树突状细胞与细胞因子诱导的杀伤细胞治疗急性白血病效果观察

目的:探讨树突状细胞(DC)与细胞因子诱导的杀伤(CIK)细胞联合治疗急性白血病的临床效果.方法:选择12例确诊的急性白血病患者(包括6例难治性急性白血病),将培养后的DC与CIK回输及行淋巴结区皮下注射,监测治疗前后的效果.结果:DC与CIK治疗过程中不良反应较小,所有患者均能耐受,治疗前后复查骨髓象,共3例获得完全缓解(3/12),其中1例从难治性白血病(1/6)获得完全缓解,骨髓中原始幼稚细胞比例下降者共6例(6/12),3例无效(3/12).结论:DC与CIK联合治疗急性白血病安全有效,为急性白血病提供了一种新的有效的免疫治疗手段,具有潜在的临床应用前景.     

树突状细胞与细胞因子诱导的杀伤细胞治疗急性白血病效果观察

目的:探讨树突状细胞(DC)与细胞因子诱导的杀伤(CIK)细胞联合治疗急性白血病的临床效果.方法:选择12例确诊的急性白血病患者(包括6例难治性急性白血病),将培养后的DC与CIK回输及行淋巴结区皮下注射,监测治疗前后的效果.结果:DC与CIK治疗过程中不良反应较小,所有患者均能耐受,治疗前后复查骨髓象,共3例获得完全缓解(3/12),其中1例从难治性白血病(1/6)获得完全缓解,骨髓中原始幼稚细胞比例下降者共6例(6/12),3例无效(3/12).结论:DC与CIK联合治疗急性白血病安全有效,为急性白血病提供了一种新的有效的免疫治疗手段,具有潜在的临床应用前景.     

参附注射液对大肠癌患者化疗后免疫功能的影响

目的:探讨参附注射液对大肠癌患者化疗后免疫功能的影响。方法:将符合条件的246例大肠癌患者随机分为单纯化疗组(对照组)、低剂量组和高剂量组,除常规化疗外,低剂量组和高剂量组分别静脉滴注参附注射液30、60mL·d-1,各组均行4周期化疗,检测化疗后各组免疫指标的变化情况。结果:从第2～4周期,免疫功能指标低剂量组较对照组无明显变化;高剂量组较对照组明显升高,且差异有逐渐增大的趋势。结论:参附注射液可减轻肿瘤化疗药物对骨髓的抑制,有效改善机体的免疫功能。     

参附注射液联合米托蒽醌为主的化疗治疗急性粒细胞白血病的临床分析

目的 探究参附注射液联合米托蒽醌为主的化疗治疗急性粒细胞白血病的有效性及安全性.方法 常规化疗组急性粒细胞白血病患者采用以米托蒽醌为主的MA方案,静脉滴注米托蒽醌10mg/ （m2·d）,第1～3d,阿糖胞苷100mg/ （m2·d）,连续滴注第1～7d.参附注射液组患者在上述MA化疗方案的基础上加滴参附注射液60 ml/d,连续滴注第1～ 14d.结果 参附注射液组患者化疗过程中的不良反应情况较轻.参附注射液组患者经治疗后WBC、Hb和PLT值均显著高于常规化疗组患者（P＜0.05）.治疗后参附注射液组患者的CD4、CD8和CD4/CD8值均明显高于常规化疗组患者（P＜0.05）.结论 参附注射液联合米托蒽醌为主的化疗对于急性髓系白血病患者的治疗具有显著减少患者不良反应、减轻化疗毒副作用、提高患者免疫力、增强疗效等优点,值得临床应用.     

生长抑素联合参附注射液治疗胆源性急性胰腺炎的临床观察

目的:观察生长抑素联合参附注射液治疗胆源性急性胰腺炎的疗效及安全性。方法:64例胆源性急性胰腺炎患者,按随机数字表法均分为对照组和研究组。两组患者均给予常规治疗,在此基础上对照组患者给予注射用生长抑素0.25 mg加入5%葡萄糖注射液250 ml中静脉滴注,qd;研究组患者在对照组治疗的基础上给予参附注射液60 ml加入5%葡萄糖注射液250 ml中静脉滴注,qd。两组患者疗程均为两周,治疗期间每日均测血淀粉酶值,待血淀粉酶值恢复正常后停止治疗,治疗结束时未恢复正常者继续治疗。观察两组患者治疗后的C反应蛋白(CRP)、内皮素(ET)-1、肿瘤坏死因子(TNF)-α、血淀粉酶指标水平,记录治愈患者血淀粉酶、血糖、血钙、白细胞恢复正常的时间,比较两组患者的临床疗效;观察两组患者胰腺假性囊肿、胰周脓肿、急性呼吸窘迫综合征、急性肾功能衰竭、心律不齐等并发症发生率及不良反应发生率。结果:研究组患者总有效率显著高于对照组,两组比较差异有统计学意义(P<0.05);研究组患者CRP、ET-1、TNF-α、血淀粉酶水平及血淀粉酶、血糖、血钙、白细胞恢复正常时间均显著优于对照组,两组比较差异均有统计学意义(P<0.05);除急性肾功能衰竭及心律不齐外,研究组患者胰腺假性囊肿、胰周脓肿、急性呼吸窘迫综合征发生率均显著低于对照组,两组比较差异均有统计学意义(P<0.05);两组患者不良反应发生率比较差异无统计学意义(P>0.05)。结论:生长抑素联合参附注射液治疗胆源性急性胰腺炎可以明显改善胰腺功能,疗效显著,且安全性较好。     

参附注射液对肾前性急性肾衰竭的保护作用

目的探讨参附注射液对肾前性急性肾衰竭的保护作用。方法82例肾前性急性肾衰竭患者被随机分为两组。对照组45例主要给予纠正低血容量等治疗。治疗组37例在纠正低血容量等治疗基础上给予参附注射液治疗。分别比较两组治疗前后收缩压及舒张压、血尿素氮及血肌酐、进入维持血液透析的比率以及死亡率。结果两组患者治疗后收缩压及舒张压均有显著增高（P〈0．01）,血尿素氮及血肌酐均有显著下降（P〈0．01）。治疗组收缩压及舒张压治疗后较对照组均有显著提高（P〈0．01）,血尿素氮及血肌酐较对照组均明显下降（P〈0．01）,两组进入维持血液透析的比率及死亡率差异无统计学意义（P〉0．05）。结论参附注射液对于肾前性急性肾衰竭患者具有保护作用。     

参附注射液对肺癌患者围手术期免疫功能的调节作用

目的研究肺癌患者围手术期免疫功能情况及参附注射液的调节作用。方法 32例肺癌患者根据病理学结果随机分为治疗组和对照组 ,治疗组患者从手术前 3天到术后 14天 ,每天静脉滴注参附注射液 5 0ml,手术过程中静脉滴注 5 0ml;对照组除不用参附注射液外 ,其它条件与治疗组相同。于术前、术毕、术后 3天、术后 14天抽取静脉血监测补体C3 、C4,免疫球蛋白IgG、IgA、IgM ,C反应蛋白 (CRR)和血常规。结果术后 3天、7天 ,治疗组患者血浆补体C3 、C4和C反应蛋白、白细胞总数明显低于对照组 (P <0 .0 5 ) ;而免疫球蛋白IgG、IgA、IgM则明显高于对照组 (P <0 0 5 ) ;中性粒细胞分类 (N % )两组无显著性差异 (P >0 0 5 )。结论参附注射液对肺癌患者围手术期免疫功能有较好的调节作用。     

急性髓细胞性白血病病人测定白血病原始祖细胞自我复制能力测定方法探讨

急性髓细胞性白血病病人的预后与其临床及生物学特性有关。测定病人白血病祖细胞自我复制能力可预测病人的预后，并可根据检测结果制定治疗方案。本报告通过实验说明白血病祖细胞自我复制能力低者预后较白血病祖细胞自我复制能力高者好。     

CD_7~+的急性髓细胞性白血病的临床意义

目的 :观察和探讨 CD7+ 的急性髓细胞性白血病 (AML )表达特征及它们对 AML患者预后的影响。方法 :采用间接免疫荧光法和流式细胞仪对 2 75例初诊的 AML患者进行了免疫表型检测 ,并对淋系分化抗原阳性表达率加髓系分化抗原阳性表达率大于 10 0 %患者的白血病细胞用流式细胞仪做双标记分析。结果 :2 75例 AML患者中 ,3 6例表达淋系分化抗原 CD7(占 13 .1% ) ;诱导化疗疗效方面 ,在同等化疗强度的基础上 ,CD34+ CD7+ AML患者的缓解率明显低于 CD34- CD7- AML 患者 (P<0 .0 5 )。结论 :CD7+ AML 的表达具有复杂性、异质性 ,属于一种预后不良的临床亚型 ,应进一步探索针对性的治疗策略     

姜黄素对马利兰耐药HL-60细胞生长的影响

目的探讨姜黄素对马利兰耐药HL-60细胞生长的影响。方法采用MTT法检测姜黄素对马利兰耐药HL-60细胞的抑制率并观察姜黄素与马利兰联用对HL-60马利兰耐药细胞的增敏作用。结果与对照组相比，姜黄素对马利兰耐药HL-60细胞的生长具有明显的抑制作用，24、48、72h的IC50分别为7．85、5．46、3．94（μg／ml），呈时间、浓度依赖性；姜黄素与马利兰联用对HL-60马利兰耐药细胞均有增敏作用。结论姜黄素对马利兰耐药HL-60细胞的生长具的明显抑制作用，且与马利兰无交叉耐药性，可作为白血病马利兰化疗的增敏剂。     

基泰体外对慢性乙型肝炎患者树突状细胞功能影响的初步研究

目的:探讨基泰对慢性乙型肝炎(简称慢乙肝)患者(chronic hepatitis B,CHB)树突状细胞(dentritic cell,DC)生物学性状的影响.方法:分离慢乙肝患者外周血单核细胞,在含GM-CSF/IL-4及不同浓度的基泰培养条件下制备DC.观察DC形态学变化,流式细胞仪(FCM)测其细胞表型分子CD1a,CD83,CD80及HLA-DR的表达,MTT法测定DC刺激同种异体淋巴细胞增殖能力.结果:与对照组相比,实验组倒置显微镜观察显示出典型的DC形态.基泰(100 μg/mL)处理组的DC膜表面分子CD1a及CD80表达均增高(P<0.05);刺激同种异体淋巴细胞增殖能力(SI)增强(P<0.05).结论:基泰一定程度上可改善CHB的DC免疫学活性.     

槲皮素对HL-60细胞周期的影响

本文报道了槲皮素对人早幼粒白血病细胞株HL-60细胞的增殖和细胞周期的影响. 结果表明槲皮素能抑制HL-60细胞的增殖， 呈剂量依赖关系， 当槲皮素作用24， 48， 72 h后， 其IC₅₀分别为 46.6, 28.7, 14.9 μmol·L^-1流式细胞仪分析表明，槲皮素能明显增加HL-60的G₂-M期细胞，而相对减少G₀/G₁细胞之百分比，且呈剂量依赖关系，当去除槲皮素时，该作用是可逆的. 结果表明槲皮素对肿瘤细胞的生长抑制作用可能与其对细胞周期的影响有关.     

Effect of quercetin on cell cycle of HL-60 cells

本文报道了槲皮素对人早幼粒白血病细胞株ＨＬ－６０细胞的增殖和细胞周期的影响．结果表明槲皮素能抑制ＨＬ－６０细胞的增殖，呈剂量依赖关系，当槲皮素作用２４，４８，７２ｈ后，其ＩＣ５０分别为４６．６，２８．７，１４．９μｍｏｌ·Ｌ－１．流式细胞仪分析表明，槲皮素能明显增加ＨＬ－６０的Ｇ２－Ｍ期细胞，而相对减少Ｇ０／Ｇ１细胞之百分比，且呈剂量依赖关系，当去除槲皮素时，该作用是可逆的．结果表明槲皮素对肿瘤细胞的生长抑制作用可能与其对细胞周期的影响有关．     

Regulation on maturation and function of dendritic cells by Astragalus mongholicus polysaccharides

Astragalus mongholicus polysaccharides(ASP) isolated from one of the Chinese herbs-A. mongholicus which are known to have a variety of immunomodulatory activity. However, little is known about their immunomodulatory effects on murine bone marrow (BM)-derived dendritic cells (DC). DC are professional antigen presenting cells, which are pivotal for initiation of primary immune response. In this study, the regulatory effects of ASP on maturation and function of cultured murine BM-derived DC were investigated in vitro. ASP (10, 50, 100, 250 microg/ml) could increase the co-expression of CD-11c and MHC class II molecules on DC surface, and the 100 microg/ml is the optimal dose. The ability of unstimulated DC to uptake FITC-dextran was higher than that of ASP- or LPS-treated DC. We analyzed the concentration of IL-12 secreted by DC using ELISA. ASP-treated DC secreted a higher level of IL-12 than untreated DC. And ASP- or LPS-treated DC displayed a more mature morphology, with long protrusions, while untreated-DC displayed shorter protrusions than stimulated DC.     

Paeoniflorin inhibits the maturation and immunostimulatory function of allergen-induced murine dendritic cells

Dendritic cells (DCs) as the front lines of defense play a crucial role in allergic contact dermatitis (ACD). Paeoniflorin (PF) has been clinically proven to be effective in the treatment of inflammatory skin diseases such as ACD. However, the mechanisms underlying the anti-inflammatory effect of PF remain unclear. The aim of this study was to explore the effect of PF on the maturation and immunostimulatory function of DCs in the murine model of ACD in vitro. Murine bone marrow-derived DCs were stimulated with the contact sensitizer 1-chloro-2, 4-dinitrobenze (DNCB) in vitro. Surface antigen expression of DCs (MHC II, CD40, CD80, and CD86), as an indicator of maturation DCs and cytokines (IL-12, IFN-γ, IL-10, and TGF-β) after DNCB stimulation in the absence or presence of PF at different doses, was detected. Then, we detected that PF-treated DCs stimulated T cells in response to DNCB. PF inhibited the up-regulation of MHC II, CD80, CD86, and CD40, decreased IL-12p70 secretion, while increased the production of IL-10 and TGF-β, and had no effect on IFN-γ cytokine production by murine bone marrow-derived DCs in response to DNCB. DCs exposed to PF had diminished capacity to stimulate allogeneic T cell proliferation and to activate IFN-γ-producing CD4⁺ T cells and induced CD4⁺CD25⁺Foxp3⁺ T cells and IL-10-producing T cell expansion from naïve CD4⁺ T cells. These results indicate that PF may be effective in preventing and treating ACD in vitro and other inflammatory responses possibly through inhibiting maturation of DCs and limiting their capacity to stimulate T cell responses.     

Triptolide affects the differentiation, maturation and function of human dendritic cells

Triptolide is a purified component from a traditional Chinese herb Tripterygium wilfordii Hook F. It has been shown to have anti-inflammatory and immunosuppressive activities by its inhibitory effect on T cells. But the effect of triptolide on dendritic cells (DC) is unknown. Dexamethasone (Dex) is a classic immunosuppressive agent known to suppress the immune response at different levels and has recently found to modulate the development of DC, thereby influencing the initiation of the immune response. In this study, we investigated the affect of triptolide on the differentiation, maturation and function of DC differentiated from human monocytes (MoDC) in vitro in the presence of GM-CSF and IL-4. Dex was included in the study as a reference. Our data show that both triptolide and Dex prevented the differentiation in immature MoDC by inhibiting CD1a, CD40, CD80, CD86 and HLA-DR expression but upregulating CD14 expression, as well as by reducing the capacity of MoDC to stimulate lymphocyte proliferation in the allogeneic mixed lymphocyte reaction. They blocked the maturation of MoDC as totally blocked induction of CD83 expression and absent upregulation of CD40, CD80, CD86 and HLA-DR. In addition, higher concentration of triptolide (20 ng/ml) and 10(-6) M Dex induced apoptosis in MoDC as measured by expression of APO2*7 and DNA fragmentation (TUNEL assay). However, the phagocytic capacity of MoDC was enhanced by triptolide but not Dex. Therefore, the suppression of DC differentiation, the function in immature DCs as well as the inhibition of DC maturation by triptolide may explain some of its immunosuppressive properties. It is suggested that DCs are a primary target of the immunosuppressive activity of triptolide.     

槲皮素单硫酸酯钠对 HL-60细胞生长的影响(英文)

通过观察槲皮素单硫酸酯钠 (SQMS)对 HL-60细胞毒作用 ,细胞周期变化 ,胞内 Ca2 +浓度([Ca2 +]i)变化及蛋白激酶 CK2活性的变化研究SQMS对 HL- 60细胞生长的影响 .发现 SQMS(2 0- 1 2 0μmol· L-1)可浓度依赖性抑制 HL- 60细胞的生长 ,阻断 HL- 60细胞于 G0 /G1期 ;SQMS(1 0 0μmol· L-1)可使 [Ca2 +]i 由 (1 0 5± 9) nmol·L-1上升到 (2 0 1± 1 3) nmol· L-1;低浓度 SQMS(0 .55-8.8μmol· L-1)可显著抑制从 HL- 60细胞中纯化的蛋白激酶 CK2的活性 .结果提示 ,SQMS可抑制HL- 60细胞生长 ,其机理可能与抑制 HL- 60细胞中蛋白激酶 CK2的活性 ,提高细胞 [Ca2 +]i 及促进细胞分化有关 .     

Antioxidant and antiapoptotic function of metallothioneins in HL-60 cells challenged with copper nitrilotriacetate

Antioxidant activity is believed to be an important intracellular function of metallothioneins (MT), yet the specific mechanisms of their antioxidant action are not known. Under conditions when cells are challenged with elevated concentrations of free copper as a result of metabolic disturbances or environmental and occupational exposures, MTs may be ideally suited for antioxidant function as effective copper chelators. In the study presented here, we tested this hypothesis using a recently established model of copper nitrilotriacetate-induced oxidative stress in HL-60 cells. Since copper-induced oxidative stress triggers apoptosis, we further investigated antiapoptotic function of MTs in HL-60 cells. Using a Sephadex G-75 chromatographic partial purification of MTs from cell homogenates with subsequent immuno-dot-blot assay, we showed that zinc pretreatment yielded a pronounced induction of MTs in HL-60 cells. We report that zinc-induced MTs were able to (i) completely bind intracellular copper, (ii) completely quench redox-cycling activity of copper, (iii) significantly inhibit copper-dependent oxidative stress in membrane phospholipids, and (iv) prevent copper-dependent apoptosis and its characteristic biochemical features (cytochrome c release from mitochondria into cytosol, caspase-3 activation, and externalization of phosphatidylserine in plasma membranes). In separate experiments, we used lung fibroblasts derived from MT1, MT2 knockout mice (MT(-)(/)(-)) and MT wild-type (MT(+/+)) mice. ZnCl(2) pretreatment resulted in a more than 10-fold induction of MTs in MT(+/+) cells, whereas the MT content in MT(-)(/)(-) cells remained low, at levels approximately 100-fold lower than in their MT wild-type counterparts. MT(-)(/)(-) cells were very sensitive to Cu-NTA and, most importantly, showed no response to ZnCl(2) pretreatment. In contrast, MT(+/+) cells were relatively more resistant to Cu-NTA, and this resistance was remarkably enhanced by ZnCl(2) pretreatment. Combined, our results demonstrate that metallothioneins function as effective antioxidants and an antiapoptotic mechanism in copper-challenged HL-60 cells.