枯否细胞条件培养基及混合血清对肝星状细胞HSC-T6的刺激作用

目的探讨枯否细胞条件培养基(KCCM)、混合的新生牛血清(NBS)和大鼠血清(RS)对肝星状细胞(HSC)增殖和胶原合成的促进作用.方法采用KCCM、单纯NBS及混合血清刺激大鼠HSC-T6细胞,用3H-TdR和3H-脯氨酸掺入法检测HSC增殖活性和胶原合成状况.结果不同刺激剂作用48 h后,HSC均体积增大,胞突增多延长,核分裂像增多.48 h的3H-TdR和96 h的3H-脯氨酸掺入明显增加.结论混合血清对HSC-T6的综合激活作用较KCCM和单纯10% NBS的作用明显,能明显促进其增殖和胶原合成,是有效的肝纤维化体外模型.     

青蒿琥酯对大鼠肝Kupffer细胞分泌肝纤维化相关细胞因子的影响

目的探讨青蒿琥酯对大鼠肝巨噬(Kupffer)细胞分泌致炎细胞因子的影响。方法 CCl4皮下注射SD大鼠进行肝纤维化造模,Percoll密度梯度离心法分离纯化大鼠肝Kupffer细胞,ELISA检测不同浓度青蒿琥酯处理LPS刺激的大鼠肝Kupffer细胞分泌致炎细胞因子TNF-α、TGF-β1和IL-6的变化。结果造模12周后,模型组大鼠出现明显的肝纤维化,Percoll密度梯度离心纯化后的大鼠肝Kupffer细胞在LPS刺激后TNF-α、TGF-β1和IL-6的表达量在模型组较对照组显著增加(P<0.05)。0μmol/L、125μmol/L、175μmol/L、225μmol/L 4个浓度的青蒿琥酯处理后,模型组较对照组致炎细胞因子TNF-α、TGF-β1和IL-6的表达量显著下调,并且175μmol/L为最佳抑制浓度(P<0.05)。结论青蒿琥酯可以抑制大鼠肝Kupffer细胞分泌致炎细胞因子     

乙醛及其刺激的Kupffer细胞对肝星状细胞活化的影响

目的 探讨乙醛及其刺激的Kupffer细胞对大鼠肝星状细胞(HSCs)活化的影响.方法 用链酶蛋白酶和胶原酶原位灌流,Nycodenz密度梯度法离心分离大鼠肝脏HSCs和Kupffer细胞,制备乙醛刺激的Kupffer细胞培养上清液(KCCM),并以MTT法观察乙醛及乙醛与Kupffer共同培养的KCCM对HSCs的增殖效应,以放射免疫法检测HSCs培养上清液中Ⅳ型胶原的含量.结果 乙醛直接作用于HSCs后HSCs明显增殖,并能合成分泌Ⅳ型胶原;未用乙醛处理和经乙醛处理后的KCCM均能使HSCs增殖并生成Ⅳ型胶原,两组之间差异无统计学意义(P＞0.05).结论 乙醛可促进HSCs活化,与酒精性肝病时肝纤维化的发生有关.乙醛不能直接作用于Kupffer细胞引起HSCs活化.     

丹参酚酸B盐对转化生长因子β1活化的大鼠肝星状细胞内细胞外信号调节激酶信号转导通路的抑制作用

目的:探讨丹参酚酸B盐(salvianolic acid B,SA-B)对转化生长因子β1 (transforming growth factor-β1,TGF-31)活化的大鼠肝星状细胞(hepatic stellate cell,HSC)内细胞外信号调节激酶(extracellular signal-regulated kinase,ERK)信号转导通路的影响.方法:采用原位灌流酶消化及Nycodenz密度梯度离心的方法分离正常大鼠HSC,将TGF-β1和SA-B直接添加于原代HSC的无血清培养液中.蛋白印记法检测HSC内磷酸化和总ERK,以及有丝分裂原激活蛋白激酶激酶MEK、有丝分裂原活化蛋白激酶激酶激酶Raf、α平滑肌肌动蛋白(α-smooth muscle actin,α-SMA)和Ⅰ型胶原蛋白的表达.结果:SA-B可抑制正常原代HSC及TGF-β1刺激的HSC内ERK上游激酶MEK的磷酸化;而对正常原代HSC及TGF-β1刺激的HSC内MEK上游激酶Raf-1的磷酸化无明显抑制.SA-B对TGF-β1刺激的HSC内α-SMA表达有明显的抑制作用,SA-B与ERK阻断剂联用,几乎接近完全阻断α-SMA的表达.SA-B对正常培养的HSC和经TGF-β1刺激的HSC Ⅰ型胶原蛋白的合成都有明显的抑制作用.结论:SA-B抑制TGF-β1刺激的HSC内ERK信号转导通路的作用环节在于抑制了MEK的磷酸化.SA-B通过抑制TGF-β1的ERK信号转导通路,减少了因HSC活化导致的α-SMA表达和Ⅰ型胶原蛋白合成增加.     

激活素A对肝星状细胞胶原合成的影响

目的探讨激活素A(ACT A)对肝星状细胞(HSC)细胞外基质(ECM)合成的影响.方法采用原位酶灌注法和密度梯度离心法分离HSC.初次传代后,HSC随机分为八组,分别加入不同浓度的ACT A和TGF-β1.加药后24h,采用放射免疫法检测培养液Ⅲ型前胶原和Ⅳ型胶原含量.结果ACT A能刺激体外培养HSC分泌ECM,在一定浓度范围内(1~100μg/L)呈剂量依赖关系;100μg/L ACT A刺激HSC分泌ECM的能力与10μg/L TGF-β1相当,而且ACT A能协同TGF-β1发挥该生物学效应.结论ACT A参与肝纤维化形成.     

丹参素对IL-1β刺激的大鼠肝星状细胞JNK、NF-κB信号通道的影响

目的 观察丹参素对活化的大鼠肝星状细胞(HSC)氨基末端蛋白激酶(JNK)以及NF-κBP65表达的影响,探讨其抗肝纤维化作用的机制.方法 分离大鼠原代HSC,MTT法检测丹参素对细胞的生长抑制,免疫细胞化学法观察Ⅲ型胶原合成,ELISA法观察Ⅲ型胶原分泌.AO/EB荧光染色观察HSC凋亡形态学变化,Annexin-V-FITC/PI联合流式细胞仪检测HSC的凋亡率,Western blotting观察丹参素对IL-1β刺激的HSCs内P-IκBα、NF-κBP65和JNK蛋白的表达.结果 和结论丹参素可抑制活化的HSC增殖,降低胶原合成和分泌,促进HSC凋亡,并抑制IL-1β刺激的HSC中JNK的磷酸化及NF-κBp65的表达.     

复方中药血清对四氯化碳刺激的肝星状细胞NO和ET-1的影响

目的:研究复方中药对体外培养的大鼠肝星状细胞(HSC)一氧化氮(NO)和内皮素1(ET-1)的影响,从细胞因子水平探讨复方中药抗纤维化和门脉高压的作用机理.方法:逆转录多聚酶链反应(RT-PCR)法检测中药血清对四氯化碳(CCl4)刺激的HSC中ET-1,iNOS mRNA的表达;SP法免疫细胞化学检测HSC ET-1,iNOS的表达.结果:CCl4刺激组HSC中ET-1 mRNA表达及其含量(7.09±1.71 vs 42.44±2.58)明显增强,与空白对照组(0.56±0.28 vs 12.25±1.56)比较显著升高(P＜0.05),中药血清对其有显著抑制作用(P＜0.05),且联合应用TGF-β1抗体对CCl4刺激HSC ET-1 mRNA的抑制作用加强;同时CCl4刺激组HSC中iNOS mRNA和蛋白表达(0.96±0.16 vs 5.31±0.86)比空白对照组0.63±0.19 vs 4.66±1.12)轻度升高,但无显著差异.药物血清处理组iNOS mRNA和蛋白的表达均高于CCl4和空白对照组(P＜0.05),且联合TGF-β1抗体作用HSC iNOS的表达高于其单独作用(P＜0.05).结论:复方中药降低CCl4诱导的HSC ET-1水平及增加HSC分泌NO途径而抑制HSC的收缩.     

外源性IL-10对大鼠肝星形细胞生物学活性的影响

目的　用白细胞介素 - 1 0 (IL- 1 0 )干预在体外培养激活的以及用血小板衍生生长因子 (PDGF)进一步激活的肝星形细胞 (HSC)模型 ,观察 HSC增殖、凋亡、收缩及胶原与纤维化相关细胞因子的表达等生物学活性 ,了解 IL- 1 0对大鼠HSC生物学活性的影响 ,探讨 PDGF对 HSC的作用机制。　方法　体外培养大鼠肝星形细胞系 ,分别用 IL- 1 0、PDGF干预以及二者共干预 ,显微镜下观察细胞收缩情况 ;采用四甲基偶氮唑盐 (MTT)比色法观察干预前后细胞增殖状况的改变 ,用半定量 RT- PCR方法检测各组 、 型胶原、转化生长因子 - β1 (TGF- β1 )、表皮生长因子 (EGF)、成纤维细胞生长因子 (FGF)及 Fas/ Fas L m RNA表达情况 ;用免疫细胞化学方法检测 IL- 1 0、PDGF干预 型胶原蛋白表达的影响。　结果　 PDGF显著增强 HSC收缩与增殖 ,促进 、 型胶原及 TGF-β1 、FGF的表达 ;IL - 1 0显著增强 HSC表达 Fas L ,并可在一定程度上抑制 HSC的增殖以及对 TGF-β1 、FGF的表达 ;IL - 1 0可显著抑制 PDGF的促收缩、增殖及促 、 型胶原、TGF-β1 表达等作用。　结论　 IL - 1 0对 HSC的增殖、收缩以及表达 、 型胶原、TGF-β1 、FGF等多方面生物学活性有一定的抑制作用。抗肝纤维化机制可能通过 Fas/ Fas L途径诱导 HSC凋亡     

丹酚酸B盐对转化生长因子-β1刺激肝星状细胞活化与胞内信号转导的作用

目的 探讨丹酚酸B盐（SA-B）抗肝纤维化的作用机理。方法 分离大鼠肝星状细胞（HSC）,于无包被的塑料培养皿上原代培1、4、7d,细胞分别处于静止,中间活化与完全活化3种活化状态,予以100pmol/L转化生长因子β1(TGF-β1）刺激,观察细胞α-肌动蛋白表达与胶原分泌的变化。选择对TGF-β1刺激最为敏感的中间活化状态HSC为细胞模型,[^3H]胸腺嘧啶掺入法观察0.1μmol/L-1mmol/LSA-B对该细胞增殖的作用,倒置显微镜观察药物对细胞形态的影响;Western印迹与Northern印迹等方法观察SA-B对TGF-β1刺激活化的HSC胞外基质基因与蛋白表达,α-肌动蛋白表达的影响;提取细胞质与细胞核蛋白,Western印迹方法观察SA-B对TGF-β1刺激的HSCSmad2/3蛋白表达,磷酸化与核转位的影响。结果 TGF-β1促进各活化状态HSC的胶原分泌,促进率分别为128.6%,207.3%与188.2%,中间活化状态HSC对TGF-β1的促胶原分泌最为敏感,除0.1mmol/L-1mmol/LSA-B引起部分细胞死亡外,0.1μmol/L-10μmol/LSA-B对细胞形态无影响,但可浓度依赖性地抑制细胞增殖,细胞内[^3H]胸腺嘧啶掺入量分别为对照组的76%,60.1%与47.8%,1μmol/L-100644mol/LSA-B明显抑制TGF-β1刺激的HSC胶原分泌量（分别为对照组的68.6%与56.1%)。抑制α-肌动蛋白与纤维蛋白酶原激活物抑制子蛋白表达,下调I型前胶原基因表达,0.1μmol/L-10μmol/LSA-B不同程度地抑制Smad2/3的蛋白表达量,明显抑制Smad2蛋白胞内磷酸化与核转位。结论 SA-B抑制TGF-β1的HSC胞内信号转导,从而拮抗TGF-β1的促HSC活化,以上作用是SA-B抗肝纤维化的主要机理。     

激活素A对肝星状细胞胶原合成的影响

目的：探讨激活素A(ACTA)对肝星状细胞(HSC)细胞外基质(ECM)合成的影响。方法：采用原位酶灌注法和密度梯度离心法分离HSC。初次传代后，HSC随机分为八组，分别加入不同浓度的ACT A和TGF-β1。加药后24h，采用放射免疫法检测培养液Ⅲ型前胶原和Ⅳ型胶原含量。结果：ACTA能刺激体外培养HSC分泌ECM，在一定浓度范围内(1～100μg/L)呈剂量依赖关系；100μg/L ACT A刺激HSC分泌ECM的能力与10μg/L TGF-β1。相当，而且ACTA能协同TGF-β1发挥该生物学效应。结论：ACTA参与肝纤维化形成。     

Effects of Kupffer cells stimulated by triglyceride and very low-density lipoprotein on proliferation of rat hepatic stellate cells

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白细胞介素10抑制枯否细胞诱导的肝星状细胞激活的研究

目的　研究白细胞介素 10 (IL 10 )对与枯否氏细胞 (KC)共培养的肝星状细胞 (HSC)激活的影响 ,并初步探讨其作用机制。方法　采用肝脏离体胶原酶灌注消化 ,及密度梯度离心的方法来分离培养HSC和KC ;将原代培养 2d的HSC和KC分为HSC单独培养、KC单独培养和HSC与KC共培养 3大组 ,分别加 2ng/ml和 2 0ng/ml的IL 10处理。 2d后 ,分别采用3 H 胸腺嘧啶脱氧核苷 (3 H TdR)掺入法检测HSC的增殖 ,Western印染法检测HSC中α 平滑肌肌动蛋白 (α SMA)的表达和酶联免疫吸附分析 (ELISA)法检测培养上清中肿瘤坏死因子 α(TNF α)的含量。结果　IL 10对单独培养的HSC的增殖 (P >0 .0 5 )和α SMA表达 (P >0 .0 5 )无明显影响。共培养组HSC的增殖和α SMA表达分别增加了 2 .4倍和 6倍 ;2ng/ml和 2 0ng/ml的IL 10分别使共培养组HSC的增殖降低了 2 3%和 33% ,α SMA表达降低了 35 %和 4 9% ,均呈浓度依赖性 ,和HSC单独培养组相比 ,差异有显著意义 (P <0 .0 5或P <0 .0 0 1)。HSC单独培养组未检测出TNF α ;共培养组的TNF α量比KC单独培养组增加了 74 %(P <0 .0 1) ;2ng/ml和 2 0ng/ml的IL 10分别使共培养组的TNF α量降低了 2 7% (P <0 0 1)和 36 % (P<0 0 1) ,使KC单独培养组的TNF α量降低了 2 9% (P <0 0 5 )和 4     

Effects of vitamin E on the proliferation and collagen synthesis of rat hepatic stellate cells treated with IL-2 or TNF-α

Objective To study the effects of vitamin E on the proliferation and collagen synthesis of rat hepatic stellate cells treated with interleukin-2 (IL-2 ) or tumor necrosis factor-α (TNF-α). Methods Hepatic stellate cells were isolated from male Sprague-Dawley rats by using modified Friedman’s method. Using the isolated cells cultured and treated with IL-2 or TNF-α, we studied the effects of vitamin E on their proliferation and collagen synthesis through an (3)H-thymidine and (3)H-proline incorporation assay, as well as through observation of these cells under a contrary phase microscope. Results Adding IL-2 increased the both proliferation and collagen synthesis of hepatic stellate cells. Their proliferation was also increased by the addition of TNF-α, although it decreased collagen synthesis. Vitamin E had marked inhibitory effects on the ability of cells treated with IL-2 or TNF-α to reproduce or synthesize collagen. Conclusion Vitamin E can inhibit the proliferation and collagen synthesis of hepatic stellate cells. It is possible that vitamin E affects liver fibrosis through these activities.     

异甘草酸镁对四氯化碳肝纤维化大鼠肝组织病理改变的影响

目的:探讨异甘草酸镁(magnesium isoglycyrrhizinate,MgIG)早期、晚期干预对四氯化碳( carbon tetrachloride,CCl4)肝纤维化模型大鼠肝组织结构和肝星状细胞(hepatic stellate cells,HSC)活化的影响.方法: 32只3月龄雄性SD大鼠随机分为对照组(10只)、CCl4模型组(10 只)、MgIG早期干预组(6 只,在CCl4造模开始同时即每日腹腔注射MgIG 30 mg/kg)和MgIG晚期干预组(6只,在CCl4造模5周后每日腹腔注射MgIG 30 mg/kg).各组大鼠在造模10周后取材,从每只大鼠肝脏等距随机抽选4个肝组织块制作石蜡包埋切片,行Masson染色和HE染色观察肝组织一般结构和胶原纤维数量和分布的变化;另从每只大鼠肝脏随机抽选5个组织块制作电镜超薄切片,在电镜下观察肝组织超微结构的改变.结果: 与对照组比较, CCl4大鼠肝组织内肝细胞出现明显的脂肪变性、坏死和再生,胶原纤维增生,假小叶形成,HSC体积增大、数量增多;MgIG早期干预或晚期干预对CCl4大鼠肝组织一般结构、超微结构以及HSC的活化增殖均无明显影响.结论: CCl4诱导大鼠肝组织发生肝纤维化或肝硬化的病理改变,可能与HSC的活化、增殖有关;MgIG对CCl4大鼠的肝纤维化病理进展没有明显的抑制或逆转作用.     

人肝细胞生长因子基因表达对CCl4损伤的人肝细胞及大鼠肝星状细胞株的影响及其机制

目的：探讨人肝细胞生长因子(hHGF) 基因的表达对CCl4损伤的人肝细胞及大鼠肝星状细胞株（CFSC-2G）生物学效应的影响及其对CCl4损伤的人正常肝细胞株（HL-7702）的保护作用,进一步探讨凋亡产生的机制。方法：将获得的稳定转染HL-7702细胞克隆,分为4组,Ⅰ组为转染PCI-neo-hHGF实验组,Ⅱ组为转染PCI-neo空载体对照组,Ⅲ组为仅加入脂质体的对照组,Ⅳ组为空白对照组。采用MTT法测定细胞增殖活性。采用Western blotting测定转染PCI-neo-hHGF的HL-7702细胞和CFSC-2G细胞中hHGF、caspase-3、caspase-8、caspase-9蛋白质的表达。结果：HL-7702细胞转染PCI-neo-HGF并培养48 h后,细胞的增殖活性明显高于PCI-neo空载体对照组、脂质体转染对照组和空白对照组HL-7702细胞（P<0.01）,而且随着转染PCI-neo-HGF剂量增加,细胞的增殖活性有一定的增长趋势,但各组间比较差异无显著性（P>0.05）;PCI-neo-HGF转染的HL-7702细胞caspase-3蛋白质表达量较CCl4损伤的HL-7702细胞和PCI-neo转染的HL-7702细胞明显降低,未检测到caspase-8和caspase-9蛋白质的表达;PCI-neo-HGF转染的CFSC-2G细胞caspase-3蛋白质表达量较CCl4诱导的CFSC-2G增加,caspase-9蛋白质表达也呈阳性。结论：PCI-neo-HGF可促进体外培养的HL-7702细胞的生长增殖,能够抑制CCl4损伤的HL-7702细胞的凋亡,促进大鼠CFSC-2G细胞的凋亡,其作用机制可能与上调caspase-3和caspase-9蛋白质表达有关。     

来氟米特抑制结缔组织生长因子诱导的肾间质成纤维细胞增殖和胶原合成的研究

目的探讨来氟米特（LEF）对人肾间质成纤维细胞增殖和胶原合成的影响。方法在体外培养的人肾间质成纤维细胞中，加入不同浓度来氟米特活性代谢产物A771726和重组人结缔组织生长因子（rhCTGF），MTT法测定两者单独及同时干预下细胞增殖情况；ELISA法测定细胞合成Ⅰ、Ⅳ型胶原的含量。结果经不同浓度的rhCTGF刺激，成纤维细胞增殖和细胞合呈Ⅰ型、Ⅳ型胶原均成剂量依赖性增加（P〈0．01）：而来氟米特作用细胞后，细胞增殖及胶原合成均呈剂量依赖性减少（P〈0．01）；在来氟米特与结缔组织生长因子（CTGF）共同作用下，细胞的增殖和胶原的合成较单用同剂量的CTGF时减少（P〈0.05）。结论rhCTGF能够促进人肾间质成纤维细胞的增殖及Ⅰ、Ⅳ型胶原合成；来氟米特则抑制细胞的增殖及细胞合成Ⅰ、Ⅳ型胶原；来氟米特对rhCTGF诱导的胶原合成增加有一定的拮抗作用。     

Effect of angiotensin Ⅱ and angiotensin Ⅱ type 1 receptor antagonist on the proliferation,contraction and collagen synthesis in rat hepatic stellate cells

Background Angiotensin Ⅱ （Ang Ⅱ） is a very important vasoactive peptide that acts upon hepatic stellate cells （HSCs）, which are major effector cells in hepatic cirrhosis and portal hypertension. The present study was aimed to investigate the effects of Ang Ⅱ and angiotensin Ⅱ type 1 receptor antagonist （AT1RA） on the proliferation, contraction and collagen synthesis in HSCs.
Methods HSC-T6 rat hepatic stellate cell line was studied. The proliferation of the HSC cells was evaluated by MTT colorimetric assay while HSC DNA synthesis was measured by ^3H-thymidine incorporation. The effects of angiotensin Ⅱ and AT1RA on HSCs contraction were studied by analysis of the contraction of the collagen lattice. Cell culture media were analyzed by RT-PCR to detect secretion of collagen Ⅰ （Col Ⅰ）, collagen Ⅲ （Col Ⅲ） and transforming growth factor β1 （TGF-β1） by enzyme linked immunosorbent assay. HSC was harvested to measure collagen Ⅰ, collagen Ⅲ and tissue inhibitor of metalloproteinase-1 （TIMP-1） mRNA expression.
Results Ang Ⅱ （（1×10^-10-1×10^-4）mol/L）stimulated DNA synthesis and proliferation in HSCs compared with untreated control cells. AT1RA inhibited angiotensin Ⅱ induced proliferation of HSCs. A linear increase in the contractive area of collagen lattice correlated with the concentration of angiotensin Ⅱ （1×10^-9-1×10^-5 mol/L） and with time over 48 hours. AT1RA blocks angiotensin Ⅱ induced contraction of collagen lattice. Col Ⅰ, Col Ⅲ and TGF-β1 levels of the Ang Ⅱ group were higher than those of control group and this increase was downregulated by AT1RA. The mRNA expressions of Col Ⅰ, Col Ⅲ and TIMP-1 were higher in HSCs from the Ang Ⅱ group than the control group and downregulated by AT1RA.
Conclusions Angiotensin Ⅱ increased DNA synthesis and proliferation of HSCs in a dose-dependent manner, stimulated the contraction of HSCs dose- and time-dependently. Angiotensin also promoted excretion of Col I, Col Ⅲ and TGF-β1 lev     

Effects of ribozyme targeting platelet-derived growth factor receptor β subunit gene on the proliferation and apoptosis of hepatic stellate cells in vitro

Background Activation and proliferation of hepatic stellate cells (HSC) is essentially involved in the development and progression of hepatic fibrosis. The most potent growth factor for HSC is platelet-derived growth factor receptor (PDGF) and PDGF receptor β subunit (PDGFR-β) is the predominant signal transduction pathyway of PDGF which is overexpressed in activated HSC. This study investigated the cleavage activity of hammerhead ribozyme targeting PDGFR-β mRNA in HSC and the effect on biological characteristics of HSC.Methods Expression vector of anti-PDGFR-β ribozyme was constructed and transfected into rat activated HSC with lipofectamin. The positive cell clones were gained by G418 selection. The expression of PDGFR-β, α-smooth muscle actin, and typeⅠand type Ⅲ collagen were detected by using Northern blot, Western blot and immunocytochemical staining, respectively. The cell proliferation was determined with MTT colorimetric assay. The cell apoptosis was analyzed by using flow cytometry, acridine orange fluorescence vital staining and transmission electron microscopy.Results The expression of PDGFR-β at mRNA and protein level was markedly reduced in ribozyme-transfected HSC by 49%-57% (P&lt;0.05-0.01). The proliferation and α-smooth muscle actin expression of ribozyme-transfected HSC were significantly decreased (P&lt;0.05-0.01), and the type Ⅰ and type Ⅲ collagen synthesis were also reduced (P&lt;0.01). In addition, the proliferative response of ribozyme-transfected HSC to PDGF BB was significantly inhibited. Otherwise, the apoptotic cells were significantly increased in ribozyme-transfected HSC (P&lt;0.01), and typical apoptotic cells could be found under transmission electron microscopy.Conclusions The anti-PDGFR-β ribozyme effectively cleaved the target RNA and significantly inhibited its expression, which blocked the signal transduction of PDGF at receptor level, inhibited HSC proliferation and collagen synthesis, and induced HSC apoptosis. These results suggest that inhibiting PDGFR-β expression of HSC may be a new target for the therapy of liver fibrogenesis, and ribozyme may be a useful tool for inhibiting PDGFR-β expression.