当归红芪超滤物对氧化损伤乳鼠心肌细胞的保护作用及其机制

目的 探讨当归红芪超滤物对H2O2致乳鼠心肌细胞氧化损伤的保护作用及其可能机制。方法 用高浓度的H2O2(400μmol/L)在 Wistar 乳鼠原代培养的心肌细胞上建立氧化损伤模型,用不同质量浓度的当归红芪超滤物 (3.75、7.5、15 mg/mL) 进行干预。在倒置显微镜下观察各实验组心肌细胞的搏动频率,用 MTT 法检测心肌细胞的存活率,用试剂盒检测细胞培养上清液中乳酸脱氢酶 (LDH)、肌酸激酶 (CK) 的活性及细胞内超氧化物歧化酶 (SOD) 的活性、丙二醛 (MDA)、髓过氧化物酶 (MPO) 的量。RT-PCR 技术检测 caspase-3、hsp70 基因在心肌细胞中的表达情况。结果 当归红芪超滤物显著提高氧化损伤心肌细胞的细胞活力;与损伤组比较,当归红芪超滤物各干预组心肌细胞 LDH、CK、MPO、MDA 量显著降低 (P〖WT＜0.01),SOD 活性显著提高 (〖WTBX〗P〖WTBZ〗＜0.01),caspase-3 基因表达显著降低 (P＜0.05),hsp70 基因表达显著提高 (P＜0.05),差异具有统计学意义;并且当归红芪超滤物的抗氧化损伤作用呈剂量依赖性。结论 当归红芪超滤物具有良好的抗氧化损伤作用,其机制可能与清除自由基、上调 hsp70 表达、抑制 caspase-3 活性有关。     

PSF-SPES共混中空纤维超滤膜制备的研究

以聚砜(PSF)、磺化聚醚砜(SPES)和醋酸纤维素(CA)为膜材料,水为内凝胶剂,采用干湿法制备了PSF-SPES共混中空纤维超滤膜,探讨了PSF-SPES铸膜液中SPES离子交换容量(IEC)、SPES浓度、添加剂、外凝胶剂的选择和热处理对膜性能的影响。所得共混超滤膜性能如下:w=0.0 0 1的Na2SO4截留率19.9%,通量62 L/(h.m2.MPa);w=0.001的PEG4000截留率78.2%,通量85 L/(h.m2.MPa)。此外,以PSF-SPES中空纤维为支撑膜,采用醋酸纤维素作为涂层液,研究了CA/PSF-SPES复合超滤膜性能,讨论了CA/PSF-SPES共混中空纤维超滤膜结构。     

膜组合技术浓缩辅羧酶

选用高抗污染聚偏氟乙烯(PVDF)超滤膜与醋酸纤维素(CA)反渗透膜相结合的技术浓缩辅羧酶,考察了膜品种的选择、浓缩倍数与通量的关系及膜通量的可恢复性等因素,确定了优化的膜组合技术,可省去一道活性炭吸附工序.由于膜工艺去除了97%的水分,使辅羧酶浓度由初始的0.25%提高到9.4%,降低了成本,缩短了生产周期.     

Protection of ultra-filtration extract from Danggui Buxue Decoction (当归补血汤) on oxidative damage in cardiomyocytes of neonatal rats and its mechanism

Objective  

To investigate whether the administration of the ultra-filtration extract from Danggui Buxue Decoction (当归补血汤, EDBD) was able to protect cardiomyocytes from oxidative injury of rats induced by hydrogen peroxide (H₂O₂) and its potential mechanism.     

连续板式超滤系统在头孢菌素C发酵液过滤提纯中的应用

目的比较连续板式超滤与间歇板式超滤在头孢菌素C发酵液过滤提纯中的效果。方法进行30批连续板式超滤与间歇板式超滤的对比试验。结果表明连续式板式超滤分离头孢菌素C发酵液具有膜污染程度小,清洗后膜通量易恢复,滤液质量好、滤液单位均一等优势。结论连续板式超滤更适应头孢菌素C的过滤分离及与后续提取工艺的整合。     

METABOLISM OF URIDINE IN EXPANDED EXTRACELLULAR VOLUME STATES

1. Uridine and uridine monophosphate (UMP) are natriuretic and a vasopressor in intact rats. In deoxycorticosterone acetate (DOCA)-salt hypertensive rats metabolic clearance rate (MCR) of uridine is raised and basal plasma uridine diminished, suggesting that metabolism of uridine is linked to changes in extracellular space. 2. Plasma uridine concentration was raised in 38 patients with chronic renal failure compared with age- and sex-matched healthy controls (8.49 μmol/L, 4.37–13.74 μmol/L median, interquartile range, and 2.64 μmol/L 2.51–2.74 μmol/L, respectively, P < 0.001). Plasma uridine was significantly diminished after isotonic fluid removal by ultrafiltration (UF) from 7.25 μmol/L (3.7–11.08) to 5.07 μmol/L (3.3–8.3), P < 0.001, whereas concentration of marker solutes urea and creatinine remained unchanged. During haemodialysis (HD), plasma uridine fell significantly from its pre-HD level. 3. In an animal model of expanded extracellular space the one-kidney, one-clip rat, plasma uridine was significantly higher (20.56±1.19 μmol/L, P < 0.01) and MCR diminished (34.93 ± 3.44 mL/kg per min, P < 0.01) compared with sham-operated animals (plasma uridine 12.14 ± 1.07 and MCR 53.59 ± 4.11 mL/ kg per min). Uridine or UMP did not inhibit Na⁺, K⁺-ATPase in either of the two assay systems. 4. It was concluded that catabolism of uridine is reduced by extracellular expansion and probably increased by volume reduction by UF. Such a function may be due to the presence of a hypertensive natriuretic factor postulated by Dahl and de Wardener (1980), but would not be consistent with the ouabain-like factor postulated by other workers in this situation because it has no inhibitory effect on Na⁺, K⁺-ATPase.     

Plasma tryptophan binding to albumin in unipolar depressives

The equilibrium binding constants of the interaction of tryptophan with albumin have been determined in plasma samples from both controls and patients suffering from affective disorders. The data corresponded with literature values for both the albumin concentration in plasma and the equilibrium constant for tryptophan binding to albumin. No differences in the equilibrium constants were detected between patients and controls but a small increase in the albumin concentration was noted in the depressives. It was agreed that this rise would be inadequate to lead to a significant effect on free tryptophan levels. Non-esterified fatty acid analysis indicated no differences between patient groups.     

上海某区学校超滤直饮水水质评价及影响因素

[目的]了解学校超滤直饮水的质量,发现相关危险因素并进行控制,保障学生饮用水安全. [方法]在某区22所中小学(小学12所,中学10所)中随机选取25台超滤直饮水机,在2014年2月及10月分别采集直饮水水样,应用水质综合指数法评价水质状况,通过比较直饮水与相应原水的水质综合指数值评估水质改善情况,以耗氧量去除率[(原水耗氧量-直饮水耗氧量)/原水耗氧量×100％]表示净水能力,并采用二分类logistic回归模型分析水质改善的影响因素. [结果] 25台超滤直饮水机均以市政管网水为原水.50份超滤直饮水水样合格率为80％,不合格项目主要为菌落总数和锌.直饮水水质综合指数(0.374± 0.100)与管网水(0.392±0.027)比较,差异无统计学意义(t=1.26,P=0.22),直饮水有机污染指标水质指数(0.084±0.039)低于管网水(0.122±0.024),差异有统计学意义(t=5.78,P=0.00).直饮水水质改善率为74％,主要来自有机污染指标的改善.使用频率低(日用水量＜50L)及设备净水能力不合格(耗氧量去除率＜25％)会增加直饮水水质恶化的危险. [结论]本研究调查的学校超滤直饮水机能改善水中的有机污染状况,但直饮水仍存在一定卫生问题,易受到多种因素的影响.     

当归红芪超滤物对氧化损伤乳鼠心肌细胞的保护作用及其机制

目的 探讨当归红芪超滤物对H_2O_2致乳鼠心肌细胞氧化损伤的保护作用及其可能机制.方法 用高浓度的H_2O_2(400 μmol/L)在Wistar乳鼠原代培养的心肌细胞上建立氧化损伤模型,用不同质量浓度的当归红芪超滤物(3.75、7.5、15 mg/mL)进行干预.在倒置显微镜下观察各实验组心肌细胞的搏动频率,用MTT法检测心肌细胞的存活率,用试剂盒检测细胞培养上清液中乳酸脱氢酶(LDH)、肌酸激酶(CK)的活性及细胞内超氧化物歧化酶(SOD)的活性、丙二醛(MDA)、髓过氧化物酶(MPO)的量.RT-PCR技术检测caspase-3、hsp70基因在心肌细胞中的表达情况.结果 当归红芪超滤物显著提高氧化损伤心肌细胞的细胞活力;与损伤组比较,当归红芪超滤物各干预组心肌细胞LDH、CK、MPO、MDA量显著降低(P<0.01),SOD活性显著提高(P<0.01),caspase-3基因表达显著降低(P<0.05),hsp70基因表达显著提高(P<0.05),差异具有统计学意义;并且当归红芪超滤物的抗氧化损伤作用呈剂量依赖性.结论 当归红芪超滤物具有良好的抗氧化损伤作用,其机制可能与清除自由基、上调hsp70表达、抑制caspase-3活性有关.     

20(S)-原人参二醇药质体的制备及体外评价

目的:研制20(S)-原人参二醇(Ppd)药质体和Brij78修饰的Ppd药质体并对其进行体外评价。方法:采用薄膜超声法制备Ppd药质体和Brij78修饰的Ppd药质体,用超速离心法测包封率,用动态光散射(DLS)考察粒径分布,以粒径和包封率为指标,分别考察温度、乙醇、酸碱和人工胃肠液等对药质体的影响。结果:薄膜超声法制备的Ppd药质体的包封率为(80.84±0.53)%,粒径100.1 nm;Brij78修饰的Ppd药质体的包封率为(72.76±0.63)%,粒径为117.3 nm。结论:该药质体制备工艺简单可行,制剂学性质较稳定。