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| 1 | 胆囊切除术后综合征显示文摘 | 郑树国 王小军 | 2008 | 中国实用外科杂志2008，28，6： | 104 |
| 2 | Inhibiting effect of antisense oligonucleotides phosphorthioate on gene expression of TIMP-1 in rat liver fibrosis显示文摘AIM To observe the inhibition of antisenseoligonucleotides (asON) phosphorthioate to thetissue inhibitors metalloproteinase-1 (TIMP-1)gene and protein expression in the liver tissue ofimmunologically induced hepatic fibrosis rats.The possibility of reversing hepatic fibrosisthrough gene therapy was observed.METHODS Human serum albumin (HSA) wasused to attack rats, as hepatic fibrosis model, inwhich asONs were used to block the gene andprotein expressing TIMP-1. According to theanalysis of modulator, structure protein, codingseries of TIMP-1 genome, we designed fourdifferent asONs. These asONs were injected intothe hepatic fibrosis models through coccygealvein. The results was observed by RT-PCR formeasuring TIMP-1 mRNA expression,immunohistochemistry and in situ hybridizationfor collagen Ⅰ, Ⅲ, special staining of collagenfiber, and electron microscopic examination.RESULTS Hepatic fibrosis could last within 363days in our modified model. The expressinglevel of TIMP-1 was high during hepatic fibrosisprocess. It has been proved by theimmunohistochemical and the electronmicroscopic examination that the asONphosphorthioate of TIMP-1 could exactly expressin vivo. The effect of colchicine wasdemonstrated to inhibit the expressing level ofmRNA and the content of collagen Ⅰ, Ⅲ in theliver of experimental hepatic fibrosis rats.However, the electron microscopy research andthe pathologic grading of hepatic fibrosisshowed that there was no significant differencebetween the treatment group and the modelgroup (P>0.05).CONCLUSION The experimental rat model ofhepatic fibrosis is one of the preferable modelsto estimate the curative effect of anti-hepaticfibrosis drugs. The asON phosphorthioate ofTIMP-1 could block the gene and proteinexpression of TIMP-1 in the liver of experimentalhepatic fibrosis rats at the mRNA level. It ispossible to reverse hepatic fibrosis, and it isexpected to study a new drug of anti-hepaticfibrosis on the genetic level. Colchicine has verylimited therapeutic effect on hepatic fibrosis,furthermore, its toxicity and side effects areobvious. | Qing He Nie Yong Qian Cheng Yu Mei Xie Yong Xing Zhou Yi Zhan Cao The Center of Infectious Disease Diagnosis and Treatment of PLA,Tangdu Hospital,Forth Military Medical University,Xi’an 710038,Shaanxi Province,ChinaDr,Qing He Nie graduated from Qinghai Medical College as a doctor in 1983,got master degree at Beijing 302 Army Hospital in 1993,got doctor degree at the Third Military Medical University in 1998,engaged in postdoctoral research at the Fourth Military Medical University from 1998 to 2000,now an associate professor,specialized in clinical and experimental research of infectious diseases,had more than 90 papers published,coauthor of ten books,first author of one book. | 2001 | World Journal of Gastroenterology2001，7，3： | 73 |
| 3 | Role of Kupffer cells in the pathogenesis of liver disease显示文摘Kupffer cells, the resident liver macrophages have long been considered as mostly scavenger cells responsible for removing particulate material from the portal circu- lation. However, evidence derived mostly from animal models, indicates that Kupffer cells may be implicated in the pathogenesis of various liver diseases including viral hepatitis, steatohepatitis, alcoholic liver disease, in- trahepatic cholostasis, activation or rejection of the liver during liver transplantation and liver fibrosis. There is accumulating evidence, reviewed in this paper, suggest- ing that Kupffer cells may act both as effector cells in the destruction of hepatocytes by producing harmful soluble mediators as well as antigen presenting cells during viral infections of the liver. Moreover they may represent a significant source of chemoattractant molecules for cy- totoxic CD8 and regulatory T cells. Their role in fibrosis is well established as they are one of the main sources of TGFβ1 production, which leads to the transformation of stellate cells into myofibroblasts. Whether all these variable functions in the liver are mediated by different Kupffer cell subpopulations remains to be evaluated. In this review we propose a model that demonstrates the role of Kupffer cells in the pathogenesis of liver disease. | George Kolios Vassilis Valatas Elias Kouroumalis | 2006 | World Journal of Gastroenterology2006，12，46： | 74 |
| 4 | 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 |
| 5 | 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 |
| 6 | 苦参素对实验性大鼠肝纤维化防治作用的研究显示文摘目的:探讨苦参素对实验性大鼠肝纤维化的预防与治疗作用.方法:采用人血清白蛋白免疫损伤Wistar大鼠造成肝纤维化模型,60只Wister大鼠,分为5组:造模组、秋水仙碱治疗组、试验组I(苦参素预防组)、试验组II(苦参素治疗组),另设正常对照组.动态观察大鼠肝组织病例变化,采用HE染色观察肝组织改变及Von-Gieson胶原纤维特殊染色观察肝纤维化程度,并采用免疫组织化学染色及肝组织原位杂交检测I型、III胶原含量及I型、III型胶原mRNA的表达.结果:试验组肝组织结构明显好转,纤维组织增生程度明显低于肝纤维化模型组;I型、III型胶原含量及I型、III型胶原的mRNA表达均低于模型组免疫诱导型肝纤维化大鼠,其效果为试验组I(苦参素预防组)效果最好,试验组II(苦参素治疗组)次之,秋水仙碱治疗组再次之,三组均优于造模组.结论:苦参素可减轻肝脏炎症活动、抑制肝内胶原合成,对实验性大鼠肝纤维化具有防治作用. | 康文臻 谢玉梅 聂青和 张岩 郝春秋 王久平 陈伟红 | 2003 | 世界华人消化杂志2003，11，2： | 53 |
| 7 | 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 |
| 8 | Effects of platelet-derived growth factor and interleukin-10 on Fas/Fas-ligand and Bcl-2/Bax mRNA expression in rat hepatic stellate cells in vitro显示文摘AIM: To investigate the effects of platelet-derived growth factor(PDGF) and interleukin-10 (IL-10) on Fas/Fas-ligand and Bcl-2/Bax mRNA expressions in rat hepatic stellate cells.METHODS: Rat hepatic stellate cells (HSCs) were isolated and purified from rat liver by in situ digestion of collagenase and pronase and single-step density Nycodenz gradient.After activated by culture in vitro, HSCs were divided into 4 groups and treated with nothing (group N), PDGF (group P),IL-10 (group I) and PDGF in combinalJon with IL-10 (group C),respectively. Semi-quantitative reverse-transcriptase polymerase chain reaction (RT-PCR) analysis was employed to compare the mRNA expression levels of Fas/FasL and Bcl-2/Bax in HSCs of each group.RESULTS: The expression levels of Fas between the 4 groups had no significant differences (P>0.05). FasL mRNA level in normal culture-activated HSCs (group N) was very low.It increased obviously after HSCs were treated with IL-10(group I) (0.091±0.007 vs 0.385±0.051, P<0.01), but remained the low level after treated with PDGF alone (group P)or PDGF in combination with IL-10 (group C). Contrast to the control group, after treated with PDGF and IL-10, either alone or in combination, Bcl-2 mRNA expression was downregulated and Bax mRNA expression was up-regulated, both following the turn from group P, group I to group C.Expression of Bcl-2 mRNA in group C was significantly lower than that in group P (0.126±0.008 vs0.210±0.024, P<0.01).But no significant difference was found between group C and group I, as well as between group I and group P (P>0.05).Similarly, the expression of Bax in group C was higher than that in group P (0.513±0.016 vs0.400±0.022, P<0.01).No significant difference was found between group I and group P (P>0.05). But compared with group C, Bax expressions in group I tended to decrease (0.449±0.028 vs 0.513±0.016,P<0.05).CONCLUSION: PDGF may promote proliferation of HSCs but is neutral with respect to HSC apoptosis. IL-10 may promote the apoptosis of HSCs by up-regulating the expressions of FasL and Bax and down-regulating the expression of Bcl-2, which may be involved in its antifibrosis mechanism. | Xiao-ZhongWang Sheng-JunZhang Yun-XinChen Zhi-XinChen Yue-HongHuang Li-JuanZhang | 2004 | World Journal of Gastroenterology2004，10，18： | 35 |
| 9 | Effect of anti-fibrosis compound on collagen expression of hepatic cells in experimental liver fibrosis of rats显示文摘INTRODUCTIONLiver fibrosis is mainly characterized by theexcessive synthesis and decreased degradation ofextracellular matrix(ECM),especially the synthesisand deposition of collagen.Almost all kinds of cellsin the liver have participated in the production ofcollagen.The most important ones are hepaticstellate cells(HSC)and hepatocytes.We | Wang LT Zhang B Chen JJ | 2000 | World Journal of Gastroenterology2000，6，6： | 31 |
| 10 | Matrix metalloproteinase-2 and tissue inhibitor of metalloproteinase-1 expression in fibrotic rat liver显示文摘INTRODUCTIONLiver fibrosis is an excessive deposition ofextracellular matrix(ECM)resulted from bothincreased synthesis and decreased degradation.Matrix metalloproteinases(MMPs)represent agroup of neutral proteinases with variable | Liu HL Li XH Wang DY Yang SP | 2000 | World Journal of Gastroenterology2000，6，6： | 31 |
| 11 | 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 |
| 12 | The regulatory role of AT 1 receptor on activated HSCs in hepat,c fibrogenesis,effects of RAS inhibitors on hepatic fibrosis induced by CCl_4显示文摘AIM To assess the effect of ACE inhibitor andAng Ⅱ type Ⅰ(AT1)receptor antagonist inpreventing hepatic fibrosis caused by CCl4administration in rats;to investigate whether ornot there are expression of AT 1 receptors onhepatic stellate cells;and to observe the effectof Ang Ⅱ on proliferation and ECM synthesis ofcultured HSCs.METHODS Studies were conducted in maleSprague-Dawley rats.Except for thehepatofibrotic model group and the controlgroup,in three treated groups,either enalapril(5 mg/kg),or Iosartan(10 mg/kg),or enalapril+Iosartan were given to the fibrotic rats bydaily gavage,and saline vehicle was given tomodel and normal control rats.After 6 weeks,liver fibrosis was assessed directly by hepaticmorphometric analysis,which has beenconsidered the gold standard for thequantification of fibrosis.The expressions of AT1 receptors and(α-mooth muscle actin,α-SMA)in liver tissue or isolated hepatic stellate cells(HSCs)were detected by immunohistochemicaltechniques.The effect of Ang Ⅱ on HSCproliferation was determined by MTT method.Effect of Ang Ⅱ on collagen synthesis of HSCswas determined by 3H-proline incorporation.RESULTS Contrasted to the fibrosis in rats ofthe model group,groups of rats treated with either enalapril or Iosartan,or a combination oftwo drugs showed a limited expansion of theinterstitium(4.23±3.70 vs 11.22±4.79,P<0.05),but no difference was observedamong three treated groups(5.38±3.43,4.96±2.96,4.23±2.70,P>0.05).Expression of AT 1receptors was found in fibrotic interstitium offibrotic rats,whereas in normal control rats theywere limited to vasculature only to a very slightdegree.AT 1 receptors were also expressed onactivated HSCs in the culture.At concentrationsfrom 10-9to 10-5mol/L,Ang Ⅱ stimulated HSCproliferation in culture in a dose-dependentmanner.Increasing Ang Ⅱ concentrationsproduced corresponding increases in 3H-prolineincorporation.Differences among groups were significant.CONCLUSION Angiotensin-converting enzyme inhibitors and AT I blocker may slow the progression of hepatic fibrosis; activated HSCs express AT 1 receptors, and Ang Ⅱ can stimulate the proliferation and collagen synthesis of HSCs in a dose-dependent manner; and activation of RAS may be related to hepatic fibrogenesis induced by CCI4. | Hong Shan Wei Han Ming Lu Ding Guo Li Yu Tao Zhan Zhi Rong Wang Xin Huang Ji Lin Cheng Qin Fang Xu Department of Gastroenterology,Xinhua Hospital,Shanghai Second Medical University,Shanghai 200092,China | 2000 | World Journal of Gastroenterology2000，6，6： | 27 |
| 13 | 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 |
| 14 | Salvia miltiorrhiza monomer IH764-3 induces hepatic stellate cell apoptosis via caspase-3 activation显示文摘AIM: To investigate the effects of IH764-3 on HSC apoptosis,and the expression of caspase-3 protein in HSC apoptoticprocess.METHODS: HSCs were cultured in medium with differentIH764-3 doses ( 10 μg@ mL-1 , 20 μg@ mL-1 , 30 μg@ mL-1,40μg @mL-1) and without IH764-3, and HSC proliferation wasquantitatively measured by 3 H-thymidine incorporation. Themorphological changes of HSCs were observed withtransmission electron microscope after exposure to the doseof 40 μg@ mL-1 of IH764-3 for 48 hr, The apoptosis rates weredetected by annexin V/PI and TdT-mediated dUTP nick endlabeling (TUNEL). The expression of caspase-3 protein wasdetermined by flow cytometry.RESULTS: (1) HSC proliferation rates induced with differentIH764-3 doses ( 10 μg@ mL-1 , 20 μg@ mL-1 , 30 μg@ mL-1 , 40 μg@mL-1) were significantly reduced compared with that of thecontrol group ( P< 0.01). (2)With the doses above, IH764-3dose-dependently produced HSC apoptosis rates of 6.7 %(9.4%),9.3 %(21.6 %),15.1%(27.2 %) and 19.0 %(28.4 %)respectively, by annexin V and PI-labeled flow cytometry assay(or TUlE L), while it was only 2.3 %(6.7 %) in the control. (3)The expression of caspase-3 protein in IH764-3 groups wassignificantly higher than that of the cortrol (P<0.05).CONCLUSION: Within the dose range used in present study,IH764-3 can inhibit HSC proliferation, as well as enhance HSCapoptosis. Furthermore, IH764-3 can significantly increasethe caspase-3 protein expression. | ZhanXL LiuL 等 | 2002 | World Journal of Gastroenterology2002，8，3： | 25 |
| 15 | 中药软肝缩脾丸对肝纤维化大鼠TIMP-1/2蛋白表达的影响显示文摘目的探索肝纤维化发生的分子机制,尤其是TIMP-1,TIMP-2的作用。方法采用免疫组化和原位杂交的方法分别测定5组肝纤维化大鼠不同治疗前后TIMP-1,TIMP-2的基因调节和蛋白表达。结果 CCl_4模型组TIMP-1,TIMP-2 mRNA及蛋白水平明显高于治疗组。正常组大鼠肝组织无一例阳性。结论 TIMP-1,TIMP-2与肝纤维化形成密切相关,软肝缩脾丸对TIMP-1,TIMP-2的基因和蛋白表达有一定的抑制作用。 | 王全楚 申德林 张成道 许丽芝 聂青和 谢玉梅 周永兴 | 2001 | 世界华人消化杂志2001，9，4： | 22 |
| 16 | Effect of compound rhodiola sachalinensis A Bor on CCI4-induced liver fibrosis in rats and its probable molecular mechanisms显示文摘AIM: To explore the anti-fibrotic effect of a traditional Chinese medicine, compound rhodiola sachalinensis A Bor on CCl4-induced liver fibrosis in rats and its probable molecular mechanisms. METHODS: Ninety healthy male SD rats were randomly divided into three groups: normal group (n=-10), treatment group of compound rhodiola sachalinensis A Bor (n=-40) and CCl4-induced model group (n=40). The liver fibrosis was induced by CCl4 subcutaneous injection. Treatment group was administered with compound rhodiola sachalinensis A Bor (0.5 g/kg) once a day at the same time. Then the activities of several serum fibrosis-associated enzymes: alanine aminotransferase (ALT), aspartate aminotransferase (AST), N-acetyl-beta-D-glucosaminidase (β-NAG) and the levels ofserum procollagen Ⅲ (PCⅢ), collagen Ⅳ (CⅣ), hyaluronic acid (HA) were assayed. The histooathol(mical chanaes were observed with HE, VG and Masson stain. The expression of TGF-β1 mRNA,αl (I) mRNA and Na+/Ca2+ exchanger (NCX ) mRNA was detected by reverse transcription polymerase chain reaction (RT-PCR) in situ.RESULTS: Compound rhodiola sachalinensis A Bor significantly reduced serum activities of ALT, AST, β-NAG and decreased the levels of PCⅢ, CⅣ, HA, improved the liver histopathological changes, inhibited the expression of TGF-β1 mRNA, α(1) mRNA and Na+/Ca2+ exchanger mRNA in rats. CONCLUSION: Compound rhodiola sachalinensis A Bor can intervene in CCI4-induced liver fibrosis in rats, in which potential mechanisms may be decreasing the production of TGF-β1, reducing the production of collagen, preventing the activation of hepatic stellate cell (HSC) and inhibiting theexpression of TGF-β1 mRNA, αl(I) mRNA and Na+/Ca2+ exchanger mRNA. | Chun-TaoLei Ming-DeJiang Xiao-BinChen YongZhang HuiXu ZhaoWang Xiao-LingWU Wei-ZhengZeng Pi-LongWang | 2003 | World Journal of Gastroenterology2003，9，7： | 21 |
| 17 | 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 |
| 18 | TGFβ-Smad信号转导通路与肝纤维化显示文摘转化生长因子β(transforming growth factor beta.TGF β)是一类能够调节细胞生长和分化的多肽,具备多种生物作用,在肝纤维化发生、发展过程中具有活化肝星状细胞(hepatocelluar stellate cell,HSC),促进胶原基因表达,促进细胞外基质合成与沉积等作用,是最重要的促肝纤维化细胞因子之一、大量研究证实,TGF β-Smad信号转导通路是TGF β发挥生物学作用的主要通路,其分子组成与分子调节复杂,与其他信号通路存在广泛的交互影响,对不同的组织、细胞及肝纤维化的不同病程的作用均有明显的差异,对TGF β-Smad信号转导通路的深入研究不仅使肝纤维化的发病机制得到进一步的阐明,也给肝纤维化的防治研究提供了新的有效途径,本文综述TGF β-Smad信号转导通路的组成与调控,在肝纤维化发病与防治中的作用的研究进展。 | 吴晓玲 曾维政 王丕龙 | 2003 | 世界华人消化杂志2003，11，10： | 19 |
| 19 | Therapeutic effects and molecular mechanisms of anti-fibrosis herbs and selenium on rats with hepatic fibrosis显示文摘AIM:To study the therapeutic effects of anti-fibrosis herbs and selenium on hepatic fibrosis induced by carbon tetrachloride (CCl4) in rats and the underlining molecular mechanisms.METHODS:Fifty-three Wistar rats were randomly divided into:normal control group, model control group, colchicine group, anti-fibrosis herbs group (AF group) and anti-fibrosis herbs plus selenium group (AS group).The last four groups were administered with CCl4 at the beginning of experiment to induce hepatic fibrosis. Then colchicine, anti-fibrosis herbs and selenium were used to treat them. The normal control group and the model control group were given normal saline at the same time. At the end of the 6^th week, rats in each group were sacrificed. Blood and tissue specimens were taken. Serum indicators (ALT, AST, HA, LN) were determined and histopathological changes were graded. Lymphocyte CD4 and CD8 were examined by flow cytometry. Expression of TGF-β1 and NF-κB was detected by immunohistochemistry and expression of TGF-β1 mRNA was detected by semiquantified RT-PCR.RESULTS: Histological grading showed much a smaller degree of hepatic fibrogenesis in AS group and AF group than that in colchicine group and model control group.The serum content of ALT, AST, HA and LN in AF group and AS group were significantly lower than that in colchicine group (ALT:65.8±26.5, 67.3±18.4 and 96.2±20.9 in AF, AS and colchicine groups respectively; AST: 150.8±34.0, 154.6±27.3 and 215.8±24.6 respectively; HA: 228±83, 216±58 and 416±135 respectively; LN:85.9±15.0, 80.6±18.6 and 106.3±14.2 respectively) (P<0.05). The level of CD4 and CD4/CD8 ratio in AF group and AS group was significantly higher that those in cochicine group (CD4:50.8±3.8, 52.6±3.4 and 40.2±2.1 in AF, AS and colchicine groups respectively;CD4/CD8 ratio:1.45,1.46 and 1.26, respectively (P<0.05).The expression level of NF-κB and TGF-β1 in the liver tissues of AF and AS treatment groups was markedly decreased compared with that in cochicine group, and TGF-β1 mRNA was also markedly decreased (1.07±0.31 and 0.98±0.14 vs2.34±0.43, P<0.05).CONCLUSION: Anti-fibrosis herbs and selenium have beneficial effects on hepatic fibrosis in rats by enhancing immunity and inhibiting NF-κB and TGF-β1 expressions. | Yu-TongHe Dian-WuLiu Li-YuDing QingLi Yong-HongXiao | 2004 | World Journal of Gastroenterology2004，10，5： | 19 |
| 20 | 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 |
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