AIM To investigate the mechanisms ofsalvianolic acid A（SA-A）against liver fibrosisin vitro.METHODS NIH/3T3 fibroblasts were culturedroutinely,and incubated with 10<sup>-4</sup>mol/L-10<sup>-7</s...AIM To investigate the mechanisms ofsalvianolic acid A（SA-A）against liver fibrosisin vitro.METHODS NIH/3T3 fibroblasts were culturedroutinely,and incubated with 10<sup>-4</sup>mol/L-10<sup>-7</sup>mol/L SA-A for 22 h.The cell viability wasassayed by[<sup>3</sup>H]proline incorporation,cellproliferation by[<sup>3</sup>H]TdR incorporation,cellcollagen synthetic rate was measured with[<sup>3</sup>H]proline impulse and collagenase digestionmethod.The total RNA was prepared from thecontrol cells and the drug treated cellsrespectively,and α（1）I pro-collagen mRNAexpression was semi-quantitatively analyzedwith RT-PCR.RESULTS 10<sup>-4</sup>mol/L SA-A decreased cellviability and exerted some cytotoxiciy,while10<sup>-5</sup>mol/L-10<sup>-7</sup>mol/L SA-A did not affect cellviability,but inhibited cell proliferationsignificantly,and 10<sup>-6</sup>mol/L SA-A had the besteffect on cell viability among theseconcentrations of drugs.10<sup>-5</sup>mol/L-10<sup>-6</sup>mol/LSA-A inhibited intracellular collagen syntheticrate,but no significant influence on extracellularcollagen secretion.Both 10<sup>-5</sup>mol/L and10<sup>-6</sup>mol/L SA-A could decrease α（1）I pro-collagen mRNA expression remarkably.CONCLUSION SA-A had potent action againstliver fibrosis.It inhibited NIH/3T3 fibroblastproliferation,intracellular collagen syntheticrate and type I pro-collagen gene expression,which may be one of the main mechanisms of thedrug.展开更多
目的探讨1 800MHz电磁辐射对NIH/3T3细胞周期和凋亡的影响。方法将NIH/3T3细胞假暴露或间断暴露（5min开,10min关）在比吸收率（specific absorption rate,SAR）为2 W/kg,模拟全球移动通信系统（global system for mobile communication...目的探讨1 800MHz电磁辐射对NIH/3T3细胞周期和凋亡的影响。方法将NIH/3T3细胞假暴露或间断暴露（5min开,10min关）在比吸收率（specific absorption rate,SAR）为2 W/kg,模拟全球移动通信系统（global system for mobile communications,GSM）通话状态信号的1 800MHz电磁场中。每天暴露5h,连续60d,期间每3~4d传代一次。暴露完毕后,用Cell Counting Kit-8（CCK-8）检测细胞活性;染色后用流式细胞仪检测细胞凋亡、细胞周期的变化;用Caspase-3活性检测试剂盒检测细胞凋亡因子Caspase-3的活性变化。结果与假暴露组相比,暴露组细胞活力下降且培养96h后明显下降（t=30.78,P=0.048）;暴露组细胞处于S期（t=3.267,P=0.022）和G2期（t=3.844,P=0.022 9）的百分数较假暴露组有明显增加;细胞凋亡率明显增加（t=3.349,P=0.047）,Caspase-3活性增高（t=13.593,P=0.013）。结论 NIH/3T3细胞经60d1 800MHz模拟手机电磁辐射后,细胞活性下降,S期和G2期阻滞,同时细胞凋亡率增加。展开更多
目的观察金钱鱼凋亡相关基因SaAR(Scatophagusargusapoptosis related gene)对成纤维细胞增殖的影响。方法体外培养NIH-3T3细胞,应用脂质体将不同浓度的pcDNA3-SaAR真核表达质粒分别转染细胞并设立对照组进行比较,应用流式细胞术测定细...目的观察金钱鱼凋亡相关基因SaAR(Scatophagusargusapoptosis related gene)对成纤维细胞增殖的影响。方法体外培养NIH-3T3细胞,应用脂质体将不同浓度的pcDNA3-SaAR真核表达质粒分别转染细胞并设立对照组进行比较,应用流式细胞术测定细胞凋亡率。结果SaAR基因可显著诱导NIH-3T3细胞凋亡,并呈现剂量依赖性(P<0.05)。结论SaAR基因对体外培养的血管外膜成纤维细胞凋亡有一定的诱导作用。展开更多
文摘AIM To investigate the mechanisms ofsalvianolic acid A（SA-A）against liver fibrosisin vitro.METHODS NIH/3T3 fibroblasts were culturedroutinely,and incubated with 10<sup>-4</sup>mol/L-10<sup>-7</sup>mol/L SA-A for 22 h.The cell viability wasassayed by[<sup>3</sup>H]proline incorporation,cellproliferation by[<sup>3</sup>H]TdR incorporation,cellcollagen synthetic rate was measured with[<sup>3</sup>H]proline impulse and collagenase digestionmethod.The total RNA was prepared from thecontrol cells and the drug treated cellsrespectively,and α（1）I pro-collagen mRNAexpression was semi-quantitatively analyzedwith RT-PCR.RESULTS 10<sup>-4</sup>mol/L SA-A decreased cellviability and exerted some cytotoxiciy,while10<sup>-5</sup>mol/L-10<sup>-7</sup>mol/L SA-A did not affect cellviability,but inhibited cell proliferationsignificantly,and 10<sup>-6</sup>mol/L SA-A had the besteffect on cell viability among theseconcentrations of drugs.10<sup>-5</sup>mol/L-10<sup>-6</sup>mol/LSA-A inhibited intracellular collagen syntheticrate,but no significant influence on extracellularcollagen secretion.Both 10<sup>-5</sup>mol/L and10<sup>-6</sup>mol/L SA-A could decrease α（1）I pro-collagen mRNA expression remarkably.CONCLUSION SA-A had potent action againstliver fibrosis.It inhibited NIH/3T3 fibroblastproliferation,intracellular collagen syntheticrate and type I pro-collagen gene expression,which may be one of the main mechanisms of thedrug.
文摘目的探讨1 800MHz电磁辐射对NIH/3T3细胞周期和凋亡的影响。方法将NIH/3T3细胞假暴露或间断暴露（5min开,10min关）在比吸收率（specific absorption rate,SAR）为2 W/kg,模拟全球移动通信系统（global system for mobile communications,GSM）通话状态信号的1 800MHz电磁场中。每天暴露5h,连续60d,期间每3~4d传代一次。暴露完毕后,用Cell Counting Kit-8（CCK-8）检测细胞活性;染色后用流式细胞仪检测细胞凋亡、细胞周期的变化;用Caspase-3活性检测试剂盒检测细胞凋亡因子Caspase-3的活性变化。结果与假暴露组相比,暴露组细胞活力下降且培养96h后明显下降（t=30.78,P=0.048）;暴露组细胞处于S期（t=3.267,P=0.022）和G2期（t=3.844,P=0.022 9）的百分数较假暴露组有明显增加;细胞凋亡率明显增加（t=3.349,P=0.047）,Caspase-3活性增高（t=13.593,P=0.013）。结论 NIH/3T3细胞经60d1 800MHz模拟手机电磁辐射后,细胞活性下降,S期和G2期阻滞,同时细胞凋亡率增加。
文摘目的观察金钱鱼凋亡相关基因SaAR(Scatophagusargusapoptosis related gene)对成纤维细胞增殖的影响。方法体外培养NIH-3T3细胞,应用脂质体将不同浓度的pcDNA3-SaAR真核表达质粒分别转染细胞并设立对照组进行比较,应用流式细胞术测定细胞凋亡率。结果SaAR基因可显著诱导NIH-3T3细胞凋亡,并呈现剂量依赖性(P<0.05)。结论SaAR基因对体外培养的血管外膜成纤维细胞凋亡有一定的诱导作用。
