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1.
水飞蓟宾对大鼠肝贮脂细胞HSC-T6增殖和胶原合成的影响 总被引:4,自引:0,他引:4
目的:观察水飞蓟宾对大鼠肝贮脂细胞HSC-T6增殖和胶原合成的影响,探讨其保护肝脏及抗硬化机制。方法:采用结晶紫染色法测定细胞增殖,^3H-脯氨酸掺入法测定胶原合成。结果:水飞蓟宾(6.25~50μg/ml)以浓度依赖方式抑制血清、巨噬细胞条件培养液以及血小板源生长因子或转化生长因子β1诱导的细胞增殖和胶原合成。结论:抑制贮脂细胞增殖和胶原合成可能是水飞蓟宾保护肝脏抗硬化机制之一。 相似文献
2.
黄颜木素对HSC—T6细胞增殖和胶原合成的影响 总被引:14,自引:1,他引:13
目的:研究黄颜木素对激活的永生型大鼠肝腑 脂细胞--HSC-T6细胞增殖和胶原合成的影响。方法:细胞增殖采用结晶紫染色法检测,胶原合成采用^3H-酸掺入法分析。结果:黄颜木素(6.25-50.00μmol/L)以剂量依赖方式显著抑制血小板源生长因子(PDGF)刺激的HSC-T6细胞增殖,并抑制生长因子因子β1(TGFβ1)诱导的细胞内胶原合成,结论:黄颜木还给具有抑制激活的肝储脂细胞增殖和胶原合成 相似文献
3.
目的:研究维生素E(VitE)对大鼠贮脂细胞增殖及胶原合成的影响。方法:以链酶蛋白酶和胶原酶液原位循环灌注法分离大鼠贮脂细胞,以肿瘤坏死因子-α作为刺激因素,采用3H-胸腺嘧啶核苷(3H-TdR)和3H-脯氨酸(3H-proline)掺入法分别测定VitE对贮脂细胞增殖和胶原合成的影响,并在倒置显微镜下观察贮脂细胞的形态。结果:(1)肿瘤坏死因子-α能明显促进贮脂细胞增殖,并能明显抑制其胶原合成;(2)VitE能显著抑制肿瘤坏死因子-α引起的贮脂细胞增殖,并能增强肿瘤坏死因子-α对贮脂细胞胶原合成的抑制作用。结论:VitE对贮脂细胞增殖及胶原合成具有抑制作用,这可能是VitE抗肝纤维化作用的重要机制之一。 相似文献
4.
核心蛋白聚糖对肝细胞和肝星形细胞体外增殖的影响 总被引:5,自引:0,他引:5
目的:探讨核心蛋白聚糖(decorin)在肝纤维化形成机制中的作用。方法:在正常人肝细胞株L-02及大鼠肝星形细胞株HSC-T6体外培养体系中,分别加入不同质量浓度(0.01,5,10μg/ml)decorin共培养不同时间后,进行细胞计数以及^3H-TdR和^3H-Leu掺入量测定。结果:实验组经0.01μg/ml decorin作用4d或6d后,HSC-T6和L-02细胞增殖数量以及^3H-T 相似文献
5.
目的;研究维生素E对大鼠贮脂细胞增殖及胶原合成的影响。方法;以链酶蛋白酶和胶原酶液原位循环灌注法分离大鼠贮脂细胞,以肿瘤坏死因子-α作为刺激因素,采用^3H-胸腺嘧啶核苷和(^3H-TdR)和^3H-脯氨酸(^3H-proline)掺入法分别测定Vit E对贮脂细胞增殖和胶原合成的影响,并在倒置显微镜下观察贮脂细胞的形态。 相似文献
6.
目的为了诱导特异性小鼠-大鼠异种移植耐受。方法采用抗体亲和层析柱制备小鼠组织相容性抗原(H-2Ag);异型双功能试剂(SPDP,2-IT)连接H-2Ag和天花粉蛋白(TCS);测定其对受体免疫细胞的特异性抑制作用;将H-2Ag-TCS用于小鼠-大鼠异种心脏移植模型(Cuf技术)诱导免疫无反应性。结果H-2Ag与TCS连接物预处理后,受体免疫细胞在体外增殖反应被特异性抑制;H-2Ag-TCS能明显延长异种心脏存活时间(6.88±1.36天,CyA组:2.83±0.75,P<0.01)。结论H-2Ag-TCS能特异性诱导异种移植耐受 相似文献
7.
王向宇 《福建医科大学学报》1996,(4)
目的以20周龄自发性高血压大鼠(SHR)和正常血压大鼠(WKY)胸主动脉平滑肌细胞(ASMC)为模型,探讨SHRASMC异常增殖和自身肾素-血管紧张素系统(RAS)的关系。方法用3H-TdR参入量和倍增时间(DT)反映ASMC的增殖能力,放射免疫法测定血管紧张素Ⅱ(AngⅡ)浓度,紫外分光光度法测定血管紧张素转换酶(ACE)活性。结果(1)SHRASMC3H-TdR参入量显著高于WKY,DT显著短于WKY(P<0.01)。基础状态下,SHRASMC合成AngⅡ、ACE以及分泌AngⅡ的量显著高于WKY(P<0.01)。(2)在含2%FCS的培养基中,10-6mol/LAngⅡ使SHR、WKY的3H-TdR参入量分别提高到对照组的3.3倍、2.2倍(P<0.01),SHRASMC在不同浓度AngⅡ刺激时的3H-TdR参入量显著高于WKY(P<0.01),10-6mol/LAngⅡ使SHRASMC细胞数增加72.5±23.1%(P<0.01),WKYASMC细胞数无显著增加,10倍浓度AngⅡ的Saralasin对SHR、WKY3H-TdR参入的抑制率分别为66.7±3.3%,44.7±9.9%(P<0.01) 相似文献
8.
尾加压素在大鼠气道平滑肌细胞增殖中的作用及其机制 总被引:8,自引:1,他引:7
目的 观察近年新发现的活性肽尾加压素(Urotensin Ⅱ,UⅡ)在大鼠气道平滑肌细胞增殖中的作用及其机制。方法 (1)采用^3H-胸腺嘧啶(^3H-TdR)掺入法测定UⅡ对原代培养的大鼠气道平滑肌细胞(ASMC)DNA合成的影响,应用不同阻断剂观察UⅡ诱导细胞DNA合成的信号转导通路。(2)采用Fura-2/AM荧光探针,测定UⅡ对胞浆游离钙浓度的影响。结果 (1)UⅡ呈浓度(10^-10~10^-6mol/L)依赖性刺激ASMC^3H-TdR掺入,10^-6mol/L时,为对照组的7倍(P〈0.01);(2)蛋白激酶C(PKC)阻断剂H7、丝裂素活化蛋白激酶(MAPK)阻断剂PD98059及钙通道阻断剂尼卡的平均能抑制UⅡ刺激的ASMC^3H-TdR掺入,其抑制率分别为29%(P〈0.05),45%(P〈 相似文献
9.
观察SH1对ADP、AA,Collagen诱导的兔血小板聚集及TXB2和6-keTO-PGF1α生成的影响。用此浊法测定了透骨草提取的单体生物碱结果SH1体外对兔血小板聚集的影响,用放免法测定TXB2和6-keTO-PGF1α的含量。结果:SH1 0.8 ̄3.0mmol/L范围内明显抑制AA,ADP,Collagen诱导的兔血小板聚集。SH1对三种诱导剂的最大抑制率分别为62.16%、45.25% 相似文献
10.
柴胡皂甙对FSC激活及合成细胞外基质的实验研究 总被引:10,自引:0,他引:10
观察柴胡有效成分柴胡皂甙对原代培养贮脂细胞(FSC)激活及合成细胞外基质(ECM)的作用。结果:治疗组库普弗细胞条件培养基(TKCncm)、治疗CCl4损伤库普弗细胞条件培养基(TKCtcm)、TKCncm加肝细胞条件培养基(PCncm)组FSC内结蛋白阳性反应明显减弱,对细胞表型转化的形态学特征有一定改善,各治疗组FSC的DNA合成及3H-脯氨酸掺入量均呈不同程度降低,FSC内Ⅰ型胶原含量明显减少。说明柴胡皂甙对肝细胞具有保护作用,直接抑制FSC内DNA的合成,还可抑制FSC的激活,从而抑制FSC合成ECM的能力。 相似文献
11.
阿魏酸钠对球囊损伤大鼠颈总动脉血管内膜增生的影响 总被引:1,自引:0,他引:1
目的 :研究阿魏酸钠对球囊损伤大鼠颈总动脉内膜增生的影响。方法 :制作球囊损伤的大鼠颈总动脉内膜增生模型 ,Wistar雄性大鼠 15只随机分为①对照组 (n =7)腹腔内注射生理盐水 (4ml/d)。②阿魏酸钠治疗组 (n =8)腹腔内注射融于生理盐水的阿魏酸钠 (2 0 0mg/d) ,球囊损伤 14d后 ,损伤区域的血管段取材固定后 ,分析血管断面组织形态学的变化 ;免疫组化方法观察增殖细胞核抗原 (PCNA)阳性细胞以了解血管壁细胞的增殖情况。结果 :阿魏酸钠可明显减少新生内膜面积 ,增加管腔面积 ,抑制平滑肌细胞的增殖。结论 :阿魏酸钠具有抑制血管内膜增生的作用。 相似文献
12.
阿魏酸钠对大鼠肺纤维化的预防作用 总被引:2,自引:0,他引:2
目的:探讨阿魏酸钠对博莱霉素所致大鼠肺纤维化的预防作用。方法:30只SD大鼠随机分为对照组,肺纤维化模型组和阿魏酸钠预防组,每组10只;模型组和预防组以气管内滴入博来霉素(5mg/kg)建立肺纤维化动物模型,预防组采用阿魏酸钠(150mg/kg)灌胃治疗;HE染色检测肺组织病理改变及细胞计数,胶原纤维染色检测总胶原纤维表达,免疫组织化学检测Ⅰ型胶原纤维。结果:与对照组比较,肺纤维化模型组肺组织内细胞数、肺内总胶原纤维及Ⅰ型胶原纤维均显著增加;阿魏酸钠预防组与肺纤维化模型组比较,肺组织内细胞数、肺内总胶原纤维及Ⅰ型胶原纤维均显著降低。结论:阿魏酸钠能有效地减轻肺纤维化大鼠肺组织的炎症和纤维化程度,对肺纤维化有一定的预防作用。 相似文献
13.
Effects of ribozyme targeting platelet-derived growth factor receptor β subunit gene on the proliferation and apoptosis of hepatic stellate cells in vitro 总被引:13,自引:1,他引:12
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<0.05-0.01). The proliferation and α-smooth muscle actin expression of ribozyme-transfected HSC were significantly decreased (P<0.05-0.01), and the type Ⅰ and type Ⅲ collagen synthesis were also reduced (P<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<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. 相似文献
14.
醛固酮与螺内酯对肝星状细胞增殖及胶原合成的影响 总被引:4,自引:0,他引:4
目的 探讨醛固酮 (ALD)、螺内酯对大鼠肝星状细胞 (HSC)增殖、胶原合成的影响。方法 大鼠HSC培养 ,在不同浓度的ALD、螺内酯作用下 ,采用3 H 胸腺嘧啶核苷 (3 H TdR)、3 H 脯氨酸 (3 H Pro)掺入法及流式细胞技术观察ALD、螺内酯对HSC增殖及胶原合成的影响。结果 ALD在 10 -4mol/L高浓度时3 H TdR、3 H Pro掺入量与对照组相比明显增多 (P <0 .0 5 ) ,螺内酯在浓度高于 10 -6mol/L时 ,HSC3 H TdR、3 H Pro掺入量明显减少 ,螺内酯阻止HSC于G1期 ,ALD +螺内酯组与对照组相比差异无显著意义 (P >0 .0 5 )。结论 高浓度ALD可以促使HSC增殖 ,其拮抗剂螺内酯明显抑制HSC的增殖及合成胶原。 相似文献
15.
来氟米特对肝星状细胞增殖和胶原合成的影响 总被引:4,自引:0,他引:4
目的:研究来氟米特活性代谢物A771726对肝星状细胞(HSC)增殖和胶原合成的影响.方法:用链蛋白酶和胶原酶原位肝灌注、Nycodenz密度离心法分离大鼠HSC和Kupffer细胞,制备Kupffer培养上清液(KCCM),并以不同浓度、不同培养时间的CCl4损伤的KCCM作为刺激因素观察了A771726对HSC增殖(3H-TdR掺入法)和胶原合成(3H-Pro掺入法)的影响.ELISA法测定KCCM内TGF-β、TNF-α和IL-1含量.结果:HSC和Kupffer细胞得到较好的分离.CCl4损伤的KCCM显著增加HSC增殖和胶原合成,并且稀释度为1:2的KCCM在培养7 d时,对HSC增殖和胶原合成的刺激作用明显.A771726(0.001~10 μmol/L)对CCl4损伤的KCCM刺激HSC增殖和胶原合成有不同程度的抑制作用,并且A771726(0.001~10 μmol/L)明显抑制CCl4损伤KCCM内升高的TGF-β、TNF-α和IL-1水平.结论:CCl4损伤的KCCM可明显刺激HSC增殖和胶原合成,而A771726对此有明显的抑制作用,并且与其抑制致HSC激活的因子如TGF-β、TNF-α和IL-1分泌有关. 相似文献
16.
Effect of angiotensin Ⅱ and angiotensin Ⅱ type 1 receptor antagonist on the proliferation,contraction and collagen synthesis in rat hepatic stellate cells 总被引:11,自引:0,他引:11
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 相似文献
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 相似文献
17.
目的 观察川芎嗪对内毒素刺激的大鼠肝星状细胞(HSC)增殖和胶原表达的影响,探讨川芎嗪抗肝纤维化的作用机制.方法 于内毒素中刺激大鼠HSC的基础上加川芎嗪分组培养;并采用MTT法检测川芎嗪对HSC生长增殖的抑制作用,免疫细胞化学染色法观察HSC α-平滑肌肌动蛋白(α-SMA)的表达,同时采用ELISA法检测其上清液Ⅰ、Ⅲ型胶原水平.结果 川芎嗪对内毒素刺激的HSC增殖有抑制作用,能下调活化HSC α-SMA的表达,对HSC Ⅰ、Ⅲ型胶原的分泌也有明显抑制作用,并呈剂量依赖性.结论 川芎嗪能抑制内毒素刺激的HSC活化增殖和分泌胶原,为探索川芎嗪抗肝纤维化的分子机制提供了实验依据. 相似文献
18.
阿魏酸钠干预雷公藤多甙致小鼠肝损伤 总被引:6,自引:0,他引:6
目的:建立雷公藤多甙致小鼠肝损伤模型,研究阿魏酸钠对其所致肝损伤的影响。方法:以血清ALT、AST和肝脏指数为指标,建立雷公藤多甙致小鼠肝损伤模型,并观察阿魏酸钠对其损伤的影响。结果:雷公藤多甙1.8 g/(kg.d)连续处理小鼠6 d,血清ALT及肝指数均明显增高(P<0.01);于雷公藤多甙处理前3 d,连续给予阿魏酸钠[150 mg/(kg.d)×9 d]能明显降低ALT(P<0.05)和AST活性(P<0.01)。结论:阿魏酸钠对雷公藤多甙致小鼠肝损伤具有保护作用。 相似文献
19.
阿魏酸钠对动脉粥样硬化鹌鹑血中NO、LPO及SOD生成的影响 总被引:4,自引:0,他引:4
目的 :观察阿魏酸钠对实验性动脉粥样硬化鹌鹑血中一氧化氮 (NO)、脂质过氧化物 (LPO)水平及超氧化物歧化酶 (SOD)活性的影响。方法 :实验分为正常对照组、高脂组和高脂 +阿魏酸钠组 ,9周后分别测定各组血浆中总胆固醇 (T ch)、NO和LPO含量及红细胞SOD比活性。结果 :高脂组与正常组相比 ,血浆T ch及LPO含量显著升高 (P均 <0 .0 1) ,血浆NO含量和红细胞SOD比活性明显降低 (P均 <0 .0 1) ;而阿魏酸钠有显著降低实验性动脉粥样硬化鹌鹑血浆T ch和LPO水平、升高血浆NO含量和红细胞SOD比活性的作用。结论 :阿魏酸钠有清除自由基和减轻膜脂质过氧化的作用 相似文献
20.
Xiang Gao Kun Liu Jinping Liu Yanfu Wang Changwei Zhang Zhijian Chen Qiutang Zeng Yuhua Liao 《南京医科大学学报(英文版)》2008,22(1):1-4
Objective To study the effects of sodium ferulate on the ultrarapid delayed rectifier K current(Ikur) in human atrial myocytes.MethodsHuman atrial myocytes were isolated by enzyme dispersion method. Ikur in human atrial myocytes were recorded by using the whole cell patch clamp. The changes of Ikur were compared in the absence and the presence of sodium ferulate. ResultsThere was no effect of 0.4 g/L sodium ferulate on I-V relation of Ikur However, 0.4 g/L sodium ferulate inhibited Ikur to some degrees at each test pulse. The current densities of Ikur at 60 mV decreased from 4.997 ± 0.35 PA/PF to 3.331 ± 0.26 PA/PF(n = 6, P < 0.05). The inhibitory effect was concentration-dependent. IC50 was(0.41 ± 0.03)g/L and the Hill coefficient was 0.95 ± 0.05. ConclusionSodium ferulate as a potassium channel blocker can inhibit Ikur in human atrial myocytes effectively. 相似文献