织化学测定肝组织desmin、α-SMA、ICAM- 1、LN、Ⅰ和Ⅲ型胶原. 结果:与模型组比较,三七总皂甙组大鼠血清PCⅢ、LN 含量均明显降低:形态学改变明显轻于模型组;肝组织desmin、α-SMA、ICAM-1染色强度均明显减弱;三七总皂甙组肝组织LN、Ⅰ和Ⅲ型胶原染色轻于模型组,但差异性不显著. 结论:三七总皂甙对实验性肝纤维化形成具有一定的抑制作用.其作用机制可能与抑制HSC活化,诱导活化的HSC凋亡, 减少Ⅰ、Ⅲ型胶原和LN表达,并减轻肝窦毛细血管化有关. | 王文兵 戴立里 郑元义 | 2004 | 世界华人消化杂志2004，12，8： | 7 |
| 9 | 复方红景天干预肝纤维化大鼠胶原代谢显示文摘目的:探讨复方红景天对四氯化碳(CCl4)诱导的肝纤维化大鼠模型胶原代谢的干预作用.方法:用CCl4皮下注射法诱导SD大鼠肝纤维化模型,同时给予复方红景天口服,观察肝组织病理变化、羟脯氨酸(Hyp)含量、Ⅰ型前胶原(α 1(Ⅰ))mRNA表达,及血清HA、CⅣ、PCⅢ、TGFβ1变化情况.结果:口服复方红景天可改善肝组织病理变化,减少Hyp含量(657±74μg/g vs 1 257±98μg/g,P<0.05)及Ⅰ型前胶原α 1(Ⅰ)mRNA表达(85.7% vs 96.7%,P<0.05),降低血清HA、CⅣ、PCⅢ、TGF β 1的水平(164±46μg/L,97±15μg/L,289±76μg/L,60±20 mg/L vs 265±98μg/L,160±30μg/L,456±113μg/L,89±23 mg/L.P<0.05,P<0.01).结论:复方红景天可有效保护CCl4诱导的大鼠肝纤维化,其作用机制可能与抑制肝脏胶原纤维合成、保护肝细胞等有关. | 曾维政 吴晓玲 蒋明德 邓桂英 陈晓斌 张勇 秦建平 徐辉 | 2003 | 世界华人消化杂志2003，11，7： | 4 |
| 10 | Construction of prokaryotic expression system of TGF-β1 epitope gene and identification of recombinant fusion protein immunity显示文摘AIM: To insert the constructed TGF-β1the el loop of C-terminus of truncated hepatitis B core antigen to increase TGF-β1expression system and to identify immunity of the expressed recombinant protein in order to exploit the possibility for obtaining anti- TGF-β1METHODS: The TGF-β1mature TGF-β1TGF-32) was amplified by polymerase chain reaction from the recombinant pGEM-7z/TGF-β1HBcAg gene fragments (encoding HBcAg from 1-71 and 89-144 amino acid residues) were amplified from PYTA1-HBcAg vector. The recombinant vector pGEMEX-1 was used to insert HBcAg1-71, TGF-β1into restrictive endonuclease enzyme and ligated with T4ligase. The fusion gene fragments HBcAg1-71-TGF-β1HBcAg89-144 were recloned to pET28a(+) and the DNA sequence was confirmed by the dideoxy chain termination method. The recombinant vector pET28a (+)/CTC was transformed and expressed in E.. Coli BL21 (DE3)under induction of IPTG. After purification with Ni+2-NTA agarose resins, the antigenicity of purified protein was detected by ELISA and Western blot and visualized under electron microscope.RESULTS: Enzyme digestion analysis and sequencing showed that TGF-β1loop of C-terminus of truncated hepatitis B core antigen.SDS-PAGE analysis showed that relative molecular mass(Mr) of the expressed product by pET28a (+)/CTC was Mr 24 600.The output of the target recombinant protein was approximately 34.8% of the total bacterial protein,mainly presented in the form of inclusion body. Western blotting and ELISA demonstrated that the fusion protein could combine with anti-TGF-β1not with anti-HBcAg. The purity of protein was about 90% and the protein was in the form of self-assembling particles visualized under electron microscope. This fusion protein had good anti-TGF-β1could be used as anti-TGF-β1CONCLUSION: A recombinant prokaryotic expression system with high expression efficiency of the target TGF- epitope gene was successfully established.The fusion protein is in the form of self-assembling particles and HBcAg can increase the antigenicity of TGF-β1immunogenicity and antigenicity. | Yong-Hong Guo Zhi-Ming Hao Jin-Yan Luo Jun-Hong Wang | 2005 | World Journal of Gastroenterology2005，11，40： | 3 |
| 11 | 反义金属蛋白酶组织抑制因子-1表达质粒对实验性肝纤维化的影响显示文摘目的 观察反义金属蛋白酶组织抑制因子 1(TIMP 1)表达质粒对实验性肝纤维化的影响。方法 运用重组DNA技术构建反义TIMP 1真核细胞表达质粒 ,经与糖化多聚赖氨酸偶联后 ,尾静脉注射将其导入猪血清诱导的免疫性大鼠肝纤维化模型体内 ;通过Northern印迹法、RT PCR、Western印迹法检测外源导入基因的表达 ,并通过肝组织间质胶原酶活性和羟脯氨酸测定 ,以及肝组织Ⅰ、Ⅲ型胶原免疫组织化学与VanGieson染色观察反义TIMP 1质粒对大鼠肝纤维化的影响。结果 外源导入基因可在肝组织中获得确切表达 ,其表达可增加间质胶原酶的活性 (P <0 .0 1) ,减少羟脯氨酸含量 (P <0 .0 1) ,促进Ⅰ、Ⅲ型胶原的降解 (P <0 .0 1) ,并促进肝脏病理形态一定程度的改善 (P <0 .0 1)。结论 反义TIMP 1表达质粒对肝纤维化有较好的改善作用。 | 蒋炜 王吉耀 杨长青 王逸青 贺伯明 刘文滨 | 2003 | 肝脏2003，8，3： | 0 |
| 12 | 正常与硬化肝组织基因表达差异的初步分析显示文摘目的:了解肝硬化的基因表达概况,寻找在肝硬化及正常肝组织中差异表达基因.方法:以各24例肝硬化及正常肝组织的总RNA混合定量后反转录合成含有α-32pdATP的cDNA为探针,与Atlas微阵列表达分析膜杂交.结果:放射自显影结果经AtlasImageTM软件分析显示:在所分析的588种已知基因中,Integrinbeta7、collagentypeⅩⅧ等17个基因在肝硬化组织中表达上调,TFDP2、BAK、ABL等98个表达下调,参与细胞增生、凋亡、分化、细胞间相互作用、与细胞侵袭相关的基因表达水平发生了明显改变.结论:通过Atlas微阵列系统分析发现的这些基因的表达改变组成了—个肝硬化特异的基因表达谱.系统地研究肝硬化的基因表达改变,与肝硬化发生相关基因的差异变化可为肝硬化诊断和治疗提供线索. | 刘连新 陈志宏 武林枫 李宏伟 刘芝华 姜洪池 王秀琴 吴旻 | 2004 | 世界华人消化杂志2004，12，2： | 0 |
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