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1.
目的 观察复方861对HSC-T6组织基质金属蛋白酶抑制因子1(TIMP1)基因表达的影响。方法复方861 0.25、0.5、1.0mg/ml等浓度作用于HSC-T6细胞48h,以逆转录定量PCR方法测定其对HSC-T6细胞TIMP1基因表达的影响。结果 复方861 0.25、0.5、1.0mg/ml等不同浓度作用后,HSC-T6细胞基因表达水平依次为2.50±0.71、0.50±0.01、0.11±0.03,与空白对照组门(3.78±0.67)比较,可明显抑制TIMP1基因表达水平(P<0.05或P<0.01)。结论 复方861抑制HSC-T6细胞TIMP1基因表达水平,从而促进胶原降解,可能是抗肝纤维化的作用机制之一。  相似文献   

2.
中药鳖甲煎丸抗肝纤维化作用的临床研究   总被引:20,自引:0,他引:20  
目的研究中药鳖甲煎丸对慢性肝炎肝纤维化的治疗作用.方法用肝穿或RIA法测定血清肝纤维化指标如透明质酸(HA)、Ⅲ型前胶原(PCⅢ)及层粘蛋白(LN)等,筛选出肝纤维化指标明显异常的慢性肝炎患者80例,随机分为鳖甲煎丸组及对照组各40例,对照组用普通保肝药治疗,疗程均为3个月,观察治疗前后的血清肝纤维化指标及肝脏组织病理学变化.结果血清HA、PCⅢ及LN水平治疗前,鳖甲煎丸组为465.3±121.5(ng/ml)、190.5±77.1(μg/L)及164.7±41.9(ng/ml),对照组为479.9士198.3(ng/ml)、206.4±87.2(μg/L)及175.2±67.5(ng/ml),两组之间无显著性差异(P>0.05);治疗后,鳖甲煎丸组为87.2±41.7(ng/ml)、126.7±53.6(μg/L)及43.4±20.7(ng/ml),对照组为261.7±105.3(ng/ml)、191.2±61.3(μg/L)及89.4±45.3(ng/ml),两组差异显著(P<0.05).鳖甲煎丸组患者血清肝纤维化指标治疗后与治疗前相比有非常显著性差异(P<0.01),且治疗后其肝纤维化指标接近正常组(P>0.05),其组织病理学显示肝纤维化组织增生程度显著减轻.结论中药鳖甲煎丸具抗纤维化作用,可用于临床.  相似文献   

3.
周健  田德英  张振纲 《中西医结合肝病杂志》2006,16(3):160-161,163,T0001
目的:研究激动素对实验性肝纤维化的影响,探讨作用机制。方法:用CCl4诱导形成大鼠肝纤维化模型,使用0.1%激动素溶液0.5ml.100g-1.d-1,背部皮下注射,治疗12周,设正常对照组和模型组。血清ALT用全自动生化分析仪检测,血清透明质酸(HA)、层黏连蛋白(LN)、Ⅲ型前胶原(PCⅢ)和Ⅳ型胶原(CⅣ)含量用RIA方法检测。肝组织学检查:采用苏木精-伊红染色观察肝组织炎症和纤维化程度。结果:激动素组ALT水平与模型组ALT水平分别为(57.40±17.49)U/L和(84.70±31.85)U/L,两组比较差异有显著性意义(P<0.05)。激动素组LN和CⅣ含量分别为(29.25±6.67)ng/ml和(14.84±5.84)ng/ml,较模型组(37.18±10.06)ng/ml、(35.69±30.84)ng/ml明显降低(P<0.05);激动素组HA和PCⅢ含量分别为(136.25±76.83)ng/ml和(11.43±3.67)ng/ml,较模型组(168.55±56.19)ng/ml、(14.64±8.00)ng/ml有不同程度降低,但无统计学意义。组织学检测结果表明,模型组肝脏炎症和纤维化程度明显高于激动素组。结论:激动素对实验性大鼠肝纤维化具有抑制作用。  相似文献   

4.
目的从临床病理学角度探讨蝎纤胶囊对慢性乙型病毒性肝炎肝纤维化的治疗作用。方法126例慢性乙型病毒性肝炎患者接受观察,分为2组,其中治疗组90例,对照组36例,治疗组给蝎纤胶囊1.5g/次,3次/日,疗程为6个月;对照组给予肝泰乐及B族维生素,疗程为6个月。治疗前3个月和治疗后1个月内,分别检测血清肝纤维化指标并进行肝穿病理检查。结果①血清肝纤维化指标检测显示,治疗组治疗前后透明质酸分别为179.27±73.21ng/ml和90.87±26.51ng/ml(P<0.05),Ⅳ型胶原分别为133.78±48.21ng/ml和72.65±37.18ng/ml(P<0.05),层黏蛋白分别为1.38±0.48U/ml和1.07±0.32U/ml(P<0.05);对照组上述指标治疗前后比较无显著性差异(P>0.05);②肝组织病理学检查显示,治疗组炎症坏死方面改善的总有效率为82.6%(P<0.05),肝纤维化改善或停止发展的总有效率为92.8%(P<0.01);对照组治疗前后在炎症坏死活动性及纤维化方面均无显著差异。结论蝎纤胶囊能有效减轻肝内炎症坏死,稳定甚至逆转肝纤维化,可用作慢性乙型肝炎的抗肝纤维化治疗。  相似文献   

5.
目的探讨急性左心衰竭(ALHF)和充血性心力衰竭(CHF)患者肝功能检测指标(LFTs)的差异。方法入选纽约心功能分级Ⅲ~Ⅳ级的心力衰竭患者137例,根据病情分为ALHF组59例和CHF组78例。收集患者的基本资料,比较两组LFTs和住院病死率的差异。结果与CHF组比较,ALHF组患者的谷丙转氨酶[(34.05±14.48)U/L比(29.41±9.16)U/L]、谷草转氨酶[(30.73±12.47)U/L比(26.64±6.81)U/L]和白蛋白[(38.62±2.70)g/L比(35.33±4.20)g/L]水平均显著升高(分别为t=-2.291,P=0.024;t=-2.454,P=0.015;t=-5.25,P<0.01),而谷氨酰氨基转移酶[(30.7±20.7)U/L比(41.5±32.3)U/L]、总胆红素[(14.22±7.21)μmol/L比(18.42±8.60)μmol/L]、直接胆红素[(6.28±3.46)μmol/L比(8.00±4.67)μmol/L]和间接胆红素[(7.99±4.82)μmol/L比(10.45±5.81)μmol/L]水平均降低(t=2.257,P=0.026;t=3.013,P=0.003;t=2.384,P=0.019;t=2.636,P=0.009)。两组患者的碱性磷酸酶[(75.93±29.01)U/L比(80.42±22.91)U/L]和总蛋白[(65.2±3.8)g/L比(65.9±7.8)g/L]水平差异无统计学意义(P>0.05)。ALHF组患者病死率较CHF组高[17例(28.8%)比8例(10.3%),χ2=7.754,P=0.005]。结论 ALHF患者以谷丙转氨酶、谷草转氨酶升高为主,与肝脏缺血相关,而CHF患者以谷氨酰氨基转移酶、总胆红素、直接胆红素、间接胆红素升高和白蛋白降低为主,与肝脏淤血相关。  相似文献   

6.
目的观察蒙药清肝九味散对酒精性肝炎患者的治疗作用。方法收集内蒙古民族大学附属医院2014年5月-2016年4月收治的酒精性肝炎患者63例,随机分为试验组(32例)和对照组(31例)。试验组给予蒙药清肝九味散治疗;对照组31例给予还原型谷胱甘肽片治疗。2组患者均治疗4周并在此期间均严格戒酒、卧床休息。计量资料组间比较采用t检验。结果对照组患者肝功能指标(ALT、AST、GGT)治疗后与治疗前比较均有明显改善[(38.7±13.3)U/L vs(77.5±16.7)U/L)、(43.8±21.8)U/L vs(176.6±40.1)U/L、(63.8±21.7)U/L vs(302.9±73.3)U/L,t值分别为10.21、16.90、17.40,P值均0.01];试验组患者治疗后与治疗前比较亦有明显改善[(37.6±14.6)U/L vs(78.1±17.5)U/L、(39.6±15.3)U/L vs(180.3±44.3)U/L、(59.9±23.8)U/L vs(304.7±66.5)U/L,t值分别为10.10、16.40、19.60,P值均0.01]。对照组患者血清中肝纤维化指标(透明质酸、Ⅲ型前胶原、层黏连蛋白、Ⅳ型胶原)治疗后均较治疗前明显改善[(122.1±36.2)ng/ml vs(369.2±139.8)ng/ml、(118.6±43.8)ng/ml vs(185.9±92.7)ng/ml、(137.2±49.9)ng/ml vs(166.1±50.4)ng/ml、(128.7±48.3)ng/ml vs(155.1±44.5)ng/ml,t值分别为9.52、3.66、2.24、2.27,P值均0.05];试验组患者治疗后与治疗前比较亦有明显改善[(101.1±27.9)ng/ml vs(367.4±149.7)ng/ml、(91.6±48.4)ng/ml vs(188.3±100.5)ng/ml、(94.8±34.6)ng/ml vs(167.6±48.7)ng/ml、(92.7±30.3)ng/ml vs(161.3±62.2)ng/ml,t值分别为9.88、4.95、5.61、6.87,P值均0.01]。2组间治疗后肝纤维化指标比较差异均有统计学意义(t值分别为2.53、2.31、3.56、3.90,P值均0.05)。结论蒙药清肝九味散可以改善酒精性肝炎患者的肝功能,降低肝纤维化指标。  相似文献   

7.
急性心肌梗死后螺内酯干预对左室重构的影响   总被引:19,自引:0,他引:19  
目的 探讨急性心肌梗死(AMI)患者应用螺内酯干预对于左室重构(LVRM)的影响。方法 4家医院共入选AMI患者88例,采用多中心、随机、对照的方法,对46例AMI患者在常规治疗的基础上加用螺内酯40mg/d(螺内酯组),对照组(n=42)常规治疗。在6个月干预期内检测两组血清Ⅲ型前胶原氨基端肽(PⅢNP)、脑钠肽(BNP)及超声心动图,以评价左室纤维化、左室功能和左室容积。结果 88例中,急性前壁心肌梗死患者43例,螺内酯组23例、对照组20例;急性下壁心肌梗死患者45例,螺内酯组23例、对照组22例。急性前壁心肌梗死组在治疗3、6个月时螺内酯组与对照组相比,血清PⅢNP和BNP明显降低[PⅢNP分别为( 260 .2±59. 9 )ng/L比( 328 .0±70 .3 )ng/L, P=0 .001, ( 197 .1±46 .3 )ng/L比( 266. 7±52 .4 )ng/L, P<0. 001 ,BNP分别为( 347 .4±84 .0)ng/L比(430 .1±62 .9)ng/L, P<0 .001, (243 .7±79. 7)ng/L比(334. 6±62. 8)ng/L, P<0. 001]。治疗6个月时螺内酯组较对照组左室舒张末期内径、左室收缩末期内径明显降低[分别为(51. 0±5 .5)mm比(55. 6±4 .5)mm, P=0 .005, (35 .7±4 .6)mm比(39 .1±5 .6)mm, P=0 .046]。急性下壁心肌梗死组在治疗6个月时螺内酯组与对照组相比血清PⅢNP、BNP水平无统计学意义,(P>0 05),并且左  相似文献   

8.
目的观察慢性乙型肝炎患者血清基质金属蛋白酶(MMPs)及金属蛋白酶组织抑制因子(TIMPs)水平与肝纤维化及炎症程度的相关性,寻找新的判定肝纤维化程度的血清学指标.方法慢性乙型肝炎患者88例,间隔半年行两次肝穿刺活检,病理组织进行炎症活动度及纤维化程度半定量计分;检测血清TIMP1、TIMP2、MMP1、MMP2、MMP9、Ⅳ型胶原、层黏连蛋白、Ⅲ型前胶原N端肽、透明质酸水平.结果血清TIMP1(r=0.540,P<0.001)、MMP2(r=0.314,P=0.003)、TIMP1/MMP1(r=0.269,P<0.001)与纤维化分级成正相关,MMP1与纤维化分级成负相关(r=-0.49 5,P<0.001),且与血清Ⅲ型前胶原N端肽、透明质酸相关;根据受试者工作特性曲线(ROC)下面积计算,MMP1以13.96(ng/ml)为临界值,判别S2及S2以上纤维化的敏感性为90.5%,特异性为52.0%;TIMP1以76.84(ng/ml)为临界值,敏感性为91.6%,特异性为64.0%.MMP1以6.86(ng/ml)为临界值,判别肝硬化(S4)期敏感性为70.7%,特异性为80.9%;TIMP1以210.04(ng/ml)为临界值,其敏感性60.5%,特异性92.3%.MMP1、TIMP1与炎症分级及计分均有相关性,而TIMP1与碎屑坏死、桥接坏死相关性最好(r=0.435,P<0.001),TIMP2与MMP9与炎症没有明显相关性.结论血清TIMP1、MMP1、MMP2水平、TIMP1/MMP1比值可作评估肝纤维化发展或减轻的指标.  相似文献   

9.
复方牛胎肝提取物片治疗肝纤维化的多中心研究   总被引:3,自引:0,他引:3  
目的观察研究复方牛胎肝提取物片治疗肝纤维化在扩大人群中的临床疗效。方法采用多中心、自身对照的研究设计。筛选肝纤维化患者共115例,所有病例给予口服复方牛胎肝提取物片治疗24周,治疗前均行肝穿刺做肝活体组织检查,其中有38例患者住治疗后再次做肝活体组织检查。患者均在治疗前、治疗后12、24周和36周,应用放射免疫法检测患者血清肝纤维化标志物HA、LN、Ⅳ型胶原(Ⅳ-C),观察用药前后各项指标及肝组织病理学变化。结果口服复方牛胎肝提取物片治疗前(0周),治疗后24周和36周,患者血清肝纤维化标志物HA值分别为(279.2±81.4)ng/ml、(136.8±56.7)ng/ml、(86.9±40.7)ng/ml,LN值分别为(170.8±73.0)ng/ml、(112.5±39.5)ng/ml、(60.8±31.8)ng/ml;Ⅳ-C值分别为(153.7±60.1)ng/ml、(112.4±43.1)ng/ml、(96.3±44.1)ng/ml,治疗后血清肝纤维化标志物较治疗前显著降低(P〈0.05)。肝活体组织病理检查显示,治疗后肝组织纤维化分期比治疗前有明显降低(P〈0.01)。结论复方牛胎肝提取物片具有改善肝纤维化的作用,对于治疗慢性肝病肝纤维化具有较好的疗效。  相似文献   

10.
氧化苦参碱防治半乳糖胺诱导大鼠肝纤维化的实验研究   总被引:53,自引:1,他引:53  
目的 观察氧化苫参碱(oxymatrine,OM)预防及治疗大鼠肝纤维化的疗效并探讨其作用机制。方法 采用半乳糖胺诱导的大鼠肝纤维化模型,观察OM(90mg/kg)干预前后血及肝组织生物化学、羟脯氨酸含量、TGF β_1 mRNA表达水平及病理组织学改变。结果 OM干预组肝组织羟脯氨酸含量 (μg/mg)较模型组显著下降(预防观察组为0.50±0.11和0.99±0.14,t=8.366,P<0.01;治疗观察组为0.44±0.04和0.70±0.06,t=9.839,P<0.01);与模型组比较,干预组血清ALT、AST亦显著下降(P<0.01);病理组织学显示干预组较模型组 Ⅰ、Ⅲ型胶原沉积减少,纤维间隔纤细,数量减少;干预织肝组织匀浆内超氧化物歧化酶活性(NU/mg)较模型组升高(预防观察组为149.81±15.28和95.22±16.33,t=7.309,P<0.01;治疗观察组为157.68±19.54和119.88±14.94,t=4.348,P<0.01), 而丙二醛(nmol/mg)低于模型组(预防观察组为2.06±0.17和4.57±0.37,t=17.529,P<0.01;治疗观察组为1.76±0.24和3.10±0.17,t=12.697,P<0.01);PT-PCR显示干预组TGF β_1 mRNA表达水平降低(预防观察组为0.21±0.01和0.50±0.01,t-48.665,P<0.01;治疗观察组为0.18±0.02和0.38±0.01,t=22.464,P<0.01)。结论 氧化苫参碱对半乳糖胺诱导的肝纤维化有预防及治疗作用,其部分机制为通过  相似文献   

11.
Inhibitory effect of Huangqi Zhechong decoction on liver fibrosis in rat   总被引:6,自引:0,他引:6  
AIM: To assess the inhibitory effect of Huangqi Zhechong decoction on hepatic fibrosis in rats induced by CCl(4) plus alcohol and high fat low protein diet. METHODS: Male SD rats were randomly divided into hepatic fibrosis model group, control group and 3 treatment groups consisting of 12 rats in each group. Except for the normal control group, all the rats were subcutaneously injected with CCl(4) at a dosage of 3 mL/kg. In 3 treated groups, either high-dose group (9 mL/kg), or medium-dose group (6 mL/kg), or low-dose group (3 mL/kg) was daily gavaged with Huangqi Zhechong decoction, and saline vehicle was given to model and normal control rats. Enzyme-linked immunosorbent assay (ELISA) and biochemical examinations were used to determine the changes of alanine aminotransferase (ALT), aspartate aminotransferase (AST), hyaluronic acid (HA), laminin (LN), type-III-procollagen-N-peptide (PIIIP), and type IV collagen content in serum, and hydroxyproline (Hyp) content in liver after sacrificing the rats. Pathologic changes, particularly fibrosis were examined by hematoxylin and eosin (HE) and Van Gieson staining. RESULTS: Compared with the model control group, serum ALT, AST, HA, LN, PIIIP and type IV collagen levels dropped markedly in Huangqi Zhechong decoction groups, especially in the medium-dose Huangqi Zhechong decoction group (1 954+/-576 U/L vs 759+/-380 U/L, 2 735+/-786 U/L vs 1 259+/-829 U/L, 42.74+/-7.04 ng/mL vs 20.68+/-5.85 ng/mL, 31.62+/-5.84 ng/mL vs 14.87+/-1.45 ng/mL, 3.26+/-0.69 ng/mL vs 1.47+/-0.46 ng/mL, 77.68+/-20.23 ng/mL vs 25.64+/-4.68 ng/mL, respectively) (P<0.05). The Hyp content in liver tissue was also markedly decreased (26.47+/-11.24 mg/mgprot vs 9.89+/-3.74 mg/mgprot) (P<0.01). Moreover, the stage of the rat liver fibrosis in Huangqi Zhechong decoction groups was lower than that in model group, and more dramatic drop was observed in medium-dose Huangqi Zhechong decoction group (P<0.01). CONCLUSION: Huangqi Zhechong decoction can inhibit hepatic fibrosis resulted from chronic liver injure, retard the development of cirrhosis, and notably ameliorate the liver function. It may be a safe and effective therapeutic drug for patients with fibrosis.  相似文献   

12.
D G Li  H M Lu  X H Li 《中华内科杂志》1990,29(8):453-6, 509
Changes in serum procollagen-III-peptide (PIIIP) and intravenous tryptophan tolerance test (ITT) were studied in 121 patients with liver cirrhosis during a follow-up period of up to 18 months. The patients received either nifedipine (31 cases, 60 mg/day), verapamil (28 cases, 120 mg/day), cinnarizine (29 cases, 150 mg/day) or tetrandrine (33 cases, 150 mg/day). The significant changes were found in ITT in any of the four drugs administrated for over three months. Serum PIIIP concentration decreased significantly in patients under tetrandrine therapy for 18 months (12.06 +/- 3.91 ng/ml vs 16.57 +/- 5.69 ng/ml before treatment). These data suggest that tetrandrine therapy may have favourable effects on hepatic fibrosis and improvement of liver function in liver cirrhosis.  相似文献   

13.
Four markers for hepatic fibrosis--N-terminal peptide of Type III procollagen (PIIIP), Laminin P1 (laminin), Type IV collagen (Type IV-C), and 7S domain (7S)--were measured in the sera of 90 patients with various chronic liver diseases diagnosed by liver biopsy--fatty liver (FL), chronic inactive hepatitis (CIH), chronic active hepatitis (CAH), and liver cirrhosis (LC)--and in the sera of 20 healthy controls. The values of markers were compared with the grade of histologic findings of the liver. Four markers were significantly raised in the CAH group and the LC group, and they were considered to be indicators of hepatic fibrosis. PIIIP reflected necrosis and inflammation as well as fibrosis of the liver. Laminin, Type IV-C, and 7S reflected severe fibrosis. 7S was considered to be useful marker for liver cirrhosis.  相似文献   

14.
目的 探讨人脐带间充质干细胞(UC-MSCs)联合苦参素治疗失代偿期乙型肝炎肝硬化患者的疗效。方法 采用随机数字表法将68例失代偿期乙型肝炎肝硬化患者分为对照组34例和观察组34例,分别给予经肝动脉行UC-MSCs移植或在UC-MSCs移植后给予苦参素口服治疗,观察12个月。结果 在治疗期间,观察组3例死亡,对照组4例死亡;在治疗12月末,观察组血清ALT为(39.3±15.6) U/L、TBIL为(26.3±10.2) μmol/L,均显著低于对照组【(71.2±17.2) U/L和(39.2±11.2) μmol/L,P<0.05】;血清层粘连蛋白为(81.2±24.1) ng/ml,透明质酸为(135.7±48.5) ng/ml,Ⅳ型胶原为(106.3±32.1) ng/ml,Ⅲ型前胶原为(98.7±25.6) ng/ml,均显著低于对照组【(113.3±29.6) ng/ml、(174.8±51.2) ng/ml、(158.4±35.6) ng/ml、(124.2±30.3) ng/ml,P<0.05】;外周血CD4+细胞百分比为(34.0±4.6)%,CD4+/CD8+比值为(1.2±0.6),均显著高于对照组【(29.3±4.1)%和(0.9±0.6),P<0.05】,CD8+为(26.5±4.9)%,显著低于对照组【(31.2±3.9)%,P<0.05】;肝移植和肝癌发生率分别为2.9%和5.9%,与对照组的5.9%和11.8%比较无显著性差异(P>0.05)。结论 HU-MSCs肝内移植联合苦参素胶囊口服治疗失代偿期肝硬化患者可明显减轻肝纤维化,改善肝功能。  相似文献   

15.
Serum type-III procollagen aminopropeptide (PIIIP) has been considered a marker of hepatic fibrogenesis. In an attempt to evaluate the clinical significance of serum PIIIP in patients with hepatitis B virus (HBV)-related liver diseases, the levels of the peptide were measured in 66 healthy adults and 200 patients with HBV-related liver diseases. As compared with the healthy adults (12.3 +/- 3.1 ng/ml), the serum PIIIP levels were significantly elevated in patients with acute hepatitis (17.4 +/- 6.6 ng/ml), chronic persistent hepatitis (18.3 +/- 4.9 ng/ml), and inactive liver cirrhosis (22.1 +/- 7.1 ng/ml). The PIIIP levels in patients with chronic active hepatitis (CAH) (33.9 +/- 23.1 ng/ml) were the highest among HBV-related liver diseases and had a tendency to increase with the severity of CAH. Of the liver-diseased patients with serum PIIIP levels greater than 30 ng/ml, 91% had a recent episode of severe hepatocellular damage, whereas 56% of patients with greatly elevated serum liver aminotransferase levels had no associated high increase in serum PIIIP levels. Thus, we suggest that fibrogenesis in HBV-related liver diseases is initiated by severe hepatocellular damage, but liver damage can also take place without prominent hepatic fibrogenesis. Serum PIIIP may be a serum marker to predict the active fibrogenesis of HBV-related liver diseases.  相似文献   

16.
Serum concentrations of both the carboxyterminal cross-linking domain (NC1) of procollagen type IV and the aminoterminal propeptide of procollagen type III (PIIIP) were measured by specific radioimmunoassays in 60 patients with chronic liver disease and 50 healthy controls. Compared with controls (5.3 +/- 1.3 ng/ml, mean +/- S.D.), NC1 concentrations were significantly elevated in patients with chronic active hepatitis (10.2 +/- 2.0 ng/ml) and liver cirrhosis (13.5 +/- 3.0 ng/ml), but not in chronic persistent hepatitis (6.0 +/- 0.9 ng/ml). The concentrations in patients with active liver cirrhosis were significantly higher than those in patients with inactive cirrhosis. Serum concentrations of PIIIP in controls, parients with chronic persistent hepatitis, chronic active hepatitis and cirrhosis were 5.8 (4.3-7.9), 5.3 (3.5-7.9), 17.5 (10.6-28.9), 16.7 (10.4-26.7) ng/ml, respectively (logarithmic mean and range of mean +/- S.D. after retransformation). Patients with liver cirrhosis had significantly higher concentrations of NC1 in serum than those with chronic active hepatitis, but there was no difference in serum PIIIP concentrations between the two groups. These data suggest an alteration of type IV collagen metabolism in chronic liver disease. In liver cirrhosis, the metabolism of collagen IV is apparently different from that of collagen type III; serum NC1 determinations may therefore provide additional information on chronic liver disease, particularly in patients with cirrhosis with a normal level of serum PIIIP. Further follow-up studies as well as investigations related to the basic mechanism of the elevation of these peptides in serum are needed in order to understand their clinical significance fully.  相似文献   

17.
复方861对HSC-T6细胞基质分解素1mRNA表达水平影响的研究   总被引:6,自引:0,他引:6  
为观察复方 86 1对HSC -T6细胞基质分解素 1(MMP3 )mRNA表达水平的影响 ,复方 86 1以 0 2 5mg/ml、0 5mg/ml、1 0mg/ml等浓度作用于HSC -T6细胞 48小时 ,以逆转录定量PCR方法测定其对HSC -T6细胞MMP3 mRNA表达水平的影响。结果表明 ,复方 86 10 2 5mg/ml、0 5mg/ml、1 0mg/ml等不同浓度的HSC -T6细胞mRNA表达水平依次为 2 75± 0 35、3 0 0± 0 0 1、3 5 0± 0 71,与空白对照组比较 ,可明显提高MMP3 mRNA表达水平 (P <0 0 5或P <0 0 1)。因此 ,复方 86 1提高HSC -T6细胞MMP3 mRNA表达水平 ,可能是其促进胶原降解 ,抗肝纤维化的作用机理之一。  相似文献   

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