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| 1 | 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 |
| 2 | 珍珠梅提取物对四氯化碳所致大鼠急性肝损伤的保护作用显示文摘目的:研究珍珠梅乙酸乙酯提取物对CCl_4所致大鼠急性肝损伤的保护作用。方法:给动物ig给药,用CCl_4造大鼠急性肝损伤模型,用比色分析法测定大鼠血清天冬氨酸转氨酶(aspartate transaminase,ALT)、丙氨酸转氨酶(alanine transaminase,AST)的活性;在大鼠血清、肝匀浆、肝线粒体测定超氧化歧化酶(superoxide dismutase, SOD)、谷胱甘肽过氧化物酶(glutathione perioxidase,GSH-PX)的活性,丙二醛(malondialdehyde,MDA)的含量;在肝线粒体测定琥珀酸脱氢酶(Succinate dehydrogenase,SDH)的活性。结果:珍珠梅能显著降低因CCl_4所致急性肝损伤大鼠血清ALT(300±50&1617±267 vs 4751±451,P<0.01)、AST(533±200&1767±217 vs 3800±383,P<0.01)的升高;明显回升CCl_4所致肝损伤大鼠肝线粒体SDH(104±18&47±10 vs 7±2,P<0.05)活性的降低;对急性肝损伤大鼠血清、肝匀浆、肝线粒体SOD(40±2&25±3 vs 14±6,P<0.05;50±8&31±9 vs 20±6,P<0.05;60±8&34±6 vs 22±9,P<0.05)、GSH-PX(73±21&59±14 vs 45±16,P<0.05;126±39&135±49 vs 89±21,P<0.05;206±39&193±50 vs 117±60,P<0.05)的活性有明显的升高作用及降低MDA(1.3±0.6&1.8±0.7 vs 2.7±0.8,P<0.05;1.3±0.4&4.0±1.7 vs 6.9±1.1,P<0.05;0.8±0.2&2.4±2.2 vs 5.1±1.7,P<0.01)的含量。结论:珍珠梅乙酸乙酯提取物对CCl_4所致大鼠急性肝损伤有保护作用。 | 金海玲 张学武 赵红 柳明洙 陈丽艳 尹宗柱 | 2002 | 世界华人消化杂志2002，10，7： | 32 |
| 3 | 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 |
| 4 | Cirrhotic portal hypertension: From pathophysiology to novel therapeutics显示文摘Portal hypertension and bleeding from gastroesophageal varices is the major cause of morbidity and mortality in patients with cirrhosis. Portal hypertension is initiated by increased intrahepatic vascular resistance and a hyperdynamic circulatory state. The latter is characterized by a high cardiac output, increased total blood volume and splanchnic vasodilatation, resulting in increased mesenteric blood flow. Pharmacological manipulation of cirrhotic portal hypertension targets both the splanchnic and hepatic vascular beds. Drugs such as angiotensin converting enzyme inhibitors and angiotensin Ⅱ type receptor 1 blockers, which target the components of the classical renin angiotensin system(RAS), are expected to reduce intrahepatic vascular tone by reducing extracellular matrix deposition and vasoactivity of contractile cells and thereby improve portal hypertension. However, these drugs have been shown to produce significant offtarget effects such as systemic hypotension and renal failure. Therefore, the current pharmacological mainstay in clinical practice to prevent variceal bleeding and improving patient survival by reducing portal pressure is non-selective-blockers(NSBBs). These NSBBs work by reducing cardiac output and splanchnic vasodilatation but most patients do not achieve an optimal therapeutic response and a significant proportion of patients are unable to tolerate these drugs.Although statins, used alone or in combination with NSBBs, have been shown to improve portal pressure and overall mortality in cirrhotic patients, further randomized clinical trials are warranted involving larger patient populations with clear clinical end points. On the other hand, recent findings from studies that have investigated the potential use of the blockers of the components of the alternate RAS provided compelling evidence that could lead to the development of drugs targeting the splanchnic vascular bed to inhibit splanchnic vasodilatation in portal hypertension. This review outlines the mechanisms related to the pathogenesis of portal hypertension and attempts to provide an update on currently available therapeutic approaches in the management of portal hypertension with special emphasis on how the alternate RAS could be manipulated in our search for development of safe, specific and effective novel therapies to treat portal hypertension in cirrhosis. | Lakmie S Gunarathne Harinda Rajapaksha Nicholas Shackel Peter W Angus Chandana B Herath | 2020 | World Journal of Gastroenterology2020，26，40： | 24 |
| 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 | Antiproliferative and proapoptotic effects of somatostatin on activated hepatic stellate cells显示文摘AIM: To assess the effects of somatostatin on proliferation and apoptosis of activated rat hepatic stellate cells (HSCs). METHODS: HSCs isolated from the livers of adult SpragueDawley rats (weighing 400-500 g) by in situ perfusion and purified by single-step density gradient centrifugation with Nycodenz, became activated after 10 days' cultivation. Then the apoptotic rate of HSCs treated with different doses of somatostatin for 72 h, was assayed by acridine orange/ethidium bromide fluorescent staining, terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling, transmission electron microscopy and flow cytometry, while the proliferation of HSCs was measured by MTT assay. Furthermore, the mechanisms of somatostatin were investigated by cytodynamic analysis. RESULTS: Somatostatin at the concentration of 10^-6-10^-99 mol/L could decrease the proliferative rate, and promote the apoptosis of activated rat HSCs in a dose-dependent way. Its action was most significant when the concentration reached 10^-6 mol/L or 10^-7 mol/L (P<0.05-0.01). An obvious cell-cycle arrest (G0/G1 arrest) was the important way for somatostatin to exert its action. CONCLUSION: Antiproliferative and proapoptotic effects of low-dose somatostatin on activated rat HSCs can be obtained. These findings reveal its potential antifibrotic action. | QinPan Ding-GuoLi Han-MingLu Liang-YongLu Yu-Qinwang Qin-FangXu | 2004 | World Journal of Gastroenterology2004，10，7： | 17 |
| 7 | 珍珠梅水提物对大鼠肝损伤的保护作用显示文摘目的:研究珍珠梅水提物的保肝作用。方法:给动物灌胃给药,用CCl_4,D-半乳糖造大鼠急性肝损伤模型,用比色分析法测定大鼠血清天冬氨酸转氨酶(aspartate transaminase,ALT)、丙氨酸转氨酶(alaninetransaminase,AST)的活性;测定大鼠血清超氧化歧化酶(superoxide dismutase,SOD)、谷胱甘肽过氧化物酶(glutathione perioxidase,GSH-Px)的活性及丙二醛(malondialdehyde,MDA)的含量。结果:珍珠梅水提物显著降低因CCl_4,D-半乳糖所致急性肝损伤大鼠血清ALT,AST的升高;对急性肝损伤大鼠血清SOD,GSH-PX的活性有明显的升高作用及降低MDA的含量。结论:珍珠梅水提物对CCl_4,D-半等糖所致大鼠急性肝损伤有保护作用。 | 张学武 朴龙 刘超 孙权 金海玲 尹宗柱 | 2003 | 世界华人消化杂志2003，11，10： | 16 |
| 8 | 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 |
| 9 | Protective effect of estradiol on hepatocytic oxidative damage显示文摘AIM: To examine the protective effect of estradiol on the cultured hepatocytes under oxidative stress.METHODS: Hepatocytes of rat were isolated by using perfusion method, and oxidative stress wes induced by a serum-free medium and FeNTA. MDA level was determined with TBA method. Cell damage was assessed by LDH assay. Apoptosis of hepatocytes was assessed with cytoflowmetric analysis. Expression of Bcl-xl in cultured hepatocytes was detected by Western blot.The radicalscavenging activity of estradiol was valued by its ability to scavenge the stable free radical of DDPH.RESULTS: Oxidative stress increased LDH (from 168 ± 25 x10-6 IU. cell 1 to 780 ± 62 x 10-6 IU. cell-1 ) and MDA(from 0.28 ±0.07 x 10-6 nmol. cell-1 to 1. 35 ± 0.12 × 10-6 nmol. cell-1 ) levelsin cultured hepatocyte, and estradiol inhibited both LDH andMDA production in a dose dependent manner. In thepresence of estradiol t0-6 mol. L-1, 107 mol. L-1 and 10-8 mol.L-1 ,the LDH levels are 410 ± 53 × 10-6 IU. cell-1 ( P < 0.01 vsoxidative group), 530 ± 37 × 10-6 IU. cell-1 ( P < 0. 01 vsoxidative group), 687 ± 42 x 10-6 IU. cell-1 ( P < 0.05 vsoxidative group) respectively, and the MDA level are 0.71 ±0.12 x 10-6 nmol. cell-1 ( P < 0.01 vs oxidative group), 0.97 ± 0.11 × 10-6 nmol. cell-1 ( P < 0.01 vs oxidative group) and 1.27 ±0. 19 x 10-6 nmol. cell-1 respectively. Estradiol suppressedapoptosis of hepatocytes induced by oxidative stress,administration of estradiol (10-6 mol/ L)decreased theapoptotic rate of hepatocytes under oxidative stress from 18.6 ± 1.2% to 6.5 ± 2.5%, P < 0.01. Bcl-xl expression wasrelated to the degree of liver cell damage due to oxidativestress, and estradiol showed a protective action.CONCLUSION: Estmdiol protects hepatocytes from oxidativedamage by means of its antioxidant activity. | Ichiro Shimizu Toshihiro Omoya Susumu Ito | 2002 | World Journal of Gastroenterology2002，8，2： | 13 |
| 10 | Effects of PPARg agonist pioglitazone on rat hepatic fibrosis显示文摘AIM: To investigate effects of pioglitazone on rat hepatic fibrosis and to explore its mechanism. METHODS: Rat hepatic fibrosis was induced by carbontet. achloride (CCI4). Forty Sprague-Dawley rats were divided randomly into 4 groups: control, model, and two treatment (PⅠ, PⅡ) groups. Except for rats in control group, all rats were given subcutaneous injection of 400 mL/L CCI4, twice a wk for 8 wk. Rats in PⅠ and PⅡ groups were also treated with pioglitazone of 3 mg/kg, daily via gastrogavage beginning on the 1^st day and at the end of the 2^nd week, administration of CCI4 respectively. Liver functions (ALT, AST), serum fibrotic markers (HA, LN, PCIII) and hepatic hydroxyproline (HP) concentration were determined respectively. Histochemical staining of formalin-fixed liver sections with HE, Masson-Trichrome, and immunohistochemical staining for m-smooth muscle actin (α-SMA) were performed. Modified Knodell and Chevallier semi-quantitative scoring system (SSS) was used to evaluate necroinflammatory activity and fibrosis degree. RESULTS: Compared with model group, pioglitazone significantly reduced the serum levels of ALT, AST, HA, LN and PCⅢ (P<0.05 or <0.01). The HP concentrations in PⅠ(210.90±24.07 μg/g), and PⅡ (257.36±30.55 μg/g) groups were also lower than those in model group (317.80±36.44) μg/g) (P<0.01). Histologic examination showed that PⅠ and PⅡ groups had milder hepatocellular degeneration, necrosis and infiltration of inflammatory cells, and thinner or less fibrotic septa than did model group. The scores for necroinflammation in P (2.80±1.03), and PⅡ (3.00±1.05) groups were significantly reduced as compared with model group (4.88±2.30) (P<0.05 or <0.01); the fibrosis scores in PⅠ (3.40±1.65), and PⅡ (4.60±1.35) groups were also markedly lower than those in model group (7.00±3.21) (P<0.05 or <0.01). Immunohistochemical staining showed that expression of α-SMA in PⅠ and PⅡ groups was ameliorated dramatically compared with model group. CONCLUSION: PPARγ, agonist pioglitazone greatly retards the progression of rat hepatic fibrosis induced by CCI4 through inhibition of HSC activation and amelioration of hepatocyte necroinflammation in rats. | Guang-JinYuan Ming-LiangZhang Zuo-JiongGong | 2004 | World Journal of Gastroenterology2004，10，7： | 11 |
| 11 | Distribution of nitric oxide synthase in stomach myenteric plexus of rats显示文摘AIM: To study the distribution of nitric oxide synthase (NOS) in rat stomach myenteric plexus.METHODS: The distribution of NOS in gastric wall was studied in quantity and location by the NADPH-diaphorase (NDP) histochemical staining method and whole mount preparation technique.RESULTS: NOS was distributed in whole stomach wall, most of them were located in myenteric plexus, and distributed in submucosal plexus. The shape of NOS positive neurons was basically similar, most of them being round and oval in shape. But their density, size and staining intensity varied greatly in the different parts of stomach. The density was 62 -± 38 cells/mm2(antrum), 43 ± 32 cells/mm2(body), and 32 ± 28 cells/mm2 (fundus), respectively. The size and staining intensity of NOS positive neurons in the fundus were basically the same, the neurons being large and dark stained, while they were obviously different in antrum. In the body of the stomach, the NOS positive neurons were in an intermediate state from fundus to antrum. There were some beadlike structures which were strung together by NOS positive varicosities in nerve fibers, some were closely adherent to the outer walls of blood vessels.CONCLUSION: Nitric oxide might he involved in the modulation of motility, secretion and blood ciroulation of the stomach, and the significant difference of NOS positive neurons in different parts of stomach myenteric plexus may be related to the physiologic function of stomach. | Xi Peng Jin-Bin Feng Hong Yan Yun Zhao Shi-Liang Wang Institute of Burn Research,Southwest Hospital,Third Military Medical University,Chongqing 400038,China | 2001 | World Journal of Gastroenterology2001，7，6： | 11 |
| 12 | Regulating effect of Chinese herbal medicine on the peritoneal lymphatic stomata in enhancing ascites absorption of experimental hepatofibrotic mice显示文摘AIM: To observe the regulatory effect of Chinese herbalmedicine on peritoneal lymphatic stomata and itssignificance in treating ascites in liver fibrosis model mice.METHODS: Two Chinese herbal composite prescriptionswere used separately to treat the carbon tetrachloride-induced mouse model of liver fibrosis. The histo-pathologicchanges of the liver sections (HE and VG stainings) wereobserved. The peritoneal lymphatic stomata was detected byscanning electron microscopy and computer imageprocessing. The changes of urinary volume and sodium ionconcentration were measured.RESULTS: In the model group, lots of fibrous tissue formedin liver and extended into the hepatic Iobulss to separatethem incompletely. In the treated and prevention groups,the histo-pathologic changes of liver was rather milder, onlyshowed much less fibrous tissue proliferation in the hepaticIobules. The peritoneal lymphatic stomata enlarged withincreased density in the experimental groups (diameter:PA, 3.07±0.69μm; PB, 2.82±0.37μm; TA, 3.25±0.82μmand TB, 2.82±0.56μm; density: PA, 7.11± 1.90 stomata@1000μm-2; PB, 8.76± 1.45 stomata@ 1000μm-2; TA, 6.55± 1.44 stomata@ 1000μm-2 and TB, 8.76 ± 1. 79 stomata@ 1000μm-2), as compared with the model group (diameter: 2.00 ±0.52μm; density: 4.45 ± 1. 05 stomata@ 1000 μm-2 ). Aftertreatment, the urinary volume and sodium ion excretionincreased in the experimental groupe ( PA, 231.28 ± 41. 09mmol@L-1; PB, 171.69± 27.48 mmol@L-1 and TA, 231.44±34.12 retool@ L-1 ), which were significantly different with thosein the model group (129.33 ± 36.75 rnmol@ L-1 ).CONCLUSION: Chinese herbal medicine has marked effectsin alleviating liver fibrosis, regulating peritoneal lymphaticstomata, improving the drainage of ascites from peritonealcavity and causing increase of urinary volume and sodiumion excretion to reduce the water and sodium retention, andthus have favorable therapeutic effect in treating ascites. | Ji-Cheng Li Shi-Ping Ding,Department of Lymphology,Department of Histology and Embryology, Medical College of Zhejiang University,Hangzhou 310031,Zhejiang Province,China Jian Xu,Hangzhou First People’ s Hospital,Hangzhou 310006,Zhejiang Province,China | 2002 | World Journal of Gastroenterology2002，8，2： | 10 |
| 13 | 刀豆球蛋白A所致实验性肝损伤模型的构建显示文摘目的建立刀豆球蛋白A(ConA)诱导小鼠实验性肝损伤的模型。方法Balb/C小鼠40只,分别尾静脉注射ConA,根据注射剂量,小鼠被随机分为4组(每组10只):A组10mg/kg;B组20mg/kg;C组30mg/kg;另设D组作为实验对照组,尾静脉仅注射生理盐水。给药后8h观察小鼠血清丙氨酸转氨酶(ALT)活性、死亡率和肝组织的病理改变。选择最佳ConA剂量,观察此剂量下不同时间点ALT活性、死亡率和肝组织的病理改变特点。结果经ConA处理后8h,A组与D组无小鼠死亡,B组死亡3只,C组小鼠全部死亡;各组血清ALT值:A组为(215.55±70.19)IU/L,B组为(2516.14±764.69)IU/L,均显著高于对照组D组的(57.30±12.21)IU/L(分别t=-8.466、t=-10.143,均P=0.000)。光镜下,A组可见肝细胞变性;B组和C组可见肝组织炎症细胞浸润和肝细胞变性、坏死,以C组为甚。20mg/kgConA尾静脉注射,小鼠死亡率、ALT活性、肝组织炎症细胞浸润和肝细胞变性、坏死在一定时间范围内(24h)随时间增加而加剧。结论ConA小鼠实验性肝损伤模型建立,ConA剂量以20mg/kg、观察时间以8h为宜。 | 刘悦晖 范学工 李宁 刘洪波 付春燕 刘征波 黄燕 | 2008 | 中国感染控制杂志2008，7，5： | 10 |
| 14 | 氯沙坦抗鼠肝纤维化的实验研究(英文)显示文摘目的探讨 CCL4 诱导的肝纤维化模型鼠肝组织 Smad2/3,Smad7,TIMP-1,TGF-β1 的表达及氯沙坦干预后对其表达的影响。方法 Wistar大鼠 40 只,随机分成正常对照组、模型组、氯沙坦预防组和治疗组,采用 CCL4 皮下注射构建肝纤维化模型。行 HE 和 VG 染色,判断肝组织炎症和纤维化的程度。免疫组化方法检测各组 Smad2,3 Smad7 和 TIMP-1,TGF-β1 的表达。结果氯沙坦预防组和治疗组的肝组织炎症和纤维化程度明显低于模型组;Sm ad2,3 TIM P-1 TG F-β1 在氯沙坦预防组和治疗组的阳性表达均低于模型组( 分别为 Smad2,3:1.69 ±0.42,1.90 ±0.59,2.51 ±0.39;TIM P-1:1.09 ±0.28,1.32 ±0.23,2.60 ±0.35;TGF-β1:1.65±0.31,2.04±0.42,2.72±0.36),P <0.05;Sm ad7 在氯沙坦预防组和治疗组的阳性表达高于模型组( 分别为2.50±0.35,2.21±0.59,0.47±0.26),P <0.05。Smad2,3 Smad7 TIM P-1 和 TGF-β1 在氯沙坦预防组和治疗组的表达差异无显著性,P >0.05。结论氯沙坦抗肝纤维化作用可能与抑制 TGF-β1,TIMP-1,Smad2,3 和促进Smad7 的表达有关。 | 李乾 张桂英 孟燕妮 | 2007 | 中国现代医学杂志2007，17，4： | 9 |
| 15 | 依那普利对CCI_4急性肝损伤大鼠抗氧化功能的影响显示文摘目的:研究依那普利对四氯化碳(CCl4)所致急性肝损伤大鼠肝损伤和抗氧化功能的作用. 方法:将50只♂SD大鼠随机分为5组(每组10只):药物干预组(10mg/kg,5mg/kg和2.5mg/kg)、模型组和正常对照组,药物干预组和模型组均给予皮下注射CCl4(用等体积的橄榄油稀释),以制备急性肝损伤的大鼠模型,正常对照组用等体积的生理盐水注射,用高(10 mg/kg)、中(5 mg/kg)、低(2.5 mg/kg)剂量依那普利分别对SD大鼠灌胃给药.全自动生化分析仪测定大鼠血清丙氨酸转氨酶(ALT)、天冬氨酸转氨酶(AST)、碱性磷酸酶(ALP)、胆汁酸(TBA)的活性;用比色分析法测定超氧化歧化酶(T-SOD)、黄嘌呤氧化酶(XOD)、谷胱甘肽过氧化物酶(GSH-Px)的活性及丙二醛(MDA)的含量. 结果:依那普利显著降低因CCl4所致急性肝损伤大鼠血清ALT(正常对照组685±63 nkat/L<10 mg干预组1 241±168 nkat/L<5 mg干预组1 705±83 nkat/L<2.5 mg干预组2 302±174 nkat/L<模型对照组3 531±776 nkat/L),AST (正常对照组1 240±158nkat/L<10 mg干预组2 430±386 nkat/L<5 mg干预组2 788±522 nkat/L<2.5 mg干预组3 151±917 nkat/L<模型对照组3 372±138 nkat/L), ALP(10mg干预组2 567±159nkat/L<正常对照组2 659±248 nkatL<5 mg干预组3 212±198 nkat/L<2.5 mg干预组3 231±261 nkat/L<模型对照组3 609±346 nkat/L)和TBA(正常对照组8.48±0.49 μmol/L<10 mg干预组16.35±5.43μmol/L<5 mg干预组16.92±2.68 μmol/L<2.5 mg干预组17.53±3.59μmol/L<模型对照组24.16±9.27μmol/L) 的升高.对急性肝损伤大鼠血清GSH-PX(模型对照组50±54 nkat/L<2.5 mg干预组149±111 nkat/L<10 mg干预组169±141 nkat/L<5 mg干预组1 70±91 nkat/L<正常对照组295±194 nkat/L)的活性有明显的升高作用及降低T SOD(正常对照组6006±639 μkat/L<10mg干预组7 135±1 560μkat/L<2.5 mg干预组7 538±938 μkat/L<5 mg干预组7 589±780μkat/L<模型对照组8 579±861μkat/L) 和XOD(正常对照组571±28 nkat/L<10 mg干预组724±18nkat/L<5mg干预组821±28nkat/L<2.5mg干预组868±58 nkat/L<模型对照组1 042±188nkat/L)的含量.以上均与模型对照组比较aP<0.05,bP<0.01. 结论:依那普利的保肝机制和抗氧化作用与其对抗自由基脂质过氧化密切相关. | 张剑平 魏红山 刘顺爱 郭晶晶 张黔英 石小红 张四平 刘志英 冯鑫 吕洪波 | 2004 | 世界华人消化杂志2004，12，11： | 8 |
| 16 | TGFβ1和AT1R基因多态性与乙肝肝硬化遗传易感性及临床表型的关联研究显示文摘目的探讨与宿主肝纤维化及门脉高压形成相关的转化生长因子β1(transforming growth fac-tor beta1,TGFβ1)和Ⅰ型血管紧张素Ⅱ受体(angiotensinⅡ type 1 receptor,AT1R)基因多态性与乙肝肝硬化遗传易感性及临床表型的关系。方法应用PCR-RFLP对102例乙型肝炎后肝硬化患者和106名随机抽样的无亲缘关系的健康献血者分别检测TGFβ1启动子区-509C/T、AT1R1166A/C基因多态性。结果肝硬化组TGFβ1启动子区-509C/T纯合子CC的基因型频率明显高于对照组(P〈0.05);肝硬化Child-PughC级组-509C/T位点CC基因型分布频率明显高于B级和A级组(P〈005);AT1R1166A/C基因型和等位基因频率在对照组和肝硬化组之间差异均无统计学意义(P〉0.05)。结论TGFβ1启动子区-509C/T基因多态性与乙型肝炎后肝硬化遗传易感性有关,并与肝硬化严重程度密切相关,AT1R1166A/C基因多态性可能与乙型肝炎后肝硬化遗传易感性无关。 | 栗华 吴洪磊 吕卉 魏红山 王洪波 王培林 | 2007 | 中华医学遗传学杂志2007，24，3： | 7 |
| 17 | 肝纤维化形成过程中肾素-血管紧张素系统的变化显示文摘目的 研究肝纤维化形成过程中肾素 血管紧张素的变化。方法 给予大鼠 1%二甲基亚硝胺 (DMN )( 1ml/kg)腹腔注射 ,共 42d。模型组在开始注射DMN后的第 1天、第 10天、第 17天、第 2 8天、第 42天及第 5 6天杀死动物 ,取血和肝组织备用。血管紧张素Ⅱ (AngⅡ )采用放射免疫法检测 ,AngⅡ 1型受体 (AT1R )及Ⅰ型胶原 (Col Ⅰ )mRNA的水平以逆转录聚合酶链反应 (RT PCR)方法检测。结果 肝组织AngⅡ从DMN注射第 10天开始出现升高 ,以后一直维持高水平直至动物实验结束 ,与正常对照组差别有高度显著性。AT1R从DMN注射第 10天开始即出现降低 ,与正常对照组差别有显著性。第 2 8天后维持稳定降低直至动物实验结束 ,与正常对照组差别有显著性 (P <0 .0 1)。结论 肝脏在DMN致病因子的作用下 ,局部肾素血管紧张素系统 (RAS)激活 ,肝纤维的分期与肝脏AngⅡ及AT1R有相关性 ,因此局部RAS与肝纤维化有密切关系。 | 申凤俊 朱跃科 李琴 贾继东 王宝恩 | 2003 | 肝脏2003，8，4： | 5 |
| 18 | 血管紧张素Ⅱ对肝星状细胞迁移和增殖的影响显示文摘目的:探讨血管紧张素Ⅱ(ANGⅡ)对肝星状细胞(HSC)增殖、迁移活性的影响.方法:体外培养HSC,在不同浓度的ANGⅡ作用下,观察HSCs生长情况并绘制生长曲线,采用MTT法测定细胞增殖、Transwell小室检测细胞迁移.结果:1,2,4,8,10 umol/L ANGⅡ可显著促进HSC增殖,与空白对照组相比有显著差异(F= 2.305,P<0.05;F=4.003,6.833,8.855,21.066,P<0.01).随作用浓度的增加,细胞增殖活性显著提高,相关分析显示呈正相关(r=0.917,P<0.01).10,8,4μmol/L的ANGⅡ可显著诱导HSC迁移,与空白对照组相比差异显著(F= 22.084,15.155,10.392,P<0.01).随ANGⅡ浓度的增加,细胞迁移率显著升高,相关分析显示呈正相关(r=0.952,P<0.01).结论:ANGⅡ可显著诱导HSC增殖与迁移,并随剂量的增加作用加强. | 杨玲 朱清静 侯晓华 胡胜军 徐敏 朱锐 | 2007 | 世界华人消化杂志2007，15，9： | 4 |
| 19 | Expression of local renin and angiotensinogen mRNA in cirrhotic portal hypertensive patient显示文摘AIM: To investigate the expression of local renin and angiotensinogen mRNA in cirrhotic portal hypertensive patients.METHODS: The expression of local renin and angiotensinogen mRNA in the liver, splenic artery and vein of PH patients was detected by RT-PCR analysis.RESULTS: Expression of local renin mRNA in the liver of control group was (0.19±0.11), significantly lower than that in splenic artery(0.45±0.17)or splenic vein(0.39±0.12)respectively, (P<0.05). Expression of local angiotensinogen mRNA in the liver was (0.64±0.21), significantly higher than that in splenic artery(0.41±0.15) or in splenic vein (0.35±0.18)respectively, (P<0.05). Expression of local renin mRNA in the liver, splenic artery and vein of PH group was (0.78±0.28),(0.86±0.35) and (0.81±0.22) respectively, significantly higher than that in the control group, (P<0.05). Expression of local angiotensinogen mRNA in the liver, splenic artery and vein of PH group was (0.96±0.25), (0.83±0.18) and (0.79±0.23)respectively, significantly higher than that in the control group,(P<0.05). There was no significant difference between the liver, splenic artery and vein in the expression of local renin or local angiotensinogen mRNA in PH group, (P<0.05).CONCLUSION: In normal subjects the expression of local renin and angiotensinogen mRNA was organ specific, but with increase of the expression of LRAS, the organ-specificity became lost in cirrhotic patients. LRAS may contribute to increased resistance of portal vein with liver and formation of splanchnic vasculopathy. | LiZhang ZhengYang Bao-MinShi Da-PengLi Chong-YunFang Fa-ZuQiu | 2003 | World Journal of Gastroenterology2003，9，7： | 2 |
| 20 | 血管紧张素Ⅱ含量及其Ⅰ型受体基因多态性与乙肝肝硬化的关系显示文摘目的:探讨血管紧张素Ⅱ(AngⅡ)含量及Ⅰ型血管紧张素Ⅱ受体(AT1R)基因多态性与乙肝肝硬化的关系。方法:对102例乙型肝炎肝硬化患者和106例健康献血者,分别应用PCR-RFLP检测AT1R1166A/C基因多态性,并用放射免疫法检测血浆AngⅡ含量。结果:肝硬化组血浆AngⅡ含量明显高于对照组(P<0.05),肝硬化Child-Pugh C级、B级组的血浆AngⅡ含量明显高于A级组(P<0 05),而C级组与B级组的血浆AngⅡ含量无明显差异(P>0.05);肝硬化伴有腹水组和重度食管静脉曲张组血浆AngⅡ含量也明显高于无腹水组和轻度食管静脉曲张组,差异有统计学意义(P<0.05)。AT1R 1166A/C基因型频率和等位基因频率在肝硬化和对照组间差异均无统计学意义(P>0.05)。结论:肝硬化患者血浆AngⅡ含量明显升高,并与肝硬化严重程度及门脉高压症的发生密切相关,AT1R 1166A/C基因多态性可能与乙肝肝硬化遗传易感性无关。 | 栗华 赵幼安 吕卉 吴洪磊 王洪波 | 2007 | 山东大学学报(医学版)2007，45，3： | 1 |
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