酯类交联剂交联丙烯酸钠吸水树脂的紫外引发制备与性能

以部分中和的丙烯酸为原料,分别以乙二醇二甲基丙烯酸（EGDMA）、二甲基丙烯酸甘油酯（GDA）与三乙二醇二甲基丙烯酸（TEGDMA）为交联剂,通过紫外引发合成了聚丙烯酸钠缩乙二醇二甲基丙烯酸（PAANa-E）、聚丙烯酸钠缩二甲基丙烯酸甘油酯（PAANa-GDA）、聚丙烯酸钠缩三乙二醇二甲基丙烯酸（PAANa-TE）3种丙烯酸钠高吸水树脂。考察了交联剂用量、单体体积分数、丙烯酸中和度、辐照时间对树脂吸液率的影响,研究了3种不同链长的酯类交联剂制备的树脂吸液率与温度、pH、盐溶液浓度的关系。采用红外、热失重分     

咖啡酸苯乙酯对大肠癌细胞增殖和凋亡的影响

目的探讨咖啡酸苯乙酯(caffeic acid phenethyl ester,CAPE)对培养的大肠癌SW480细胞增殖、细胞周期和细胞凋亡的影响。方法不同浓度CAPE处理培养的大肠癌SW480细胞后,采用MTT法检测细胞的增殖活性,流式细胞仪检测细胞周期分布和细胞凋亡率,TUNEL染色观察凋亡细胞。结果CAPE对SW480细胞的生长具有明显的抑制作用,其作用表现为剂量依赖性和时间依赖性。流式细胞仪检测发现2.5、5.0、10mg/L的CAPE对SW480处理24h后,G0/G1期细胞比例上升,S期细胞比例下降,细胞凋亡率上升,呈剂量依赖性。TUNEL染色也发现CAPE作用后凋亡细胞数量增加。结论CAPE对大肠癌SW480细胞株具有明显的增殖抑制作用,其作用机制与阻滞细胞周期G期和诱导细胞凋亡有关。     

Chemoprevention of liver cancer by plant polyphenols

Primary liver cancer or hepatocellular carcinoma (HCC) is one of the most frequent tumors representing the fifth commonest malignancy worldwide and the third cause of mortality from cancer. Currently, the treatments for HCC are not so effective and new strategies are needed for its fight. Chemoprevention, the use of natural or synthetic chemical agents to reverse, suppress or prevent carcinogenesis is considered an important way for confronting HCC. Many of the chemopreventive agents are phytochemicals, namely non-nutritive plant chemicals with protective or disease preventive properties. In this review, we focus on plant polyphenols, one of the most important classes of phytochemicals, their chemopreventive properties against HCC and discuss the molecular mechanisms accounting for this activity.     

The Impact of Polyamine Analogues on the Blood Pressure of Normotensive and Hypertensive Rats

The impact of the antineoplastic polyamine analogues N¹N¹⁴-diethylhomospermine (DEHSPM) and N¹N¹¹-diethylnorspermine (DENSPM) on the blood pressure and heart rate of normotensive and hypertensive rats are described. DEHSPM was administered to both normotensive and spontaneously hypertensive rats (SHR), while the DENSPM analogue was given only to the normotensive animals. The intravenous administration of DEHSPM a t doses of 5 or 10 mg/kg resulted in a profound and long-lasting drop in the test animals' blood pressure, with no appreciable change in their heart rate. This was true for both the normotensive and the hypertensive animals. When administered at equivalent molar dosages, DENSPM was one fifth as effective as DEHSPM at reducing blood pressure. The impact of NG-nitro-L-arginine- methyl ester (L-NAME) and L-arginine on the analogues' activity is consistent with the involvement of nitric oxide.     

EFFECTS OF NITRIC OXIDE SYNTHESIS INHIBITION ON FK506-INDUCED NEPHROTOXICITY IN RATS

This study was designed to evaluate the role of nitric oxide (NO) in FK506-induced nephrotoxicity by administering an inhibitor of NO synthesis, Nω-nitro-L-arginine methyl ester (L-NAME) to rats treated with FK506. After one week of treatment with FK506 (3.2 mg/kg/day, intramuscularly) and/or L-NAME (5 mg/100 mL of L-NAME in the drinking water), the arterial pressure, urinary NOx, and parameters for renal function were measured, and histological analysis of the kidney was made. In the L-NAME without FK506 group, L-NAME administration effectively inhibited urinary NOx excretion and increased mean arterial pressure (MAP) without any change in renal function. In the FK506 without L-NAME group, FK506 treatment showed increase in urinary NOx excretion and mild renal dysfunction. In the FK506 with L-NAME group, urinary NOx excretion was decreased by L-NAME administration and renal function was significantly worsened than FK506 without L-NAME group. The plasma creatinine, BUN and urinary N-acetyl-β-D-glucosaminidase increased 2-, 3-, and 3-fold, respectively and the creatinine clearance was reduced by 50% as compared with that in the FK506 without L-NAME group. Histological analysis revealed severe interstitial fibrosis and tubular atrophy in the FK506 + L-NAME treatment group. Thus, results suggest that NO synthesis is enhanced in the kidney during FK506-induced nephrotoxicity and that NO synthesis inhibition aggravates FK506-induced nephrotoxicity. NO may play a protective role attributable to the balance of vasoactive substances in FK506-induced nephrotoxicity.     

羧基末端截短型乙型肝炎病毒X蛋白在肝细胞癌与癌旁组织中的表达及其在术后预后中的作用

目的 探讨肝细胞癌（HCC）患者肝癌组织和癌旁组织中羧基末端截短型乙型肝炎病毒X蛋白（Ct-HBx）的表达及其与患者术后预后的关系。方法 采用免疫组织化学染色法检测462例肝癌组织、配对的263例癌旁组织和配对的25例癌栓组织中Ct-HBx蛋白的表达,分析其与临床病理参数的关系,探讨Ct-HBx蛋白的表达与HCC患者术后预后的关系。结果 Ct-HBx蛋白表达在配对的263例肝癌组织和癌旁组织中阳性率分别为43.73%（115/263）和11.79%（31/263）;多因素Cox风险回归模型分析结果显示年龄、门静脉癌栓（PVTT）、术前天冬氨酸转氨酶（AST）、术前甲胎蛋白（AFP）、主瘤旁微小子灶、术前巴塞罗那临床肿瘤（BCLC）分期和术后抗病毒治疗是HCC患者术后复发的独立危险因素（P均<0.05）,门静脉癌栓、术前AFP、肿瘤包膜、术前BCLC分期和Ct-HBx蛋白表达是HCC患者术后生存的独立危险因素（P均<0.05）。在263对配对样本中,肝癌组织中Ct-HBx蛋白的表达与性别、糖类抗原19-9（CA19-9）、术后抗病毒治疗有关（P均<0.05）。肝癌组织和癌旁组织中Ct-HBx蛋白均为阴性表达的患者术后3年无瘤生存率高于Ct-HBx蛋白在肝癌组织阴性表达且在癌旁组织阳性表达的患者（P=0.050 1）。结论 当HCC患者肝癌组织中Ct-HBx蛋白表达呈阴性时,癌旁组织中Ct-HBx蛋白的表达情况可能与术后预后有关,可作为预测术后肿瘤生存和复发的标志物。     

A novel antioxidant agent caffeic acid phenethyl ester prevents shock wave-induced renal tubular oxidative stress

The aim of this study was to evaluate the effects of the novel free radical scavenger caffeic acid phenethyl ester (CAPE) on extracorporeal shock wave lithotripsy (ESWL) induced renal impairment. The study was performed using 30 rabbits which were divided into two groups, each exposed to 3,000 shock waves at 18 kV: (1) control group, (2) ESWL+CAPE treated group. Malodialdehyde (MDA), urine N-acetyl--glucosaminidase (NAG) activity, uric acid and white cell counts were used as markers of oxidative stress. Following shock wave exposure there was a significant rise in MDA, NAG and uric acid and white cell counts. CAPE reduced the rise in MDA, NAG, uric acid and white cell counts. Thus CAPE treatment to a great extent prevented the induction of these renal changes. Our results suggest that the antioxidant capacity of the kidney tissue was reduced after ESWL treatment and that the tissue was exposed to oxidant stress. We conclude that CAPE treatment provided significant protection against ESWL induced free radical damage.     

胆固醇酯转运蛋白-TaqIB基因多态性与冠心病的相关研究

目的探讨胆阿醇酯转运蛋白（CETP）-TaqIB基因多态性与冠心病的相关性。方法采用聚合酶链反应-限制片长多态性分析方法对238例冠心病患者（冠心病组）和203例非冠心病者（对照组）进行检测。结果所有受试者中CETP．TaqIB等位基因B1、B2的分布频率分别为59．4％（262／441）和40．6％（179／441）。冠心病组B181基因型频率高于对照组[39．9％（95／238）比29．6％（60／203）．P〈0．05],而B182基因型频率低于对照组[44．1％（105／238）比53．7％（109／203）,P〈0．05]。B1B1基因型高密度脂蛋门胆固醇（HDL-C）水平及载脂蛋白（apo）AI水平显著低于B282基因型[（1．19±0．36）mmol／L比（1．38±0．39）mmol／L,（1．17±0．33）g／L比（1．30±0．31）g/L,P〈0．05]。在57例行冠状动脉造影的冠心病患者中,B1纯合子冠状动脉狭窄程度显著高于等位基因B2携带者（P〈0．05）。多因素Logistic回归结果显示B181基因型作为独立危险因素未达到有统计学意义（P：0．147）。结论CETP-TaqIB基因多态性可影响脂蛋n水平,B181基因型与低HDl-C、低apoAI水平有密切关系.CETP-TaqIB基因型与冠状动脉狭窄程度相关,但作为冠心病的独立危险因素未能证实．     

咖啡酸苯乙酯干扰β-连环蛋白通路对大肠癌的影响

目的 观察咖啡酸苯乙酯(CAPE)对大肠癌SW480细胞β-连环蛋白相关通路中β-连环蛋白、c-myc和细胞周期蛋白D1基因表达的影响.方法 采用RT-PCR和Western blot方法 检测不同浓度CAPE作用24、48 h后,细胞β-连环蛋白、c-myc及细胞周期蛋白D1 Mrna和蛋白表达的变化.结果 经不同浓度的CAPE作用后,SW480细胞β-连环蛋白、c-myc、细胞周期蛋白D1 Mrna和蛋白表达均有不同程度的下降,分别从1.05±0.26下降到0.67±0.10、0.87±0.09下降到0.51±0.14、0.63±0.09下降到0.32±0.14和204±52下降到52±16、111±11下降到52±16、87±7下降到32±12,与对照组(CAPE浓度为0 mg/L)比较差异有统计学意义(F=5.724,6.793,7.026,15.936,14.889,14.162,31.147,28.881,6.322,17.647,9.584,P<0.05),并呈剂量和时间依赖性.结论 CAPE可干扰β-连环蛋白相关通路,下调β-连环蛋白及通路靶基因c-myc和细胞周期蛋白D1的转录和表达.CAPE抗肿瘤作用可能与下调β-连环蛋白通路相关基因表达有关.