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| 1 | 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 |
| 2 | 酒精性肝病大鼠模型的建立显示文摘目的为深入研究酒精性肝病的发病机制,提供一个简单可行的动物模型,并利用此模型检测血浆PDGF含量在酒精性肝病发生发展中的变化。方法本研究在平衡饮食的条件下,以400mL·L^(-1)乙醇,8g·kg^(-1)·d^(-1),日3次灌胃至4wk末,自5wk,以500 mL·L^(-1)乙醇,9g·kg^(-1)·d^(-1),日3次灌胃至8 wk末,自9 wk,以500mL·L^(-1)乙醇,10g·kg^(-1)·d^(-1)日3次灌胃至12wk末,诱导酒精性肝病大鼠动物模型,分别于4wk末、8wk末、12wk末观察肝脏病理学改变,并用生物活性法测定了对照组及实验组不同病理阶段血浆中血小板源性生长因子(PDGF)的含量。结果光镜显示对照组肝细胞以中央静脉为中心呈放射状排列,酒精摄入4wk末,肝细胞中重度脂肪变性,8wk末肝细胞变性坏死,炎性细胞浸润,Mallory染色可见胶原于中央静脉沉积增加,12wk末变性坏死及炎性细胞浸润明显,Mallory染色可见胶原自中央静脉向窦周隙伸展,呈现轻度肝纤维化改变,PDGF含量结果可见与同时期对照组相比,实验组PDGF含量(kU·L^(-1))均有显著增高,4,8,12wk分别为67±15 vs 31±18(P<0.05),130±30vs33±19(P<0.001),202±20 vs 36±6(P<0.001);实验组不同时期差异明显,随病程进展病变加重,8wk与4wk相比,P<0.01,12wk与8wk相比,P<0.001。结论灌胃为一种简单可行的造模方法;PDGF可能在酒精性肝纤维化的发生发展中起重要作用,但详细机制有待进一步探讨。 | 林红 吕淼 张义侠 王炳元 傅宝玉 | 2001 | 世界华人消化杂志2001，9，1： | 67 |
| 3 | 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 |
| 4 | Effects of Yigan Decoction on proliferation and apoptosis of hepatic stellate cells显示文摘AIM: To investigate the effects of Chinese herb YiganDecoction on proliferation and apoptosis of the hepaticstellafe cells (HSC) in vitro.METHODS: The study in vitro was carried out in the cultureof HSC lines. Various concentrations of Yigan Decoctionwere added and incubated. Cell proliferation was detectedwith MTT colorimetric assay. Cell apoptosis was detected byelectron microscopy, flow cytometry and TUNEL.RESULTS: The proliferation of HSC was inhibited by YiganDecoction, which depending on dose and time significantly.The HSC proliferation rates ofgroups at the endconoentrations 144 and 72 (g@L-1 ) were 21.62 % and 140.54 %respectively, significantly lower then that of normal controlgroup( P < 0.01 ). The HSC proliferation rates of groups atthe end concentratiors 36, 18 and 9(g@L-1 ) were 54.05 %,45.95 % and 51.35 % respectively, lower than that of controlgroup( P < 0.05). When the end concentration was 4.5 g@L-1, the proliferation rate was 83.78 %, which appeared nosignificant differences compared with control group. At thesame concentrations of 18 g@L-1, the inhibitory effects ofYigan Decoction at 24 h, 48 h and 72 h time point wereobserved, the effects were time-dependent, and reached apeak at 72 h. Meanwhile, it was showed that the inducingeffects of Yigan Decoction on HSC apoptosis were dose-dependent and time-dependent. The apoptosis index (Al)was detected by TUNEL. After Yigan Decoction had beenincubated for 48 h at the end concentration of 18 g@ L-1 , tieAl (14.5 + 3. 1 ) % was significantly higher than that ofcontrol group (4.3+ 1.3) % (P<0.01). When visualizedunder transnission electron microscopy, some apoptoticsfellafe cells were found, i. e. dilated endoplasmicreticulum, irregular ntclei, chromatin condensation andheterochromatin ranked along inside of nuclear membrane.By flow cytometry detection, after HSC was treated withYigan Decoction at different concentrations of 36, 18 and 9(g@ L-1 ) for 48 h, Al ( % ) were 13.3 ± 3.2, 10.7 ± 2.7 and 10.1 ±2.5 respectively, which were significantly higher than that ofcontrol group(4. 1 ± 1.9) (P < 0.01). At the sameconcentration of 18g@ L-1 for 24h, 48h and 72h, Al (%) were9.3± 1.8、10.7± 2.7 and 14.6±4.3 respectively, which weresignificantly higher than that of control group ( P< 0.01).CONCLUSION: Yigan Decoction could significantly inhibitHSC proliferation and increase the apoptosis index of HSCdosedependently and time-dependently, which may berelated to its mechanism of antifibrosis. | YaoXX TangYW 等 | 2002 | World Journal of Gastroenterology2002，8，3： | 44 |
| 5 | ROC curves in evaluation of serum fibrosis indices for hepatic fibrosis显示文摘AIM: Use Receiver operating characteristic (ROC) curves to find out the relationship between serum level of hyaluronic acid (HA), type Ⅲ procollagen (PCⅢ), N-terminal procollagen Ⅲ peptide (PⅢNP), laminin (LN), type Ⅳ collagen (C-Ⅳ) and hepatic fibrosis, as well as to determine their value in clinical practice.METHODS: 114 serum samples from chronic hepatitis patients were assayed for fibrosis indices including HA, PCⅢ, PⅢNP, LN and Ⅳ-C with radioimmunoassay (RIA). Liver biopsy was also performed in all these patients and the biopsy material was examined histopathologically.RESULTS: ROC curves analysis showed that area under the curve (AUC) of PⅢNP, HA, PCⅢ, C-Ⅳ and LN was 0.800,0.728, 0.727, 0.583 and 0.463, respectively. The analysis also showed that PⅢNP (r=0.452), HA (r=0.497) and PCⅢ (r=0.404) have greater diagnosis performances than C-Ⅳ (r=0.238) and LN (r=0.128) according to fibrosis staging. The sensitivity of HA plus PⅢNP was 55.1%, it was the most sensitive combination. Combined three or more than three indices that based on HA, the specificity was 100 %.Using combination assays can improve the specificity, but its sensitivity was not high. Serum fibrosis indices increased as the grade of inflammation aggravated. But only PⅢNP and PCⅢ had significant difference between G1 and G2 (PⅢNP: 13.16±8.07 VS8.32±5.09; PCⅢ: 164.22±65.69 VS 138.23±77.63). The coefficient correlation of the results of inflammation grade and fibrosis staging to HA was 0.525 and 0.553 respectively, that to PCⅢ, 0.446 and 0.412, that to LN, 0.234 and 0.194, and that to Ⅳ-C, 0.363 and 0.351, respectively.CONCLUSION: Serum fibrosis indices can indicate tendency of hepatic fibrosis, but it cannot replace liver biopsy. However, as diagnostic markers, more efficient serum fibrosis indices for the diagnosis of hepatic fibrosis need to be explored. | Min Zheng Wei-Min Cai Hong-Lei Weng Rong-Hua Liu,Institute of Infectious Diseases,First Affiliated Hospital,School of Medicine,Zhejiang University,Hangzhou 310003 Zhejiang Province,China | 2002 | World Journal of Gastroenterology2002，8，6： | 29 |
| 6 | 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 |
| 7 | 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 |
| 8 | 肝星状细胞与肝纤维化的研究进展显示文摘活化肝星状细胞(HSC)数量的增加是肝纤维化形成的中心环节,凋亡则导致其数量的减少.HSC是纤维化过程中产生细胞外基质(ECM)的主要细胞,ECM过多产生是形成肝纤维化,最终导致肝硬化、肝功能衰竭的主要原因.因此,可从抑制 HSC激活、促进 HSC凋亡两方面进行抗肝纤维化治疗.加强HSC的激活和凋亡调控机制的研究,有助于我们认识HSC激活和凋亡及肝纤维化发生的本质. | 蒋业贵 李兆申 | 2003 | 世界华人消化杂志2003，11，9： | 17 |
| 9 | Extraction and purification of TGFβ and its effect on the induction of apoptosis of hepatocytes显示文摘AIM To extract and purify the transforming growth factor β (TGF β), and to demonstrate its biological activity in vivo and induction of apoptosis of hepatocytes in vitro.METHODS TGF β was isolated from fresh bovine platelets by acid/ethanol extraction method and purified with ion exchange and gel chromatography. The extracted TGF β was injected subcutaneously to mice, and its biological activity in vivo was observed 72 hfs post-injection by HE staining. The morphological changes were observed by HE staining and the occurrence of apoptosis was detected by TUNEL method after the human normal hepatic cell line QZG was treated with 8 μg@L 1 TGFβ for 12 hrs in vitro.RESULTS The molecular mass 25 ku TGF β protein was successfully extracted. It was able to induce localized granulation tissue formation in vivo. TGF β-treated hepatocytes showed obvious apoptotic morphological changes, including the pyknosis and dense-stained nuclei and cytoplasm, the fragmentary, annular or crescent nuclei, and the 'bubbling' cytoplasm. Moreover, its apoptotic rate was significantly higher than that of the control group (P<0.05).CONCLUSION Biological active TGF β protein is extracted and purified successfully from bovine platelets, and it is able to induce the apoptosis of hepatocytes. | Xiao-Hui Si Lian-Jun Yang Research Institute of Stomatology,the Ninth People’s Hospital,Shanghai Second Medical University,Shanghai 200011,ChinaDepartment of Pathology,Fourth Military Medical University,Xi’an 710033,Shaanxi Province,China | 2001 | World Journal of Gastroenterology2001，7，4： | 15 |
| 10 | Influence factors of serum fibrosis markers in liver fibrosis显示文摘AIM: To analyze the factors which influence the serum levels of hyaluronic acid (HA), type Ⅲ pro-collagen (PCIII), laminin (LN) and type Ⅳ collagen (C-Ⅳ) in liver fibrosis.METHODS: The serum specimens from 141 chronic hepatitis patients were assayed for fibrosis indexes including HA, PCIIT,LN and C-Ⅳ with radioimmunoassay (RIA) and liver function indexes by an automatic biochemistry analyzer. The patients were then divided into consistent group and inconsistent group. The patients'clinical manifestations were recorded,routine blood pictures were done by a blood counter and analyzer (AC-900). Liver biopsy specimens were examined path-morphologically. The inner diameters of portal vein,splenic vein and thickness of spleen were all measured by ultrasonography.RESULTS: Sixteen patients (14.16 %) had serum fibrosis indexes inconsistent with histological stage of their hepatic fibrosis. Their serum fibrosis indexes did not correlate with the stage of hepatic fibrosis (P>0.05), but were positively correlated with the grade of inflammation (X2=12.07, P<0.05).At the same time, serum albumin (ALB) and the ratio of albumin and globulin (A/G) were significantly increased (t=3.06, P<0.01), (t=3.70, P<0.01). Serum levels of glutamicpyruvic transaminase (ALT), glutamic-oxaloacetic transaminase (AST), γ-glutamyl transferase (GGT) and globulin (GLB) were all significantly decreased (t=2.45, P<0.05), (t=2.33,P<0.05), (t=2.08, P<0.05), (t=3.03, P<0.01). Weary degree also decreased more obviously (X2=7.52, P<0.05), but other clinical manifestations, routine blood indexes, serum levels of alkaline phosphatase (AKP), total bilirubin (TBTL), total protein (TP), width of main portal vein, width of splenic vein and thickness of spleen had no significant change (P>0.05).CONCLUSION: Serum fibrosis indexes can be influenced by the grade of inflammation, some liver function indexes and clinical manifestations. Comprehensive analysis is necessary for its proper interpretation. | Jun Tao Hui-Qin Peng Wei-Min Cai Feng-Qin Dong Hong-Lei Weng Rong-Hua Liu, Institute of Infectious Diseases, First Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou 310003 Zhejiang Province, China | 2003 | World Journal of Gastroenterology2003，9，11： | 15 |
| 11 | Expression changes of activin A in the development of hepatic fibrosis显示文摘AIM To examine the expression of activin A, amember of the transforming growth factor (TGF-β) superfamily, recently has been reported to beoverexpressed in liver cirrhosis, in the course ofcarbon tetrachloride-induced rat hepaticfibrosis.METHODS Hepatic fibrosis was induced in ratsby subcutaneous injections of 40% carbontetrachloride oily solution for a period of 1 to 7weeks. At the end of 1, 2, 3, 4, 5, 6 and 7 weeksafter carbon tetrachloride injections, the ratswere killed in group (6- 10 rats each time) forstudy. The activin A messenger RNA expressionand its protein localization were assessed bysemi-quantitative reverse transcriptionpolymerase chain reaction ( RT-PCR ) andimmunohistochemistry.RESULTS The normal rat liver expressedactivin A mRNA and protein, and its expressionwas transiently decreased and becameundetectable after carbon tetrachlorideinjections for 2 or 3 weeks and then increasedgradually. After injection of carbon tetrachloridefor 6 and 7 weeks, activin A mRNA and proteinexpressions were significantly enchanced in ratliver. Compared with that of the normal ratliver. Activin A mRNA expression levels in ratsreceiving carbon tetrachloride injections for 6and 7 weeks were 1.6 and 2.2 times that of thosein normal rat liver respectively (0.456±0.094 vs0.286± 0.0670, P<0.01; 0.620± 0.134 vs 0.286±± 0.0670, P<0.01). Immunohistochemistryshowed that activin A expressed in hepatocytesof normal liver, and its expression wasdecreased in rats receiving carbon tetrachloridefor 2 or 3 weeks. Compared with normal liver,activin A expression distribution mode changedin fibrotic liver, being increased significantly inhepatocytes around fibrotic areas.CONCLUSION Activin A expression wasincreased in latestage of hepatic fibrosis, andthis may be involved in hepatic fibrosisformation in this period. | Xin Huang1 Ding Guo Li1 Zhi Rong Wang1 Hong Shan Wei1 Ji Lin Cheng1 Yu Tao Zhan1 Xin Zhou1 Qin Fang Xu1 Xin Li2 Han Ming Lu1 1Xinhua Hospital, Shanghai Second Medical University, Shanghai 200092, China2Ninth Hospital. Shanghai Second Medical University, Shanghai 200011. China | 2001 | World Journal of Gastroenterology2001，7，1： | 12 |
| 12 | Preparation and identification of anti-transforming growth factor β1 U1 small nuclear RNA chimeric ribozyme in vitro显示文摘AIM: To study the preparation and cleavage activity of antitransforming growth factor (TGF)β1 U1 small nuclear (sn)RNA chimeric hammerhead ribozymesin vitro.METHODS: TGFβ1 partial gene fragment was cloned into T-vector at the downstream of T7 promoter. 32p-labeled TGFβ1 partial transcripts as target RNA were transcribed in vitro and purified by denaturing polyacrylamide gel electrophoresis (PAGE). Anti-TGFβ1 ribozymes were designed by computer, then synthetic ribozyme fragments were cloned into the U1 ribozyme vector pZeoU1EcoSpe containing U1 snRNA promoter/enhancer and terminator.32p-labeled U1 snRNA chimeric ribozyme transcripts were gel-purified, incubated with target-RNAs at different conditions and autoradiographed after running denaturing PAGE.RESULTS: Active UlsnRNA chimeric ribozyme (U1Rz803)had the best cleavage activity at 50 °C; at 37 °C, it was active, Km=34.48 nmol/L, Kcat=0.14 min-1; while the point mutant ribozyme U1Rz803m had no cleavage activity, so these indicated the design of U1Rz803 was correct.CONCLUSION: U1Rz803 prepared in this study possessed the perfect specific catalytic cleavage activity. These results indicate U1 snRNA chimeric ribozyme U1Rz803 may suppress the expression of TGFβ1in vivo, therefore it may provide a new avenue for the treatment of liver fibrosis in the future. | Ju-ShengLin Yu-HuSong Xin-JuanKong BinLi Nan-ZhiLiu Xiao-LiWu You-XinJin | 2003 | World Journal of Gastroenterology2003，9，3： | 11 |
| 13 | Decorin对肝星形细胞合成胶原的影响显示文摘目的探讨decorin对肝星形细胞合成胶原及层粘连蛋白功能的影响。方法体外培养的肝星形细胞株(HSC-T6细胞)经decorin(10mg·L^(-1))作用后,采用免疫组化和细胞原位核酸杂交技术分析观察胶原及层粘连蛋白水平的变化。经灰度扫描,随机计数30个细胞,计算单个细胞的灰度值,并进行统计学处理,其灰度值与蛋白水平或mRNA表达量成反比。结果 Decorin(10mg·L^1)作用24h,免疫组化染色HSC-T6细胞灰度值分别为(α1)Ⅰ、Ⅲ型胶原和层粘连蛋白在处理组为114.7±35.2、133.4±36.7和149.4±34.3,而对照组为97.5±30.1、123.0±27.7和142.7±32.6,表明处理组细胞(α1)Ⅰ、Ⅲ型胶原蛋白和层粘连蛋白水平比对照组细胞分别减少17.6%(P<0.01)、8.4%(P<0.05)和4.7%(P<0.05);细胞原位核酸杂交其灰度值分别为Ⅰ、Ⅲ型胶原和层粘连蛋白在处理组为75.7±11.6、77.0±10.8和79.0±11.6;对照组为65.9±13.1、69.6±14.5和76.8±17.0,表明其(α1)Ⅰ、Ⅲ型前胶原mRNA表达量比对照组分别降低14.8%和10.6%(P<0.01),层粘连蛋白mRNA表达无明显变化(P>0.05)。结论 Decorin能使HRC-T6细胞转录合成胶原等细胞外基质水平降低,提示对肝星形细胞合成功能有负调控作用。 | 王桂琴 陆慧琦 王皓 孔宪涛 仲人前 黄超 高锋 | 2001 | 世界华人消化杂志2001，9，12： | 9 |
| 14 | Effect of endotoxin on portal hemodynamic in rats显示文摘AIM: To study the effects of endotoxin on portalhemodynamic of normal and noncirrhotic portal hypertensiverats.METHODS: Normal rats were intraperitonealy injected with 0.1,0.25, 0.5, 1.0, 2.0, 4.0 mg@kg-1 of lipopolysaccharide( LPS ) respectively, portal vein ligation ( PVL ) andintrahepatic portal occlusion (IPO) rats as well as sham-operated rats were treated with an intraperitoneal injection of1.0 mg@kg-1 of LPS, the portal vein pressure(PVP), portalvenous flow(PVF), inferior vena cava pressure(IVCP) andportal vein resistance (PVR) were detected 4 hours afterinjection.RESULTS: PVF of the 5 groups of rats acceptingintraperitoneal injection of LPS were increased from 14.0 to18.0, 22.2, 266.2, 34.8, 39.66, 38.8 mL@min-1 4 hours afterinjection of LPS ( P < 0. 01 ). PVP of the 4 groups of ratsaccepting more than 0.1 mg/kg@ b. w of LPS was increasedfrom 1.04 to1.25, 1.50, 1.80, 1.95, 2.05 kPa(P<0.01). Theincrements of PVF and PVP were in a dose-dependentmanner of LPS. PVR of the 5 groups of rats was decreasedfrom 51 to 42,44,48,45,44,47 kPa@min@ L-1 ( P< 0.05) and nodosedependent manner wes observed. PVF of PVL, IPOand sham-operated rats increased from 22.66 to 32.8, 22.0 to28.0, 14.0 to 34.8 mL@min1 ( P< 0.01), and PVP increasedfrom 1.86 to 2.24, 1.74 to 1.95, 1.04 to 1.80 kPa(P<0.01),PVR decreased from 71 to61, 67 to61, 52 to 44 kPa@min@ L-1after intraperitoneal injection of 1 mg@ kg-1 of LPS. Theincrements of PVF and PVP of PVL and IPO rats weresignificantly less than the sham-operated rats ( P < 0. 01 ),There wes no significant difference between the amounts ofPVR decreased in the two groups of PHT model rats andsham-operated rats( P> 0.05) after intraperitoneal injection 1mg@kg1 of LPS.CONCLUSION: Endotoxin could prompt portal hypertensionof the normal and noncirrhotic portal hypertensive rats byincreasing portal blood flow mainly. | BiXJ ChenMH | 2002 | World Journal of Gastroenterology2002，8，3： | 9 |
| 15 | 卵泡抑素对肝纤维化大鼠细胞增殖及激活素A的影响显示文摘目的研究基因重组人卵泡抑素(recombinant humanfollistatin,rh-FS)对实验性肝纤维化大鼠增殖细胞核抗原(proliferating cell nuclear antigen,PCNA)、溴脱氧尿苷(bromodeoxyuridine,BrDU)核标记及激活素 A(activin A,ActA)表达的影响.方法采用400 mL·L^(-1)四氯化碳(CCl_4)sc 制备大鼠实验性肝纤维化模型,将16只肝纤维化模型组大鼠随机分成 rh-FS 处理组和假手术组,另外8只大鼠不作任何处理作为正常对照.rh-FS(1μg)经大鼠回结肠静脉注入 rh-FS 处理组大鼠门静脉内,24 h 后处死动物,免疫组织化学法检测正常大鼠肝脏、rh-FS 处理组和假手术组 PCNA,BrDU 核标记及 Act A 的表达.结果 rh-FS 可明显增强肝纤维化大鼠肝细胞 PCNA(FS 处理组 PCNA 核标记19%±7%,假手术组3%±2%,n=8,P<0.01)和 BrDU(FS 处理组 DrDU 染色+,假手术组染色-,n=8)核标记,二者变化相似;肝纤维化时 Act A 表达增加(正常大鼠肝脏+,肝纤维化时++~+++),且其分布发生改变,rh-FS 短时间作用对 Act A 表达无明显影响.结论 rh-FS 可促进纤维化肝脏肝细胞增殖. | 黄新 李定国 王志荣 魏红山 程计林 展玉涛 徐芹芳 陆汉明 | 2000 | 世界华人消化杂志2000，8，9： | 8 |
| 16 | 肝硬化血清胰岛素样生长因子-Ⅰ与肝功能和数字连接试验的关系显示文摘目的观察肝硬化患者血清胰岛素样生长因子-1(IGF-1)的浓度,同时进行数字连接试验(NCT)测定,比较IGF-1与NCT、肝功能不同Child分级的关系,探讨IGF-1与肝硬化预后及亚临床肝性脑病(SHE)的相关性。方法夹心免疫法测定45例肝硬化患者和34例正常对照者血清IGF-1浓度,肝硬化组另行NCT测定及Child-pugh分级。结果肝硬化组血清IGF-1浓度(68±66)μg·L^(-1)明显低于健康对照组(246±94)μg·L^(-1),P<0.01.且随着Child A、B、C分级的升高而递减,Child A级血清IGF-1浓度(135±80)μg · L^(-1),明显高于Child B级(44±29)μg·L^1、Child C级(27±10)μg·L^(-1),P<0.01.Child B与 Child C级血清IGF-1浓度虽有递减,但无统计学差异(P>0.05).NCT低于66s组患者的血清IGF-1浓度(78±16)μg·L^(-1),明显高于NCT高于66s组患者的血清IGF-1浓度(18±4)μg·L^(-1),P<0.01。结论肝硬化患者血清IGF-1浓度与肝功能Child-pugh分级、与NCT测值密切相关,提示IGF-1与肝硬化严重程度及肝硬化亚临床肝性脑病的发生有关。 | 吴巍 张曙 吴云林 叶静 奚容平 | 2001 | 世界华人消化杂志2001，9，12： | 5 |
| 17 | 大鼠肝硬变病程中血清透明质酸的动态变化显示文摘目的通过系统测定大鼠肝硬变病程中血清透明质酸 HA 的动态变化,来探讨其用于肝纤维化的测试和监控的临床价值.方法利用 CCl_4损伤 SD 大鼠造成肝硬变模型(n=6),综合分析不同时间取材的实验组和正常对照组(n=6)之间血清肝纤维化指标-血清 HA 浓度、肝组织病理改变以及 HA 在肝组织中的免疫组织化学定位.结果在大鼠肝硬变的病变发展过程中,血清 HA 含量在3(7.98 ng/mL),6(20.10 ng/mL),9(229.73 ng/mL),12(324.74 ng/mL)周时,均较正常组(0周:0.21 ng/mL)有极显著升高(P<0.01),其中9 wk 和12 wk 的血清 HA 含量比正常对照组分别高出1094和1546倍.而在0→3 wk、3→6 wk、6→9wk、9→12wk 时,血清 HA 平均增加的倍数依次为38,2.5,11.4和1.4倍.同时,肝组织病理学结果(HE 染色)显示,CCl_4诱发的肝纤维化大鼠在9 wk 以前无明显变化;9 wk~12 wk 时,与正常肝组织相比,有明显肝细胞坏死,同时伴有肝细胞质分布不均匀程度的加深及红细胞增多成团现象.此外,12 wk 组还出现明显的肝细胞气球样变性现象及局部炎症细胞浸润.同期用免疫组化法观察 HA 在不同期肝硬变大鼠肝内的分布,镜检发现只在12 wk 有少量 HA 的特异性分布.结论动态观察血清 HA 数值可用于早期肝纤维化的预测和肝纤维化的分期. | 马岚 赵力生 李春华 吕琦 李仁宽 邓双胜 | 2000 | 世界华人消化杂志2000，8，12： | 4 |
| 18 | 清肝利湿汤对兔胆囊炎胆石症模型局部组织的影响显示文摘目的研究“清肝利湿汤”对兔胆囊炎胆石症局部组织的疗效。方法采用胆总管不全结扎及胆囊内注入大肠杆菌的方法造成兔胆囊炎胆石症的动物模型。40只家兔随机分为空白对照组、模型对照组、龙胆泻肝汤组及清肝利湿汤组,每组10只。除空白对照组外,其余3组均手术造模,空白对照组及模型对照组每日插胃管饲以蒸馏水一次,龙胆泻肝汤及清肝利湿汤组每日插胃管饲以相应药物一次,连续7d后全部处死,抽取胆汁送测粘滞度,取胆囊组织200mg均浆,离心后测肿瘤坏死因子α(TNF-α)及β内啡肽(β-EP)等指标。结果清肝利湿汤组局部组织TNF-α、β-EP含量(分别为17.8ng·g^(-1)±12.7ng·g^(-1)和2163pg·g^(-1)±726pg·g^(-1))均明显低于模型组(分别为112.6ng·g^(-1)±22.7ng·g^(-1)和4919pg·g^(-1)±1100pg·g^(-1)(P<0.01),死亡率及胆汁粘滞度(分别为0和1.61±1.26mPas)也低于模型组(分别为40%和3.12±1.32mPas)(P均<0.05)。且清肝利湿汤组局部组织内TNF-α含量明显低于龙胆泻肝汤组(50.15±22.03ng/g)(P<0.05)。结论清肝利湿汤在改善胆囊局部动力学,局部镇病抗炎方面作用显著。 | 刘盛 陈泽奇 | 2001 | 世界华人消化杂志2001，9，11： | 2 |
| 19 | 反应停对重症肝炎外周血单个核细胞细胞因子的影响显示文摘目的观察反应停(Thal)对重症肝炎外周血单个核细胞(PBMCs)细胞因子的影响及其对重症肝炎的治疗作用.方法用淋巴细胞分离液从11例重症肝炎患者的外周血中分离 PBMCs,体外培养,用酶联免疫吸附、免疫组化和半定量斑点杂交法,观察 Thal 对 PBMCs TNFα和其他细胞因子的影响.结果 Thal 可抑制 PBMCs TNFα和其他细胞因子的产生(从1923 ng·L^(-1)±697 ng·L^(-1)下降至713 ng·L^(-1)±224 ng·L^(-1),P<0.05)以及 TNFα mRNA 的表达(相对灰度值从13.6±4.5下降至8.3±2.7,P<0.05).结论 Thal 对重症肝炎的治疗有重大的意义. | 刘树人 张雁 彭齐荣 李灼亮 余宙耀 陆汉明 | 2000 | 世界华人消化杂志2000，8，12： | 2 |
| 20 | 复方中药木疏胶囊抗大鼠肝纤维化的免疫机制显示文摘目的:探讨木疏胶囊抗大鼠肝纤维化的免疫作用机制.方法:400g/LCCl4诱导大鼠肝纤维化模型.Wister大鼠随机分为正常对照组,模型对照组,木疏胶囊预防组和治疗组,鳖甲软肝片预防组和治疗组.HE染色和Masson染色观察肝右叶相同部位组织病理改变.放免法测定血清细胞因子IL-2、IL-6、IL-8及TNF-α,流式细胞术检测血淋巴细胞CD4、CD8表达.结果:木疏胶囊与鳖甲软肝片各组两两比较,对IL-2和IL-6作用均无显著性差异;对IL-8的降低作用木疏胶囊优于鳖甲软肝片(预防组:0.4±0.2mg/Lvs0.6±0.1mg/L;治疗组:0.5±0.2mg/Lvs0.6±0.2mg/L;均P<0.05);对TNF-α的降低作用为木疏胶囊预防组优于鳖甲软肝片(1.1±0.3mg/Lvs1.4±0.3mg/L,P<0.05),而治疗组无显著差异.与模型对照组比较,木疏胶囊预防组和治疗组使CD4和CD4/CD8均显著升高(CD4:36.4%±7.5%,34.6%±5.0%vs28.0%±5.1%;CD4/CD8:1.9%±0.4%,1.8%±0.3%vs1.5%±0.2%;均P<0.01),鳖甲软肝片预防组使CD4显著升高(33.4%±4.9%vs28.0%±5.1%,P<0.05),治疗组无显著性差异,鳖甲软肝片使CD8和CD4/CD8升高,但均无显著性差异;木疏胶囊和鳖甲软肝片对CD4、CD8、CD4/CD8的作用无显著性差异.结论:木疏胶囊可升高肝纤维化大鼠血清IL-2,降低IL-6、IL-8和TNF-α水平,升高CD4、CD4/CD8. | 高萍 程留芳 刘春 邵泽勇 | 2008 | 世界华人消化杂志2008，16，12： | 1 |
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