血清IL-6、PCT水平与急性胰腺炎严重程度的相关性研究

目的探讨血清促炎细胞因子白细胞介素-6（IL-6）及降钙素原（PCT）水平在早期评估急性胰腺炎（AP）患者严重程度及预后的价值。方法以28例重症急性胰腺炎（SAP）和36例轻症急性胰腺炎（MAP）患者为研究对象,另以47名健康体检者作为对照组。采用酶联免疫吸附试验（ELISA）检测血清IL-6及PCT水平,分析二者与患者Ranson评分、APACHEⅡ评分、BahhazarCT评分、血清生化指标及预后的关系。结果SAP组、MAP组、健康对照组血清IL-6水平分别为（531．37±168．67）pg／ml、（261．32±178．55）pg／ml、（15．31±3．15）pg／ml,三组间差异均有统计学意义（P均〈0．01）。SAP组、MAP组、健康对照组血清PCT水平分别为（4．22±2．84）ng／ml、（0．45±0．33）ng／ml、（0．12±0．11）ng／ml,三组间PCT值差异均有统计学意义（P均〈0．05）。血清IL-6和PCT水平与Ranson评分、APACHE11评分、BalthazarCT评分均呈正相关。结论血清IL-6和PCT水平与急性胰腺炎病情的严重程度和并发症显著相关。     

高效液相色谱-荧光检测法测定复合维B片中维生素B1含量

目的建立测定复合维B片中维生素B1含量的高效液相色谱-荧光检测法。方法样品用0．1mol／L盐酸提取，碱性铁氰化钾氧化，正丁醇萃取；采用Kromasil 100—5 C18柱（150mm×4．6mm，5μm）为色谱柱，以0．02mol／L乙酸铵-甲醇（70：30）为流动相，流速为1.0mL／min，荧光检测激发波长365nm，发射波长475nm。结果维生素B1质量浓度在0．5～20μg／mL范围内与峰面积线性关系良好，平均回收率为100.37％，RSD为1．34％，方法检出限（S／N=3）为2．3ng。结论高效液相色谱-荧光检测法快速、简便、准确，适用于复合维B片中维生素B1的含量测定。     

Deacetylation of 4-(5-acetylamino-2-furyl)thiazole and formation of 1-(4-thiazolyl)-3-cyano-1-propanone by rat liver tissues

The reductive metabolism of the rat carcinogen 4-(5-nitro-2furyl)thiazole (NFT) to 1-4-thiazolyl)-3-cyano-1-propanone (TCP) is reported. Formation of TCP from NFT involved furan ring fission. This could have occurred through involvement of either aminofuran or N-hydroxylaminofuran as precursors. To examine if 4-(5-amino-2-furyl)thiazole is a precursor for TCP, a stable model compound, 4-(5-acetylamino-2-furyl)thiazole (AAFT), was prepared and subjected to enzymatic deacetylation, using rat liver tissue homogenates. AAFT was synthesized by catalytic hydrogenation of NFT with 5% palladium on activated carbon, followed by acetylation with acetic anhydride. AAFT, a white crystalline powder, melted at 168–170°, had an extinction coefficient of 17.9 mM^?1 cm^?1 at 293 nm in ethyl acetate, and exhibited spectroscopic and mass spectral characteristics consistent with the assigned structure. Incubation with rat liver 10,000 g supernatant preparations resulted in the biotransformation of AAFT as evidenced by a decrease in absorption at 290 nm. Incubation of ¹⁴C-labeled AAFT followed by extraction with chloroform-diethyl ether (1:1) resulted in the recovery of a major portion (56%) of the radioactivity in the organic phase when the label was at the 2-position of the thiazole ring, while the major amount (82%) of radioactivity was recovered in the aqueous phase when the 1-¹⁴C-acetyl group was labeled. The radioactivity from the aqueous phase was extractable into the organic phase following acidification to pH 1, an observation consistent with deacetylation. Furthermore, the deacetylation product exhibited a mass spectrum, and retention times in gas and high pressure liquid chromatography, similar to those of synthetic TCP. These data establish 4-(5-amino-2-furyl)thiazole, derived from AAFT by deacetylation, as a precursor for TCP.     

线粒体与吗啡诱导的肝损伤作用

我们用药掺食法培养吗啡依赖大鼠模型，研究了吗啡依赖大鼠肝线粒体自由基损伤及其结构与功能的变化。结果发现：超氧化物歧化酶（ＳＯＤ）活性明显降低、丙二醛（ＭＤＡ）含量明显升高；细胞色素Ｃ氧化酶活性、心磷脂含量和膜流动性都明显降低。这表明吗啡依赖大鼠肝线粒体自由基清除能力降低，导致自由基损伤增加，并进一步影响到线粒体的结构与功能。线粒体结构与功能的这种改变可能在吗啡诱导的肝损伤中有重要作用。     

有机磷农药解毒剂——4-叔丁基-1-[(3-取代酰基)吡啶基]甲氧甲基-吡啶季铵碘盐的合成

为了寻找有机磷农药解毒剂,合成了10个未见文献报道的双吡啶季铵盐化合物,Ⅰ_(1～100)制备中间体4-叔丁基吡啶(2)时,得一副产物,熔点135℃,通过光谱测定,确定其结构为2-(4-吡啶基)-丙醇-2。我们推测了副产物的生成原因,从而改进实验条件,提高了(2)的产率。     

肝移植术治疗肝病终末期围手术期处理体会

目的探讨肝移植治疗肝脏终末期病变围手术期处理的方法。方法回顾性总结11例肝移植的围手术期处理方法。11例均行术前人工肝血浆置换，改良背驮式或经典式肝移植术，术中、术后加强重要脏器的监测和维护、抗捧斥反应及防治感染。结果11例病人均顺利度过围手术期。随访：生存1年以上2例，6～10个月2例，3个月3例，1个月3例，其中1例术后6个月因脑出血死亡。结论肝移植是治疗肝脏终末期病变的可靠方法，规范围手术期处理方法是提高手术成功率和长期存活率的关键。     

利尿剂治疗肝硬化腹水疗效的部分影响因素分析

目的探讨利尿剂治疗肝硬化腹水疗效的部分影响因素。方法收集93例肝硬化腹水患者的临床相关指标,通过单因素分析和Logistic回归分析,分析临床各项指标与利尿剂治疗肝硬化腹水疗效的关系。结果在利尿剂治疗肝硬化腹水有效和无效组中,肝硬化并发症、肝功能分级、血电解质水平、尿量、血肌酐水平和腹水程度比较差异具有显著性(P<0.05);将具有显著性差异的影响因素纳入Logistic回归模型,结果显示,肝硬化腹水利尿剂治疗有效的主要预测因素为肝功能分级(P=0.006,OR=0.326)和血肌酐水平(P=0.044,OR=0.169)。结论肝功能分级和血肌酐水平是影响肝硬化腹水利尿剂疗效的重要因素。     

A novel compound RS-0466 reverses beta-amyloid-induced cytotoxicity through the Akt signaling pathway in vitro

In order to determine whether 5-[bis(carboxymethyl) amino]-2-carboxy4-cyano-3-thiopheneacetic acid distrontium salt (S12911-2) inhibits bone resorption by acting on the differentiation and/or function of osteoclasts, its effects were assessed on the 1,25-dihydroxyvitamin D(3)-induced expression of carbonic anhydrase II and vitronectin receptor in chicken bone marrow cells, and on the resorbing activity of authentic rat osteoclasts cultured on bone slices. S12911-2 dose-dependently inhibited, after a 6-day exposure, the expression of carbonic anhydrase II and vitronectin receptor in stimulated osteoclasts (46% and 40%, respectively, at 10(-3) M Sr(2+), P<0.05). A pre-incubation of bone slices with S12911-2 induced a dose-dependent inhibition of bone resorbing activity from 32% at 10(-4) M Sr(2+) to 66% at 10(-3) M Sr(2+) (P<0.05 in each case). A continuous incubation (10(-3) M Sr(2+)) induced a greater inhibition of bone resorbing activity (73%, P<0.05). The inhibition of bone resorption obtained specifically with S12911-2 is related to an inhibition of the differentiation and resorbing activity of the osteoclasts.     

护肝颗粒对小鼠急性肝损伤的保护作用

目的:研究护肝颗粒对模型小鼠急性肝损伤的保护作用。方法:以0.12%氯仿-花生油溶液经腹腔注射,制备小鼠肝损伤模型,显微镜下观察肝组织病理学变化;测定丙氨酸氨基转移酶(ALT)、天冬氨酸氨基转移酶(AST)、超氧化物歧化酶(SOD)活性及丙二醛(MDA)含量;计算肝脏指数。结果:高、中、低剂量护肝颗粒均能显著降低急性肝损伤模型小鼠血清中ALT、AST活性,提高其SOD活性,降低其MDA含量及肝脏指数。结论:护肝颗粒对急性肝损伤有一定的保护作用。     

黄芪甲苷调节PI3K/Akt/FoxO1通路抑制糖尿病大鼠肝糖异生

目的:探讨黄芪甲苷对2型糖尿病(T2DM)大鼠肝损伤保护潜在机制及肝组织磷酯酰肌醇3-激酶(PI3K)/蛋白激酶B(Akt)/叉头框转录因子1(FoxO1),磷酸烯醇式丙酮酸羧基酶(PEPCK)和葡萄糖6-磷酸酶(G6Pase)蛋白表达的影响。方法:6周高糖高脂饮食后,链脲佐菌素(STZ)一次性腹腔注射(0.035 g·kg^-1)建立T2DM大鼠模型,随机分为正常组、模型组、黄芪甲苷低、中、高剂量组及二甲双胍组。黄芪甲苷低、中、高剂量组灌胃黄芪甲苷0.02,0.04,0.08 g·kg^-1·d^-1,二甲双胍组灌胃二甲双胍0.2 g·kg^-1·d^-1;给药8周后,于末次灌胃24 h禁食不禁水后处死,测血清肝生化指标,肝脏指数等;采用苏木素-伊红(HE)染色观察肝脏组织病理形态学变化;马松(Masson)染色观察纤维化程度;过碘酸希夫(PAS)染色反应观察细胞内糖原等变化;免疫组化及蛋白免疫印迹法(Western blot)检测各组肝中PI3K/Akt/FoxO1信号蛋白及PEPCK,G6Pase蛋白表达水平。结果:与正常组比较,模型组肝脏指数显著升高(P<0.01),肝功能指标丙氨酸氨基转移酶(ALT),天门冬氨酸氨基转移酶(AST),总胆固醇(TC),甘油三酯(TG)的含量显著升高(P<0.01),高密度脂蛋白胆固醇(HDL-C)显著降低(P<0.01),大鼠体质量显著减轻(P<0.01),PI3K/Akt/Fox O1信号减弱(P<0.01),PEPCK,G6Pase蛋白表达水平显著增强(P<0.01);与模型组比较,黄芪甲苷中、高剂量组及二甲双胍组肝功能指标ALT,AST,TC,TG的含量明显降低(P<0.05,P<0.01),大鼠体质量明显增加(P<0.05,P<0.01),肝组织Fox O1,PEPCK及G6Pase蛋白水平明显降低(P<0.05,P<0.01),Fox O1的磷酸化水平明显增强(P<0.05,P<0.01)。结论:黄芪甲苷可能通过调节PI3K/Akt/Fox O1信号通路抑制高脂高糖加小剂量STZ诱导T2DM肝糖异生,从而起到延缓T2DM大鼠肝脏损伤作用。