三氧化二砷对HepG2细胞表达基因调节作用

目的 应用基因芯片技术，阐明低剂量三氧化二砷作用于肝HepG2细胞之后，无机砷对差异表达基因的调节作用。方法 应用基因表达谱芯片技术，对5μmol／L三氧化二砷诱导的HepG2细胞和以生理盐水处理的相同细胞的mRNA进行差异显示分析，研究三氧化二砷诱导人HepG2细胞后的差异表达基因。结果 HepG2细胞经5μool／L三氧化二砷诱导后。所检测的4096条目的基因中有123条产生差异表达，其中48条基因表达上调，75条基因表达下调。结论 应用基因表达谱芯片成功筛选了低剂量三氧化二砷诱导肝细胞后的差异表达基因，无机砷对肝细胞有双向调节作用。     

Effects of arsenic trioxide on drug transporting molecules in multidrug resistance malignant neoplasma MR2 cell line

INTRODUCTIONIn recent ye ars, some studies have introducedAs2O3 into the treatment of acute promyelocyticleukemia (APL) with the complete clinical remission(CR) rate of 52.3￣93.7%[1,2]. Studies in vitro haveconfirmed that As2O3 can induce apoptosis of retinoicacid-resistant APL cell line[3]. As2O3 has been also ap-plied in the treatment for refractory primary hepaticcancer [4] with satisfactory result [5]. The drug resis-tance of tumor is correlated with the drug transport-ing molec…     

Mechanism of Arsenic Trioxide Inhibiting Angiogenesis in Multiple Myeloma

Duringthelast decade,the efficacy of arsenic tri-oxide(As2O3)in both newly diagnosed and relapsedpatients with acute promyelocytic leukemia(APL)hasbeen established.And now,As2O3is used with otheragentsintreating patients with relapsed and refractorymultiple myeloma(MM)in clinical practice[1].Theinitial researches demonstratedthat As2O3couldinhibitproliferation andinduce apoptosisin MMcellsin vitroandin vivo[2,3].In addition to affecting tumorgrowth,As2O3has been showntoinhibit angiogenes…     

化妆品中新银盐法测定砷的问题研究

目的：通过对聚乙烯醇-硝酸银-乙醇分光光度法测定化妆品中砷的存在问题的实验研究分析，完善国家卫生规范检验方法。方法：消化处理后样品中的五价砷在碘化钾和氯化亚锡的作用下还原为三价砷经聚乙烯醇-硝酸银-乙醇溶液吸收形成黄色胶态银，比色测定。对不同室温下的标准系列的显色数据进行了方差分析。结果：不同室温下混合吸收液对同一含量的砷氢的吸收显色存在的差异有统计学意义（P〈0．01）。结论：作为国家的卫生规范检验方法，聚乙烯醇＋硝酸银＋乙醇混合吸收分光光度法存在缺陷，为此建议增加相应的实验必要条件。     

三氧化二砷诱导尤文肉瘤细胞凋亡及对EWS—FLil融合蛋白的影响

目的：探讨三氧化二砷（Arsenic trioxide，As2O3）诱导尤文肉瘤细胞凋亡及对融合蛋白EWS—FLi1表达的影响，．方法：应用噻唑蓝（MTF）法、形态学观察、原位末端标记法（TUNEL）、流式细胞术（FCM）观察As2O3对体外生长的尤文肉瘤RD—ES细胞系生物行为的影响：应用半定量RT—PCR测定应用As2O3前后c—mye基因mRNA水平的变化；应用免疫细胞化学及固定化蛋白印迹法（Western blot）观察用药前后EWS—FLi1融合蛋白表达水平的变化、结果：As2O3对体外生长的RD—ES细胞系具有明显抑制作用，并可诱导细胞凋亡、c-mye基因mRNA表达水平和EWS—FLil融合蛋白表达量随As2O3作用时间延长逐渐降低结论：常规治疗浓度的As2O3对体外生长的尤文肉瘤细胞具有明显的杀伤作用，其作用机制与改变线粒体膜通透性和抑制EWS—Flil融合蛋白、降低c一myc基因表达有关。     

The Synergistic Inhibitory Effect of STI571 in Combination with Arsenic Trioxide (As2O3) on Multidrug-Resistant Leukemic Cells

OBJECTIVE To study the synergistic effect of STI571, an inhibitor of tyrosine kinase, in combination with arsenic trioxide As2O3 on a multidrug-resistant leukemia cell line expressing bcr-abl.METHODS The cytotoxic effect of STI571 alone or in combination with different concentrations of As2O3 on the bcr-abl and mdr1 -positive leukemia cell line, K562-n/VCR, was examined by the MTT method.RESULTS One μmol/L of STI571 alone had no significant cytotoxic effect on K562-n/VCR cells. However the cytotoxic effect increased markedly when combined with As2O3 at concentrations of 10-5, 10-6, 10-7 and 10-8 mol/L. The IC50 of K562-n/VCR cells in As2O3 group was 1.879 μmol/L, with. Upon addition of STI571, the IC50 decreased to 0.155 μmol/L resulting in a synergistic cytotoxic effect on K562-n/VCR ceils that was increased 12.1 times.CONCLUSION A combination of STI571 with As2O3 has a more powerful inhibitory effect on leukemia cells expressing positive bcr-abl and positive mdrl compared to the effect with As2O3 alone.     

砒石对哮喘小鼠气道壁厚度及c-myc与c-sis表达的影响

气道重构是哮喘的主要病理特征之一,平滑肌细胞(SMC)、成纤维细胞(FB)是气道粘膜下的主要结构细胞,具有合成和降解细胞外基质(ECM)的双重功能,其大量增殖引起ECM大量沉积,是引起基底膜增厚、导致气道重构的关键因素.近年来研究发现,c-myc 、 c-sis与SMC、FB增殖密切相关,三氧化二砷能抑制哮喘豚鼠的气道炎症.本研究通过建立小鼠哮喘模型,探讨c-myc、c-sis在哮喘气道重构中的作用及砒石对它们的影响,进一步探讨砒石治疗哮喘的可能机制,为哮喘的防治开辟新途径提供理论依据.     

救急行军散中雄黄的含量测定

目的:建立救急行军散中雄黄的含量测定方法.方法:采用分光光度法对散剂中雄黄所含有的砷进行定量分析.结果:砷的线性范围为2.5～22.5μg,r=0.9995,平均回收率为100.1%,RSD为1.0%.结论:方法简便可行、重线性好,适用于该制剂的质量控制.     

Arsenic-induced hepatic mitochondrial toxicity in rats and its amelioration by diallyl trisulfide

The present investigation was aimed to investigate the possible protective role of diallyl trisulfide (DATS) against arsenic (As)-induced hepatic mitochondrial toxicity in rats. Mitochondria were isolated from the liver tissue of rats from all the groups. Lipid profile, lipid peroxidation, antioxidant enzyme activities, hepatic function enzymes, mitochondrial swelling, cytochrome c oxidase activity, mitochondrial Ca⁺-ATPase and Na⁺/K⁺-ATPase activity, mitochondrial calcium content and mitochondrial enzyme activities were measured. Short-term As exposure (5?mg/kg?bw/d for 28?d) caused liver damage as evidenced by changes in activities of liver enzymes. The effects of As were coupled with enhanced reactive oxygen species generation, mitochondrial swelling, inhibition of cytochrome c oxidase, complex I-mediated electron transfer, decreased Ca²⁺-ATPase and Na⁺/K⁺-ATPase activity, a reduction in mitochondrial calcium content, changes in indices of hepatic mitochondrial oxidative stress, significant increase in mitochondrial lipid peroxidation products and alterations in mitochondrial lipid profile. Significant decreases in mitochondrial antioxidants and tricarboxylic acid cycle enzymes were also found in the liver mitochondria of As-induced hepatic mitochondrial toxicity in rats. As also increased hepatic caspase-3 activity and DNA fragmentation. All these apoptosis-related molecular changes caused by As could be alleviated by supplementation with DATS, which likely suggests a protective role against As-induced hepatotoxic changes and hepatic mitochondrial toxicity. The protective effect of DATS on the liver mitochondria was evidenced by altering all the changes induced by As. Free radical scavenging and metal chelating activities of DATS may be the mechanism, responsible for the protective action against As-induced mitochondrial damage in liver.