大黄对实验性急性化脓性胆管炎早期血浆内毒素含量的影响

取ＳＤ大鼠，随机分为三组：正常组、盐水组、大黄组。利用大肠杆菌诱发急性化脓性胆管炎，盐水组和大黄组分别经口灌服生理盐水和大黄１ｍｌ／１００ｇ·日。以血浆内毒素及血清酶学为指标，观察了大黄对大鼠急性化脓性胆管炎早期血浆内毒素及肝功的影响。结果显示：１．盐水组术后３天内死亡４只，大黄组死亡２只，正常组无死亡。２．盐水组大鼠术后３天血浆内毒素含量明显升高，大黄组含量较盐水组明显降低（Ｐ＜０．０１）。３．术后３天血清ＡＫＰ和ＧＰＴ与正常组比均有明显增高，而盐水和大黄组之间无显著性差异（Ｐ＞０．０５）。结果表明大黄具有降低化脓性胆管炎大鼠的早期死亡率及显著降低内毒素血症的作用。     

栀子提取液对大鼠急性胰腺炎时TNF-α和IL-6改变的影响

目的：探讨急性胰腺炎时血清TNF-α和IL-6的变化以及栀子提取液对其的影响。方法：SD大鼠造模后口服给予栀子提取液进行药物治疗，24h后呆血测淀粉酶、TNF-α和IL-6，并分组对比，取胰腺组织做病理学检查。结果：急性胰腺炎时血淀粉酶、TNF-α和IL-6水平显著升高，镜下见大量炎细胞浸润，栀子提取液可改善上述变化。结论：栀子提取液对大鼠急性胰腺炎有治疗作用。     

美法仑治愈荷瘤小鼠的过程与TNFα的关系

目的探讨单一剂量的美法仑治愈荷瘤野生型C57BL/6小鼠的过程与肿瘤坏死因子α(TNFα)的关系。方法以3种遗传背景相同、肿瘤坏死因子受体1(TNFR1)基因型不同的TNFR1 / 、TNFR1 /-和TNFR1-/-C57BL/6小鼠为实验动物,皮下接种数量相同的小鼠淋巴瘤EL4细胞。接种瘤细胞后12d,给基因型不同的各组荷瘤小鼠腹腔内单次注射7.5mg/kg的美法仑。以荷瘤野生型C57BL/6小鼠(TNFR1 / )为对照,观察美法仑对荷瘤TNFR1 /-C57BL/6小鼠和荷瘤TNFR1-/-C57BL/6小鼠的治疗效应。结果在美法仑(7.5mg/kg)治疗后的1周内,基因型不同的各组荷瘤小鼠肿瘤消退的速度基本相同。在随后的2月内,荷瘤TNFR1 / 和TNFR1 /-C57BL/6小鼠的肿瘤结节逐渐消退、肿瘤治愈;而多数荷瘤TNFR1-/-C57BL/6小鼠的肿瘤结节缩小后又再次出现并逐渐长大、肿瘤复发。结论TNFα与美法仑治愈肿瘤的过程密切相关,其中美法仑的抗肿瘤作用与荷瘤小鼠TNFR1的表达无关,但在美法仑治疗后,机体预防或避免肿瘤复发方面需要TNFR1在机体细胞的表达,而不是在肿瘤细胞的表达。     

雌激素性肝内胆汁淤积发病机制的研究进展

肝内胆汁淤积是指肝细胞分泌胆汁障碍 ,致使正常的胆汁成分淤积肝内和返流入血 ,生理上表现为胆汁流速降低 ,临床上有黄疸、瘙痒伴淤胆的生化和病理异常。通常把由雌激素引起的肝内胆汁淤积称为雌激素性肝内胆汁淤积。随着口服避孕药及雌激素替代疗法的应用 ,其发病率明显增高。本文拟在介绍正常胆汁分泌的基础上 ,从细胞、分子水平概述雌激素性肝内胆汁淤积发病机制的研究进展。1　胆汁的形成胆汁由肝细胞产生 ,胆汁酸盐 (简称胆盐 )是其溶质中的主要成分。胆汁分泌是一种继发于肝细胞主动分泌胆盐及其它胆汁溶质的渗透性扩散过程。胆盐及其它胆汁溶质进入毛细胆管后 ,由于不能经肝细胞间紧密连接返流入血 ,故在毛细胆管内产生渗透梯度 ,并吸引着水分及其它电解质经细胞旁路(ｐａｒａｃｅｌｌｕｌａｒｐａｔｈｗａｙ)或跨细胞途径 (ｔｒａｎｓｃｅｌｌｕｌａｒｐａｔｈｗａｙ)进入毛细胆管 ,从而产生了胆盐依赖性胆汁流 (ｂｉｌｅｓａｌｔｄｅｐｅｎｄｅｎｔｆｌｏｗ ,ＢＳＤＦ) (由胆盐渗透梯度产生 )与胆盐非依赖性胆汁流 (ｂｉｌｅｓａｌｔｉｎｄｅｐｅｎｄｅｎｔｆｌｏｗ ,ＢＳＩＦ) (由非胆盐渗透梯度形成 )。胆汁形成至少涉及肝细胞血窦面细胞膜...     

反相高效液相色谱法测定桅子中京尼平甙和京尼平的含量

应用高效液相色谱法同时测定了栀子中京尼平甙和京尼平的含量。采用YWG -C18柱 ,0 0 5mol/L磷酸氢二钠—甲醇 ( 72∶2 8) ,用磷酸调节pH6 80为流动相 ,于 2 4 0nm波长处检测 ,京尼平甙和京尼平的平均加样回收率分别为 99 10 % ,98 2 8% ,RSD分别为 1 0 5% ,1 2 1% (n=5)。本法简单、准确、重现性好     

肝复康对实验性大鼠肝纤维化肝组织Ⅰ、Ⅲ型胶原含量的影响

目的研究肝复康对实验性大鼠肝纤维化的肝组织Ⅰ、Ⅲ型胶原含量及其比值的影响.方法采用四氯化碳皮下注射制备肝纤维化模型,于造模60 d后给予肝复康治疗3个月,以秋水仙碱及肝脾康为对照药.检测肝组织羟脯氨酸含量,苦味酸天狼星红染色法偏振光显微镜显示肝组织Ⅰ、Ⅲ型胶原,并结合图像分析计算Ⅰ、Ⅲ型胶原面积及面积比.结果肝复康治疗后肝组织Ⅰ、Ⅲ型胶原的含量较模型对照组明显减少,Ⅰ型胶原面积明显降低(P《0.01),Ⅲ型胶原面积明显降低(P《0.01),Ⅰ、Ⅲ型胶原含量的比值明显降低(P《0.01).结论肝复康可明显降低肝组织Ⅰ、Ⅲ型胶原表达,降低Ⅰ、Ⅲ型胶原含量比,使细胞外基质的成分趋于正常.     

肝复康对实验性大鼠肝纤维化肝组织Ⅰ、Ⅱ型胶原含量的影响

目的 :研究肝复康对实验性大鼠肝纤维化的肝组织 、 型胶原含量及其比值的影响。方法 :采用四氯化碳皮下注射制备肝纤维化模型 ,于造模 6 0 d后给予肝复康治疗 3个月 ,以秋水仙碱及肝脾康为对照药。检测肝组织羟脯氨酸含量 ,苦味酸天狼星红染色法偏振光显微镜显示肝组织 、 型胶原 ,并结合图像分析计算 、 型胶原面积及面积比。结果 :肝复康治疗后肝组织 、 型胶原的含量较模型对照组明显减少 , 型胶原面积明显降低(P<0 .0 1) , 型胶原面积明显降低 (P<0 .0 1) , 、 型胶原含量的比值明显降低 (P<0 .0 1)。结论 :肝复康可明显降低肝组织 、 型胶原表达 ,降低 、 型胶原含量比 ,使细胞外基质的成分趋于正常。     

十全大补汤对荷膀胱癌小鼠大剂量化疗的减毒增效作用

Objective To investigate the toxicity attenuation and efficacy potentiation effects of Shiquan Dabu Tang (SDT) on high dose chemotherapy in T739 mice with bladder carcinoma. Methods Mouse bladder carcinoma tissue was inoculated subcutaneously into T739 mice to establish tumor-beating mice model. The tumor-bearing mice were randomly divided into a CTX group (100, 200, 400 mg/Kg respectively), a SDT group (high or low dose respectively), a high-dose SDT combined with 200 mg/Kg CTX group and a control group. The body weight, diameter of tumor nodules and complete blood count were observed subsequently. Results Different doses of SDT could effectively inhibit tumor growth in mice. SDT + CTX treatment significantly prolonged the survival time of mice by 49.4±23.3 days (P<0.01, 0.05, 0.01), compared with high dose SDT treatment (17.4±5.77) days, 200 mg/kg CTX treatment (23±14.02) days and control group (11.75±2.06) days respectively. The peripheral platelet count increased more significantly in mice treated with SDT within a week as compared to mice without SDT treatment (P<0.05). The peripheral RBC count and liB concentration increased more significantly in mice treated with SDT for 2 weeks as compared to mice without SDT treatment (P<0.05). Conclusions SDT could enhance the anti-tumor effects of high dose CTX on tumor-bearing mice and reduce toxicity in its peripheral red blood cells. The results showed that SDT combined with high dose of CTX chemotherapy had toxicity attenuation and efficacy potentiation effects in tumor-beating T739 mice.     

十全大补汤对荷膀胱癌小鼠大剂量化疗的减毒增效作用

Objective To investigate the toxicity attenuation and efficacy potentiation effects of Shiquan Dabu Tang (SDT) on high dose chemotherapy in T739 mice with bladder carcinoma. Methods Mouse bladder carcinoma tissue was inoculated subcutaneously into T739 mice to establish tumor-beating mice model. The tumor-bearing mice were randomly divided into a CTX group (100, 200, 400 mg/Kg respectively), a SDT group (high or low dose respectively), a high-dose SDT combined with 200 mg/Kg CTX group and a control group. The body weight, diameter of tumor nodules and complete blood count were observed subsequently. Results Different doses of SDT could effectively inhibit tumor growth in mice. SDT + CTX treatment significantly prolonged the survival time of mice by 49.4±23.3 days (P<0.01, 0.05, 0.01), compared with high dose SDT treatment (17.4±5.77) days, 200 mg/kg CTX treatment (23±14.02) days and control group (11.75±2.06) days respectively. The peripheral platelet count increased more significantly in mice treated with SDT within a week as compared to mice without SDT treatment (P<0.05). The peripheral RBC count and liB concentration increased more significantly in mice treated with SDT for 2 weeks as compared to mice without SDT treatment (P<0.05). Conclusions SDT could enhance the anti-tumor effects of high dose CTX on tumor-bearing mice and reduce toxicity in its peripheral red blood cells. The results showed that SDT combined with high dose of CTX chemotherapy had toxicity attenuation and efficacy potentiation effects in tumor-beating T739 mice.     

siRNA表达框架对TNF-α和IL-1的特异性抑制

[目的]利用siRNA表达框架研究RNA干扰技术对小鼠腹腔活化巨噬细胞分泌TNF-α和IL—1的抑制作用及其干扰序列的特异性。[方法]原代培养小鼠腹腔巨噬细胞,构建针对小鼠TNF—α和IL-1的siRNA表达框架,转染细胞,用ELISA方法检测TNF-α和IL-1分泌情况。[结果]TNF-α干扰组TNF-α分泌量（21．87±1．20）pg／mL较IL-1干扰组（28．02±1．03）pg／mL及对照组（27．64±1．92）pg／mL均明显降低,差异有显著性意义（P〈0．05）。IL-1干扰组IL-1分泌量（40．37±4．02）pg／mL较TNF—α干扰组（57．86±3．91）pg／mL及对照组（59．55±3．57）pg／mL均明显降低,差异有显著性意义（P〈0．05）。[结论]构建的针对TNF-α和IL-1的siRNA表达框架能够明显抑制巨噬细胞分泌TNF-α和IL-1,且干扰作用具有序列特异性。