鹿茸醇提物抗氧化作用的实验研究

用鹿茸醇提物对用环磷酰胺处理后的小鼠进行灌胃实验,以探讨鹿茸醇提物对该小鼠抗氧化作用的影响。实验结果表明:鹿茸醇提物组(即实验组)小鼠每50μL血中的红细胞内SOD的活性为191±07u,而对照组为152±09u,两组相比较,差异显著(P<0.05);实验组小鼠肾脏中丙二醛(MDA)的含量为327±02nmol/g,而对照组为356±05nmol/g,两组相比较,差异显著(P<0.05)。结果提示,鹿茸醇提物可增强该小鼠的抗氧化作用     

钩藤提取物与阿片受体结合特点分析

用放射配体结合实验方法确定钩藤提取物是否能与阿片受体发生相互作用,具体以3H-diprenorphine为标记配体,反应体系及反应条件同饱和结合实验,选用不同浓度的吗啡(10-10~10-5nmol/L)或钩藤提取物(0.125~4mg/mL)为竞争药物,考察钩藤提取物与转染阿片受体的结合水平.结果表明,钩藤提取物(0.125~4 mg/mL)浓度依赖地竞争3H-diprenorphine(1nmol/L)与μ、δ、κ3种阿片受体的结合,其IC50值分别为(1.27±0.86)mg/mL(n=3)(、0.59±0.21)mg/mL(n=4)和(1.20±0.24)mg/mL(n=3),其Ki值分别为(0.41±0.27)mg/mL(n=3)、(0.26±0.09)mg/mL(n=4)和(0.38±0.08)mg/mL(n=3),说明钩藤提取物非选择性地与μ、δ、κ三种阿片受体结合.     

解读米非司酮在妇产科疾病治疗中的应用及临床效果

妇产科作为医院内部的重要科室,主要研究女性生殖系统疾病的诱因、诊治方法、妊娠、分娩、妇科保健等,其就诊的许多女性患者患有外阴疾病、阴道疾病、卵巢疾病等,这些疾病严重影响了患者的日常生活,所以需要加强疾病治疗.药物治疗是控制患者病情发展的重要举措,米非司酮作为强抗孕激素,与孕酮受体、糖皮质激素受体亲和力较强,现已广泛应用...     

大鼠心脏胞浆胞核雌激素受体的羟磷灰石放射分析法

用羟磷灰石放射分析法分析大鼠心脏胞浆、胞核雌激素受体,表明大鼠心脏雌激素受体具有可饱和性、低容量和高亲和力、甾体特异性和稳定结合等特性;饱和分析表明雌、雄鼠心脏胞浆雌激素受体最大结合容量分别为6.91±1.08fmol/mg蛋白质和6.05±0.93fmol/mg蛋白质((?)±SD),雌鼠心脏胞核雌激素受体最大结合容量为138.3±23.8 fmol/mg DNA((?)±SD);单点分析测得雌、雄鼠心脏胞浆雌激素受体的饱和容量分别为4.25±0.72fmol/mg蛋白质(n=10)和3.98±0.87fmol/mg蛋白质(n=10)((?)±SD),雌鼠心脏胞核雌激素受体的饱和容量为113.45±2.87fmol/mg DNA(n=10)((?)±SD)。相同5份雌鼠心脏胞浆、胞核雌激素受体的最大结合容量的变异系数分别为3.69％和7.46％,表明此方法重复性好。     

米非司酮（RU486）对人子宫肌瘤组织雌,孕激素受体的影响

孕酮促进子宫肌瘤生长，米非司酮则可缩小肌瘤体积。为进一步了解米非司酮的抗孕酮作用，本文研究米非司酮治疗后子宫肌瘤细胞的雌、孕激素受体状况。方法：将有子宫肌瘤症状的妇女２２人随机分成２组（对照组１２人，米非司酮组１０人）。患者年龄为３０～５０岁，平均４２０９岁。米非司酮组在手术前一周，每天口服米非司酮２５ｍｇ。切除子宫后立即取一块肌瘤组织及子宫内膜，在福尔马林固定，以后用石蜡包埋。肌瘤样品经单克隆抗体及ＬＳＡＢ反应后，用于研究雌、孕激素受体的表达情况。利用计算机分析系统测定平均密度做受体的定量分析。子宫内膜组织用于月经周期的组织学分期。结果：与对照组相比，米非司酮组显示（１）雌激素受体含量在增生期明显增加（Ｐ＜００５）；（２）雌激素受体含量在分泌期无明显变化（Ｐ＞００５）；（３）孕激素受体含量无论是在增生期还是分泌期均明显减少（Ｐ＜００５）。结论：米非司酮能降低肌瘤细胞的孕激素受体含量，这样它可抑制孕酮促肌瘤组织生长的作用     

胎膜早破对新生儿脐血免疫球蛋白及补体的影响

目的:研究胎膜早破时新生儿脐血免疫球蛋白、补体的变化规律。方法:应用速率透射比浊法检测79例新生儿脐血IgG、IgA、IgM和补体C3、C4水平,追踪新生儿出生1周内感染发生的情况,其中有胎膜早破史的研究组38例,无胎膜早破史的对照组41例。结果:胎膜早破组脐血IgA(0.16±0.12)g/L,对照组(0.06±0.03)g/L,(P<0.01);胎膜早破组IgM(0.24±0.15)g/L,对照组(0.16±0.03)g/L,(P<0.01),差异有统计学意义;脐血IgG水平无明显变化;脐血IgA浓度在胎膜早破72h为0.234±0.156)g/L,较胎膜早破<12h的0.091±0.047g/L明显增加,差异有统计学意义(P<0.05);脐血补体C3(0.76±0.35)g/L,对照组(0.93±0.21)g/L,(P<0.05),C4(0.16±0.09)g/L,对照组0.20±0.05g/L,(P<0.05),研究组明显低于对照组,差异有统计学意义。结论:有胎膜早破史的新生儿,脐血免疫球蛋白IgA、IgM浓度升高,IgG不受胎膜早破的影响,脐血补体C3、C4水平下降。脐血IgA、IgM及补体C3、C4均能反映胎膜早破个体合并宫内感染。     

抗人绒毛膜促性腺激素（HCG）单克隆抗体的研制和特性分析

以HCG为抗原,免疫BALB/c小鼠,取其脾细胞与小鼠Sp2/0—Ag14骨髓瘤细胞融合,经反复筛选和再克隆化,获得8株能稳定分泌抗HCG特异单克隆抗体的杂交瘤细胞株。对其中6个高效价单抗进行了特异性和抗原决定簇检测,选出两个抗相距较远不同决定簇的单抗(2D_4,4F_4)作进一步特性分析。结果显示:免疫球蛋白亚类鉴定,2D_4为IgGl亚类,4F_4为IgG2a亚类;亲和力常数(K_(affi)),2D_4为5.41±0.94×10~(-10)mol/L,4F_4为1.37±0.33×10~(-9)mol/L。证实该两种单克隆抗体可用于研制有关临床诊断试剂盒。     

SLE患者淋巴细胞凋亡及血清新蝶呤、γ-干扰素水平研究

探讨SLE患者体内淋巴细胞凋亡率、巨噬细胞功能相关的细胞因子(新蝶呤、γ-干扰素)水平及两者间相互关系,并同时与抗ds-DNA抗体滴度、疾病活动性评分(SLAM评分)进行相关性分析.应用Annexin V凋亡检测试剂盒及流式细胞仪检测淋巴细胞凋亡率;采用ELISA法检测血清γ-干扰素、新蝶呤水平.结果发现:(1)SLE活动期患者外周血淋巴细胞凋亡率((13.07±7.39),n=30)明显高于非活动期患者((4.08±3.55),n=8,P<0.001)及正常人((5.13±3.37),n=11,P<0.001).(2)抗ds-DNA抗体阳性组患者淋巴细胞凋亡率((12.98±9.25),n=20)与阴性组((9.35±4.76),n=18)相比无差异(P=0.14).淋巴细胞凋亡率与抗ds-DNA抗体滴度无相关性(r=0.112,P=0.77).(3)SLE患者血清新蝶呤水平((1.39±1.10)μg/L,n=20)极显著高于正常人((0.36±0.19)μg/L,n=20,P<0.01).(4)SLE活动期患者血清γ-干扰素水平((58.97±34.52)ng/L,n=15)显著高于正常人((28.06±2.35)ng/L,n=16,P<0.05).(5)SLE患者淋巴细胞凋亡率与血清新蝶呤水平呈正相关(r=0.446,P<0.05,n=22),与SLAM评分呈正相关(r=0.533,P<0.001,n=38),血清新蝶呤水平与SLAM评分亦呈正相关(r=0.485,P<0.05,n=22).未发现SLE患者淋巴细胞凋亡与抗ds-DNA抗体产生相关,未发现明显升高的细胞凋亡率与血清新蝶呤     

HCG日孕酮水平与体外受精-胚胎移植治疗结局的关系探讨

目的:探讨在体外受精-胚胎移植(IVF-ET)控制性促排卵(COH)过程中,人绒毛膜促性腺激素(HCG)日孕酮(P)浓度与IVF-ET治疗结局的关系.方法:分析350个IVF-ET取卵周期,均采用黄体中期垂体降调节方案,按HCG日血清孕酮浓度分为3组,分别为A组67例(1.0≤P2.0 nmol/L)、B组133例(2.0≤P3.0 nmol/L)、C组150例(3.0≤P4.77 nmol/L).比较3组患者的基本临床资料、卵子及胚胎资料、周期取消及妊娠结局情况.结果:HCG日血清孕酮浓度在3.0~4.77 nmol/L组时,获卵数、MII卵数及受精数均高于其他组;同时种植率及妊娠率亦最高.结论:HCG日血清孕酮浓度水平在3.0~4.77 nmol/L之间能获得更成熟的卵子,同时不增加因多卵泡发育引起卵巢过度刺激综合征(OHSS)导致的周期取消率.     

药物流产150例临床分析

米非司酮是一种新型孕酮拮抗剂,通过其对子宫内膜及脱膜靶细胞的孕激素受体的结合,阻止了体内孕酮对子宫内膜或脱膜的作用,所以产生较强的抗孕酮作用。我院选择自愿要求用药物终止妊娠的健康妇女150例,停经49天以内,血CHG检查阳性,B超检查确诊宫内妊娠。米非司酮25mg/片,每天早上口服2片,晚上口服1片,连服2天,第3天晨来院空腹顿服米索前列醇600ug,留院观察6小时。结果:完全流产130例(86.6%),不全流产10例(6.6%),失败10例(6.6%),阴道大出血行清宫术3例,本药使用方便安全,副反应小,效果满意。     

Requirement of hormone for thermal conversion of the glucocorticoid receptor to a DNA-binding state

A central question arising from the model of eukaryotic gene regulation by steroid hormone receptors is whether or not proteins represent pre-existing gene regulatory proteins that are activated on exposure to the extracellular signal. It has been generally believed that the ligand-binding of steroid hormone receptors triggers an allosteric change in receptor structure, manifested by an increased affinity of the receptor for DNA in vitro and nuclear target elements in vivo, as monitored by nuclear translocation. But this model has been challenged by recent reports indicating that glucocorticoid and progesterone receptors bind specifically in vitro to target DNA sequences even in the absence of hormone. On the other hand, it appears that the hormone induces protection in vivo of the glucocorticoid response element of the tyrosine amino transferase gene. Here we show that under conditions permitting minimal in vitro manipulation, the steroid-free glucocorticoid receptor in crude cytosol associates with the hsp90 heat shock protein (relative molecular mass Mr approximately equal to 90,000) to form a large 300K complex, rather than the 94K liganded receptor monomer. More importantly, we have developed an assay to demonstrate the requirement of hormone to dissociate the 300K complex by heat treatment. Specific DNA-binding activity of the receptor becomes apparent in this process, showing that DNA binding occurs but is inhibited in the large heteromeric complex. We propose a model in which receptor function is repressed by association of the receptor with hsp90. Dissociation of this complex is induced by the binding of steroid and is apparently an irreversible process.     

Bis(7)-Tacrine, a promising anti-Alzheimer's agent, attenuates glutamate-induced cell injury in primary cultured cerebrocortical neurons of rats

The effects of bis(7)-tacrine, a novel dimeric acetylcholinesterase (AChE) inhibitor, on glutamate-induced cell injury were investigated in primary cerebral cortical neurons of rats. Exposure of cultured neurons (12 days after plating) to 0.5 mmol/L glutamate for 30 min resulted in significant cell damage. Pretreatment with bis(7)-tacrine (0.03–1.0 μmol/L) reduced the glutamate-induced neurotoxicity in a concentration dependent manner and the maximal response was seen at 1 μmol/L with approximately, 30% protection. A receptor binding assay showed that bis(7)-tacrine can completely displace MK-801 binding to rat cortical membrane with an IC₅₀ of 0.57 μmol/L. These findings suggest that bis(7)-tacrine can directly interact with N-methyl-D-aspartate receptor channel complex, which may contribute to the inhibitor's protective effects against glutamate-induced excitotoxicity. Thus, it is possible that anti-glutamate/anti-AChE synergism is responsible for potentially better Alzheimer's therapy of bis(7)-tacrine relative to tacrine. Biography: Zhang Bai-fang (1974-), female, Ph. D. candidate, research direction: Alzheimer's disease and ischemia     

Influence of site-directed mutation of cytochrome b5 Phe35 on the protein’s structure and properties

Kinetic studies of the heme dissociation from the wild type and Phe35Tyr, Phe35Leu mutants of bovine liver microsomal ferricytochrome b 5 indicate that the oxidized Phe35Tyr mutant is more stable towards denaturant than wild type but Phe35Leu mutant proceeded with a different mechanism compared with wild type cytochrome b 5 and Phe35Tyr mutant protein. Because of the decrease of side chain volume in Phe35Leu mutant, a cavity produced in the interior of the protein may offer a channel for urea molecule to enter the hydrophobic pocket. When urea concentration is larger than 5 mol/L, the urea molecule may compete to coordinate the iron of heme with His39, that results in sharp increase of the rate of heme dissociation. The interaction between cytochrome b 5 and cytochrom c demonstrated that a 1:1 protein complex was formed between the two proteins. The binding constants of cytochrome b 5 with cytochrome c are: wild type K A=4.2(±0.01)×10 6(mol/L) -1 , Phe35Tyr K A=3.7(±0.01)×10 6(mol/L) -1 and Phe35Leu K A=4.7(±0.01)×10 6(mol/L) -1 respectively ( I =1 m mol/L, pH 7.0 soldium phosphate buffer, 25℃). These results clearly show that the mutation at Phe35 has no influence on the binding of cytochrome b 5 with cytochrome c and that the hydrophilic patch residues are not involved in the binding of cytochrome b 5 and cytochrome c.     

组织胺对大鼠DRG神经元ATP-激活电流的抑制作用

目的:探讨组织胺对大鼠DRG神经元ATP-激活电流的调制作用.方法:采用全细胞膜片钳技术,在新鲜分离的大鼠背根神经节细胞上进行.结果:实验观察到组织胺在DRG神经元可引起内向电流,并有明显的浓度依赖性.在被检测的DRG神经元中,85%(30/35)的细胞对ATP敏感,可引起一浓度依赖性的去敏感的内向电流.预加10-8、10-7、10-6、10-5、10-4mol/L组织胺后,对ATP-激活电流的抑制分别是:(12.50±3.2%(n=5)、(24.49±3.5%(n=5)、(35.18±4.5%(n=6)、(32.62±5.8%(n=8)、(23.53±4.2%(n=5),呈浓度依赖性.结论:组织胺对大鼠DRG神经元ATP-激活电流有明显的抑制作用.     

Involvement of Oxidative Stress and Down-Regulation of Bcl-2 in Arachidonic Acid-Induced Apoptosis in HUVECs

0IntroductionAraacicdhi,diosn fiocu ancidd p(reAdAo)m i,naanntelsys eantt itahle p sonl-y2u npsoastiutiroante doff actetl-ylular phospholipids . Normal free AAconcentrationin humanblood ranges from5 .8μmol/Lto 49 .3μmol/L[1].It is re-leased mostlythroughactivation of phospholipase A2by physi-ological and pathological sti muli[2]. Free AAcan be metabo-lizedinto various eicosanoids via specific enzymes such as cy-clooxygenases ( COX) , lipoxygenase and cytochromesP-450[3]. During AA met…