重楼皂苷Ⅰ对人卵巢癌细胞株体外生物学效应的影响

目的探讨重楼皂苷Ⅰ(P-Ⅰ)作用于人卵巢癌细胞株SKOV3的体外生物学效应。方法不同浓度的P-Ⅰ作用于SKOV3细胞的不同时间后,观察细胞的体外增殖情况和细胞周期的变化以及细胞的凋亡过程;所使用的检测和观察方法有CCK-8比色法、流式细胞术检测、ROS检测法。结果 P-Ⅰ给药浓度在1.0~5.0μg/ml范围内时,细胞增殖抑制率随药物浓度增加而明显增加(P<0.05),当P-Ⅰ浓度在1.0~3.0μg/ml时,同一药物浓度,细胞增殖抑制率随用药时间延长而显著增加,但P-Ⅰ浓度为4.0~5.0μg/ml时,细胞增殖抑制率随用药时间延长增加不明显。结论 P-Ⅰ对SKOV3细胞有显著的生物学作用,抑制体外癌细胞增殖、干扰细胞分裂、诱导癌细胞凋亡。     

药食植物提取物影响肺癌细胞YTMLC-90生长的血清药理学研究

目的在营养领域内建立血清药理学方法,为评价药食植物的防癌效果提供一种新技术;同时观察药食植物提取物(HFE)对肺癌细胞生长和增殖的作用,为预防癌症提供有效可行的营养措施。方法用正交设计探讨建立血清药理学方法的适宜条件;用MTT、群体倍增时间和集落形成实验研究含HFE动物血清对肺癌细胞生长和增殖的作用。结果针对HFE,在对小鼠每天灌胃2次、共连续灌胃3天、体外实验含药血清浓度10%的实验条件下,为建立血清药理学方法的较好条件。各浓度(0.5、1.0和2.0g/ml)的HFE对肺癌细胞的生长和增殖均有一定的抑制作用;高浓度组(HFE2.0g/ml)灌胃3日和低浓度组(HFE0.5g/ml)灌胃10日的抑制作用尤为明显,且二者作用无显著差异。结论用血清药理学方法能更直接深入地观察受试物的抑癌作用。药食植物对防癌抗癌有较好的效果,在长期防癌过程中有较好的实用价值。     

他克莫司在体外对HepG2细胞增殖及细胞周期的影响

目的研究他克莫司在体外对肝癌细胞HepG2的细胞增殖、细胞周期及细胞周期蛋白A(cyclin A)表达的生物学影响。方法选择肝癌细胞HepG2进行体外培养,经含有不同浓度的他克莫司(低、中和高浓度组剂量分别为50μg/L、100和500μg/L、1 000和3 000μg/L,对照组0μg/L)的培养基干预后,采用四甲基偶氮唑盐微量酶反应比色法(MTT)及流式细胞技术,分别检测细胞增殖、细胞周期及cyclin A水平。结果①中浓度(500μg/L)和高浓度(1 000和3 000μg/L)的他克莫司对HepG2细胞有增殖抑制作用,且抑制作用随浓度的增加而增加,而低浓度的他克莫司则无抑制作用。②他克莫司对HepG2细胞周期的影响:中浓度(500μg/L)和高浓度(1 000和3 000μg/L)的他克莫司作用时,HepG2细胞停止在G0/G1期,从而对肿瘤细胞的生长有抑制作用,且抑制作用随浓度的增加而增加,而低浓度的他克莫司则无抑制作用。③他克莫司可以降低HepG2细胞中cyclin A的表达,且与浓度相关,他克莫司浓度越高,cyclin A表达越少。结论他克莫司在体外对HepG2增殖有抑制作用,其中cyclin A发挥一定的作用。     

脱氧雪腐镰刀菌烯醇对小鼠成骨细胞Pax1表达的影响

目的探讨脱氧雪腐镰刀菌烯醇(DON)对小鼠成骨细胞骨骼发育相关基因Pax1表达的影响。方法麻醉后取胎鼠的顶骨,采用改良的组织块培养法体外培养小鼠成骨细胞,碱性磷酸酶法鉴定成骨细胞,将浓度为100、200、500、1000和1500mg/L的DON分别作用于对数生长期的成骨细胞,噻唑蓝(MTT)比色法检测DON对成骨细胞增殖的作用。半定量RT-PCR和Western blotting检测不同剂量DON对体外培养小鼠成骨细胞Pax1 mRNA和蛋白质表达的影响。结果培养的细胞鉴定为成骨细胞,不同浓度DON能降低小鼠成骨细胞的增殖速度,并可增加小鼠成骨细胞Pax1 mRNA和蛋白质表达,随着DON浓度增加,小鼠成骨细胞Pax1基因表达增多越显著。结论 DON促进小鼠成骨细胞Pax1基因的表达,进而影响骨骼的发育。     

脱氧雪腐镰刀菌烯醇对小鼠成骨细胞Pax1表达的影响北大核心CSCD

目的探讨脱氧雪腐镰刀菌烯醇(DON)对小鼠成骨细胞骨骼发育相关基因Pax1表达的影响。方法麻醉后取胎鼠的顶骨,采用改良的组织块培养法体外培养小鼠成骨细胞,碱性磷酸酶法鉴定成骨细胞,将浓度为100、200、500、1000和1500mg/L的DON分别作用于对数生长期的成骨细胞,噻唑蓝(MTT)比色法检测DON对成骨细胞增殖的作用。半定量RT-PCR和Western blotting检测不同剂量DON对体外培养小鼠成骨细胞Pax1 mRNA和蛋白质表达的影响。结果培养的细胞鉴定为成骨细胞,不同浓度DON能降低小鼠成骨细胞的增殖速度,并可增加小鼠成骨细胞Pax1 mRNA和蛋白质表达,随着DON浓度增加,小鼠成骨细胞Pax1基因表达增多越显著。结论 DON促进小鼠成骨细胞Pax1基因的表达,进而影响骨骼的发育。     

2种除草剂对小鼠骨髓细胞DNA损伤作用

目的 研究2种代表性除草剂二甲戊灵和烯草酮在体外、体内条件下对小鼠骨髓细胞DNA的损伤作用.方法 应用彗星实验检测不同浓度二甲戊灵和烯草酮对小鼠骨髓细胞DNA的损伤情况.结果 在体外实验中,二甲戊灵在10,20 mg/L浓度下与溶剂对照组比较差异有统计学意义(P<0.05,P<0.01);而烯草酮仅在高浓度(20mg/L)下与溶剂对照组比较差异有统计学意义(P<0.05);体内实验中,二甲戊灵500和1 000 mg/(kg·bw)与溶剂对照组比较差异有统计学意义(P<0.05,P<0.01);而烯草酮250～1 000 mg/(kg·bw)与溶剂对照组比较差异无统计学意义(P>0.05).结论 在体外和体内条件下,二甲戊灵均可明显造成小鼠骨髓细胞DNA的损伤;而烯草酮对小鼠骨髓细胞DNA损伤不构成明显的阳性反应.     

乙草胺和胺苯磺隆对小鼠骨髓细胞DNA损伤作用

目的 观察2种代表性除草剂(乙草胺和胺苯磺隆)对小鼠骨髓细胞DNA的损伤作用.方法 应用彗星实验检测在体外、体内2种条件下不同剂量的乙草胺和胺苯磺隆对小鼠骨髓细胞DNA的损伤作用.结果 体外给予5、10和20 mg/L乙草胺,小鼠骨髓细胞尾部DNA含量分别为(9.64±1.84)%、(23.67±4.5)%和(41.37±4.21)%,尾长分别为(8.80 ±2.57)、(34.90±6.33)和(44.70±7.64)px,尾矩分别为(0.95±0.24)、(5.76±1.12)和(24.82±3.22)TM,明显高于空白对照组,差异有统计学意义(P＜0.01);体内给予100、200和400 mg/kg乙草胺,小鼠骨髓细胞尾部DNA含量分别为(9.72±3.16)%、(23.51±3.60)和(29.63±4.07)%,尾长分别为(7.40±2.67)、(20.60±3.72)和(24.50±4.32)px,尾矩分别为(0.93±0.30)、(7.27±0.71)和(14.46±2.60)TM,明显高于空白对照组,差异有统计学意义(P＜0.01);体外、体内给予一定剂量的胺苯磺隆对小鼠骨髓细胞DNA无明显影响.结论 乙草胺对小鼠骨髓细胞DNA具有损伤作用,而胺苯磺隆对小鼠骨髓细胞DNA无明显影响.     

甲醛和甲苯联合染毒对小鼠骨髓细胞的遗传毒性研究

目的研究甲醛和甲苯联合吸入染毒对小鼠骨髓细胞的遗传毒性作用。方法 72只健康清洁级昆明纯系小鼠,雌雄各半,按3×3析因设计随机分为9组,每组8只,分别为:对照组(清洁空气),低甲醛(1 mg/m3)、高甲醛(5 mg/m3)剂量组,低甲苯(400 mg/m3)、高甲苯(2 000 mg/m3)剂量组,低甲醛+低甲苯(1 mg/m3+400 mg/m3)、低甲醛+高甲苯(1 mg/m3+2 000 mg/m3)、高甲醛+低甲苯(5 mg/m3+400 mg/m3)、高甲醛+高甲苯(5 mg/m3+2 000 mg/m3)剂量组。采用静式吸入染毒,每天2 h,连续14 d。染毒结束次日处死小鼠,采用微核试验和彗星试验检测甲醛和甲苯联合染毒致骨髓细胞的遗传毒性作用。结果微核试验结果显示,甲醛和甲苯致小鼠骨髓细胞微核的形成具有统计学意义(P0.05),且随着染毒浓度的增加微核率增大,二者在高浓度时微核率最高(33.83‰),甲醛和甲苯对小鼠骨髓细胞微核率的影响有交互作用(P0.05)。彗星试验结果显示,甲醛和甲苯对骨髓细胞彗星尾部DNA含量、彗星细胞尾矩形成均有影响(P0.05);二者联合染毒对小鼠骨髓彗星细胞尾部DNA含量、尾矩形成均有交互作用(P0.05)。结论甲醛和甲苯对小鼠骨髓细胞均有遗传损伤作用,二者联合吸入对小鼠骨髓细胞的遗传损伤具有一定的协同作用。     

挥发性有机物对小鼠脑组织形态学和氨基酸类递质的影响

目的通过挥发性有机物(VOCs)对小鼠脑组织中递质类氨基酸含量的影响,探讨VOCs对小鼠神经系统的毒性。方法采用静式吸入染毒,小鼠亚急性暴露于挥发性有机物,设置对照、低(甲醛1.5mg/m3;VOCs20mg/m3)、中(甲醛4.5mg/m3;VOCs60mg/m3)、高浓度暴露组(甲醛13.5mg/m3;VOCs180mg/m3),染毒结束后,做脑组织常规病理,采用高效液相色谱法测定小鼠脑组织(皮质和海马)氨基酸类递质[包括兴奋性氨基酸类递质谷氨酸(Glu)、门冬氨酸(ASP);抑制性氨基酸类递质氨基丁酸(GABA)、甘氨酸(Gly)]含量。结果暴露组小鼠脑组织皮质和海马兴奋性氨基酸类递质含量随染毒浓度增加而降低,而抑制性氨基酸类递质含量随染毒浓度增加而增加。脑组织病理表现为VOCs暴露组神经元变性坏死。结论挥发性有机物引起小鼠学习记忆能力下降和麻醉作用。     

甲醛对小鼠离体和体内骨髓细胞DNA的损伤作用

目的探讨甲醛对离体和体内小鼠骨髓细胞DNA的损伤作用。方法采用单细胞凝胶电泳技术检测骨髓细胞DNA的损伤作用。以6、30、60、120μmol/L甲醛浓度处理离体小鼠骨髓细胞。以0.2、2、20 mg/kg的甲醛腹腔注射染毒,连续5 d。结果6、30、60μmol/L剂量的甲醛对小鼠骨髓细胞DNA迁移显著高于对照组(P<0.01),30μmol/L时DNA损伤最为明显(P<0.001),但甲醛浓度为120μmol/L时DNA迁移与对照组差异无显著性。腹腔注射0.2、2、20 mg/kg的甲醛组小鼠骨髓细胞DNA迁移显著高于对照组(P<0.01),以2 mg/kg组DNA迁移最为明显(P<0.001)。结论甲醛对小鼠离体和体内骨髓细胞DNA均有明显的损伤作用,进一步证实甲醛具有遗传毒性。     

Sensitivity to bleomycin of JTC-11 cells modified by serum concentration and underlaid 3T3 cells

The sensitivity to bleomycin of JTC-11 cells derived from Ehrlich ascites tumor was modified by both serum concentration and superinoculation on a sheet of Swiss 3T3 cells. The dose-survival curve of the JTC-11 cells was biphasic or triphasic, with a sensitive phase at lower doses (less than 10 micrograms/ml) and a resistant one at higher doses (more than 40 micrograms/ml). Sensitivity of JTC-11 cells to bleomycin decreased with increases in the serum concentration. When JTC-11 cells were superinoculated on the sheet of Swiss 3T3 cells, the sensitivity of JTC-11 cells to bleomycin did not change with increases in the serum concentrations.     

不平衡氨基酸对肿瘤生长的影响

目的：比较几种不平衡氨基酸营养支持对肿瘤生长的影响。方法：荷Walker-256癌肉瘤SD大鼠，空肠喂饲营养制剂10天，根据所喂饲制剂中氨基酸组成的不同，分为A组（平衡氨基酸组）B组（增量精氨酸不平衡氨基酸组）、C组（去甲硫氨酸不平衡氨基酸组）、D组（去缬氨酸不平衡氨基酸组）、C组（增量精氨酸、去甲硫氨酸和缬氨酸不平衡氨基酸组）。以肿瘤体积增长速度，肿瘤重量，肿瘤重量／尸重，肿瘤组织PCNA指数，肿瘤细胞周期各时相百分比，以及DNA倍性作为观察肿瘤生长速度的指标。结果：上述各指标值显示：B、C、D组与A组相比，除DNA倍性外，其余各指标值均非常显著降低，但B、C、D组间比较无显著差异。E组与B、C、D组相比较，所有指标值均显著降低。结认：平衡氨基酸促进肿瘤生长；量精氨酸、去甲硫氨酸和去缬氨酸三种平衡氨基酸对肿瘤生长有不同等抑制作用；增量精氨酸，去甲硫氨酸和去缬氨氨酸复合不平衡氨基酸对肿瘤生长抑制作用更显著。     

Specific inhibition of spermatozoal energy metabolism by oxidized spermine

Oxidized spermine, an iminoaldehyde [N,N′-bis(3-propionaldehyde)1,4-diaminobutanel inhibits the energy metabolism of human spermatozoa with striking specificity as compared with other mammalian cell types. Low concentrations of oxidized spermine virtually abolished the conversion of glucose to CO₂ and lactate in human spermatozoa while in Ehrlich ascites-carcinoma cells, in human peripheral lymphocytes and in human vaginal minces, the iminoaldehyde caused little, if any, inhibition of glucose degradation. In contrast to oxidized spermine, some other aliphatic aldehydes with long carbon chain, which likewise were inhibitory to human spermatozoa, did not show any cell specificity depressing equally well the metabolism of all cell types tested.The inhibitory action exerted by oxidized spermine on human sperm metabolism could be prevented, but not reversed, with heparin. The latter compound, however, did not prevent the inhibition produced by other aliphatic aldehydes.Although the mechanism of inhibition by oxidized spermine, and other aliphatic aldehydes as well, is not completely clear, it possibly involves an interaction of the compounds with cell membranes, since no inhibition was found when cell free extracts of spermatozoa were used as the source of glycolytic enzymes.The idea that the inhibition by oxidized spermine was not entirely an unspecific detergent-like effect was supported by the finding that Triton X-100 depressed the glucose metabolism in Ehrlich ascites cells and human spermatozoa in a similar manner, while under the same conditions oxidized spermine, being strongly inhibitory to the sperm cells, failed to depress the glucose degradation by ascites cells.Oxidized spermine also inhibited the conversion of radioactive pyruvate to carbon dioxide in human sperm cells.     

Role of dietary magnesium and/or manganese variables on ehrlich ascites tumor‐bearing mice

Female Swiss albino mice were placed on seven dietary regimens for five weeks. These regimens differed only in magnesium and/or manganese contents. At the end of the feeding period, the animals were inoculated with Ehrlich ascites tumor. Ten days after transplantation, Ehrlich ascites carcinoma (EAC) cells were harvested, and all animals were killed. EA C cells and plasma samples were subjected to several biochemical tests. The results suggest several conclusions. 1. Dietary supplements of magnesium and/or manganese have no effect on retarding tumor growth in vivo. 2. Dietary restriction of manganese and combined magnesium and manganese gave promising effects on retarding tumor growth in vivo. 3. Dietary magnesium deficiency, per se, had no significant effect on tumor regression in vivo. 4. In contrast to in vitro studies, manganese supplementation appeared to exert no effect on tumor progression in vivo. 5. Magnesium supplementation seemed to have no effect on tumor progression in vivo, which is in agreement with in vitro studies.     

Chlorella vulgaris Modulates Immunomyelopoietic Activity and Enhances the Resistance of Tumor-Bearing Mice

We studied the effects of Chlorella vulgaris (CV) on the interaction between stromal and hematopoietic stem cells in normal and Ehrlich ascites tumor (EAT)-bearing mice. Long-term bone marrow culture (LTBMC), cytokine production, spleen mononuclear cells (SMC) proliferation (SCP), colony stimulating activity (CSA), and NK cells activity were evaluated. In tumor bearers, reduced capacity of stromal cell layer to support the growth and differentiation of granulocyte-macrophage progenitor cells (CFU-GM), concomitantly to decreased numbers of total nonadherent cells in LTBMC and reduced local production of IL-6 and IL-1α, were observed. Presence of the tumor has not altered the number of stromal adherent cells. CV treatment restored the ability of stromal cells from EAT-bearing mice to produce IL-6 and IL-1α, which was consistent with increased number of nonadherent cells and higher ability to display CFU-GM in vitro. EAT growth increased SCP, serum CSA, and IL-10 production and concurrently depressed NK cell activity and the secretion of IL-2, IFN-γ, and TNF-α. Treatment of tumor-bearing mice with CV augmented CSA, SMC proliferation, NK cell activity, and the production of IL-2, IFN-γ, and TNF-α, whereas IL-10 levels where reduced. Our results suggest that CV modulates immunehematopoietic cell activity and disengages tumor-induced suppression of these responses.     

Role of dietary magnesium and/or manganese variables on Ehrlich ascites tumor-bearing mice

Female Swiss albino mice were placed on seven dietary regimens for five weeks. These regimens differed only in magnesium and/or manganese contents. At the end of the feeding period, the animals were inoculated with Ehrlich ascites tumor. Ten days after transplantation, Ehrlich ascites carcinoma (EAC) cells were harvested, and all animals were killed. EAC cells and plasma samples were subjected to several biochemical tests. The results suggest several conclusions. 1. Dietary supplements of magnesium and/or manganese have no effect on retarding tumor growth in vivo. 2. Dietary restriction of manganese and combined magnesium and manganese gave promising effects on retarding tumor growth in vivo. 3. Dietary magnesium deficiency, per se, had no significant effect on tumor regression in vivo. 4. In contrast to in vitro studies, manganese supplementation appeared to exert no effect on tumor progression in vivo. 5. Magnesium supplementation seemed to have no effect on tumor progression in vivo, which is in agreement with in vitro studies.     

Chlorella vulgaris modulates immunomyelopoietic activity and enhances the resistance of tumor-bearing mice

We studied the effects of Chlorella vulgaris (CV) on the interaction between stromal and hematopoietic stem cells in normal and Ehrlich ascites tumor (EAT)-bearing mice. Long-term bone marrow culture (LTBMC), cytokine production, spleen mononuclear cells (SMC) proliferation (SCP), colony stimulating activity (CSA), and NK cells activity were evaluated. In tumor bearers, reduced capacity of stromal cell layer to support the growth and differentiation of granulocyte-macrophage progenitor cells (CFU-GM), concomitantly to decreased numbers of total nonadherent cells in LTBMC and reduced local production of IL-6 and IL-1α, were observed. Presence of the tumor has not altered the number of stromal adherent cells. CV treatment restored the ability of stromal cells from EAT-bearing mice to produce IL-6 and IL-1α, which was consistent with increased number of nonadherent cells and higher ability to display CFU-GM in vitro. EAT growth increased SCP, serum CSA, and IL-10 production and concurrently depressed NK cell activity and the secretion of IL-2, IFN-γ, and TNF-α. Treatment of tumor-bearing mice with CV augmented CSA, SMC proliferation, NK cell activity, and the production of IL-2, IFN-γ, and TNF-α, whereas IL-10 levels where reduced. Our results suggest that CV modulates immunehematopoietic cell activity and disengages tumor-induced suppression of these responses.     

Abnormal plasma amino acid profiles in patients undergoing bone marrow transplant

Amino acid concentrations in plasma have been measured during total parenteral nutrition in patients undergoing bone marrow transplantation. Profound hyperaminoacidemia was noted in the immediate para-transplant period. The increase was due mainly to high levels of phenylalanine and methionine. During the radiation treatment period these amino acids plus valine, proline, serine and glycine were exceptionally high. Levels of cystine and asparagine tended to be low. The results suggest that infusion of a mixture of amino acids which is lower in phenylalanine and methionine might result in better nitrogen utilization.     

不平衡氨基酸对肿瘤生长的影响

目的 比较几种不平衡氨基酸营养支持对肿瘤生长的影响。方法 荷Walker-256癌肉瘤SD大鼠,空肠喂饲肠外营养制剂10天,据所喂饲制剂中氨基酸组成的不同,分为：A组（平衡氨基酸组）、B组（增量精氨酸不平衡氨基酸组）、C组（去蛋氨酸不平衡氨基酸组）、D组（去缬氨酸不平衡氨基酸组）、E组（增量精氨酸、去蛋氨酸、去缬氨酸不平衡氨基酸组）。肿瘤体积增长速度、肿瘤重量、肿瘤重量／尸重,肿瘤组织PCNA指数,肿瘤细胞周期各时相百分比以及DNA倍性作为观察肿瘤生长速度的指标。结果 上述各指标值显示：B、C、D组与A组相比,除DNA倍性外,其余各项指标值均降低（P＜0．01）,但B、C、D组间比较无显性差异（P＞0．05）。E组与B、C、D组相比较,所有指标值均显降低（P＜0．05）。结论 平衡氨基酸促进肿瘤生长;增量精氨酸、去蛋氨酸、去缬氨酸三种不平衡氨基酸对肿瘤生长有同等抑制作用;增量精氨酸、去蛋氨酸、去缬氨酸复合不平衡氨基酸对肿瘤生长抑制作用更显。     

Antioxidant effects in the development of Ehrlich ascites carcinoma

The effect of Ehrlich ascites tumor growth on selenium-turnover rates and selenium-75 distribution in liver, kidney, and immunological tissues (spleen, thymus, and lymph nodes) was investigated in Swiss Webster mice that had been prelabeled with selenium-75. Ehrlich ascites tumor caused a decrease in the selenium-75 content of liver, kidney, and thymus; it also decreased the rate of the total-body selenium-turnover. In liver, depletion of selenium-75 was almost as great as that produced by a selenium and vitamin E-deficient diet. When mice had been fed an antioxidant-deficient diet, considerable quantities of selenium-75 were accumulated by the tumor; the specific activity of the tumor increased 9-fold over that in antioxidant-supplemented mice. The same diet produced a premature, and in some cases drastic, contraction in tumor volume. The possible significance of tumor-induced antioxidant deficiencies to the etiology of certain paraneoplastic syndromes is discussed.