新型抗蝰蛇毒血清对不同喹蛇毒作用的实验研究

目的　探讨新型抗蝰蛇毒血清对国产圆斑蝰蛇毒及缅甸蝰蛇毒的作用 .方法　采用免疫电泳、SDS -聚丙烯酰胺电泳及动物实验等方法 .结果　国产圆斑蝰蛇毒的LD50 (腹腔注射 )为 0 .3 0 6± 0 .0 0 3mg/kg ,缅甸蝰蛇毒的LD50 (腹腔注射 )为 0 .2 90± 0 .0 0 3mg/kg .免疫电泳结果表明国产圆斑蝰蛇毒和缅甸蝰蛇毒均和新型抗蝰蛇毒血清产生明显的免疫沉淀线 .体外中和实验表明抗蝰蛇毒血清对国产圆斑蝰蛇毒的中和抗体效价为 2 75 0 μg/ml(约45 0LD50 ) ,对缅甸蝰蛇毒的中和抗体效价为 2 490 μg/ml(约 43 0LD50 ) .体内保护实验表明给予 0 .0 5ml抗蝰蛇毒血清可抵御 2 5 4μg(约41 5LD50 )国产圆斑蝰蛇毒或 116μg(约 2 0LD50 )缅甸蝰蛇毒的攻击 ,使小鼠全部存活 .结论　新型抗蝰蛇毒血清对国产圆斑蝰蛇毒及缅甸蝰蛇毒的中和抗体效价均较高 ,有较大的应用价值 .     

抗蝰蛇毒血清治疗蝰蛇伤临床疗效考察

目的：对国产抗蝰蛇毒血清治疗蝰蛇伤的疗效、治疗剂量、不良反应等进行临床疗效的考察。方法：蝰蛇伤患者335例，抗蝰蛇毒血清治疗组322例，不使用抗蝰蛇毒血清治疗患者13例。结果：使用抗蝰蛇毒血清治疗组、死亡7例（2．2％），未见不良反应。没用抗蝰蛇毒血清治疗患者，死亡9例（69．2％），结论：抗蝰蛇毒血清是治疗蝰蛇伤的特效、高效和安全的急救药物。     

抗蝰蛇毒血清治疗蝰蛇伤临床疗效考察

目的对国产抗蝰蛇毒血清治疗蝰蛇伤的疗效、治疗剂量、不良反应等进行临床疗效的考察. 方法蝰蛇伤患者335例,抗蝰蛇毒血清治疗组322例,不使用抗蝰蛇毒血清治疗患者13例. 结果使用抗蝰蛇毒血清治疗组,死亡7例(2.2%),未见不良反应.没用抗蝰蛇毒血清治疗患者,死亡9例(69.2%), 结论抗蝰蛇毒血清是治疗蝰蛇伤的特效、高效和安全的急救药物.     

圆斑蝰蛇毒中性磷脂酶A2对不同种类血管条作用的比较

本文比较了福建圆斑蝰蛇毒中性磷脂酶Ａ２（ＰＬＡ２－３）对人胃网膜动脉条、兔和大鼠主动脉条的作用，表面ＰＬＡ２－３对处于静息状态和预收缩状态的人网膜动脉能诱发松弛反应，而对大鼠和兔主动脉诱发剂量依赖性收缩反应，表明该ＰＬＡ２的血管作用具有血管种类差异性。ＰＬＡ２－３对大鼠主动脉的收缩反应是内皮细胞非依赖性的，去除内皮细胞能增强ＰＬＡ２－３所诱发的收缩反应；ＰＬＡ２－３所诱发的大鼠主动脉条收缩反应可能     

圆斑蝰蛇毒中性磷脂酶A2对大鼠心脏的药理作用

本文研究了福建圆斑蝰蛇毒中性磷脂酶Ａ２（ＰＬＡ２）对大鼠心脏的药理作用。实验结果显示，ＰＬＡ２使麻醉大鼠心率减慢，Ｐ－Ｒ间期延长、但ＱＲＳ波群变化较小。对离体大鼠右心房诱发正性频率作用，而对大鼠Ｌａｎｇｅｎｄｏｒｆｆ心脏诱发心率减慢型心率失常。这种房室率分离现象与从整体心电图上所观察到的Ｐ－Ｒ间期延长结果相吻合，表明ＰＬＡ２影响到心脏传导系统，尤其是房室交界区。对离体Ｌａｎｇｅｎｄｏｒｆｆ心脏产生     

蝰蛇毒压电免疫传感器固定方法的研究

目的：为研制蝰蛇毒压电免疫传感器，研究抗蛇毒抗体固定于石英晶体银电极表面的固定技术。方法：采用马抗蝰蛇毒血清抗体和抗蝰蛇毒鸡卵黄抗体作为生物敏感材料，对比研究了胱胺自组装-PSS反相吸附法和PEI粘附-戊二醛交联法：比较了采用两种固定方法所制的压电免疫传感器的性能。结果：鸡卵黄抗体采用PEI粘附-戊二醛交联法效果较好，其制备的IgY压电免疫传感器检测蝰蛇毒灵敏度为0．5ug／mL；而马血清抗体用胱胺自组装-PSS反相吸附法较好，其制备的IgG’免疫传感器检测蝰蛇毒灵敏度为10ug／mL。结论：以PEI粘附-戊二醛交联法固定抗蝰蛇毒鸡卵黄抗体所制备的蝰蛇毒压电免疫传感器的性能稳定，特异性好，可实现蛇毒的快速检测。     

蝰蛇毒压电免疫传感器的研制

采用聚乙烯亚胺(PEI)科学仪黏附、戊二醛(Glu)交联的方法,将抗蝰蛇毒IgY固定于石英品体表面,制成蝰蛇毒压电免疫传感器.该传感器用于检测浓度范围为0.5～100μg/mL的蝰蛇毒时,呈线性相关,相关系数为0.962,具有良好的选择性.     

精制抗蝮蛇毒血清治疗蝮蛇咬伤920例临床报告

我院自1990年至1994年应用精制抗蝮蛇毒血清治疗蝮蛇咬伤920例，现报道如下。     

双价抗蛇毒IgY灌胃对眼镜蛇、蝰蛇伤小鼠的保护作用

目的： 比较双价抗蛇毒鸡卵黄抗体(IgY) 经腹腔注射或灌胃对蝰蛇、眼镜蛇伤小鼠保护作用的差异,为其口服制剂的应用奠定理论基础。方法：2种单一抗原按顺序依次交替注入单只鸡体内,水稀释法制备双价抗蛇毒IgY;间接ELISA法观察双价抗蛇毒IgY在体外及其灌胃后小鼠血浆中的效价,通过胃排空试验确定灌胃给药的最佳时间,在此基础上,比较双价抗蛇毒IgY腹腔注射或灌胃对蛇伤小鼠的保护作用。结果：初次免疫后28 d至第42 d,以水稀释法提取的双价抗蛇毒IgY对眼镜蛇毒及蝰蛇毒的效价分别为1∶12 800和1∶6 400。不同浓度的双价抗蛇毒IgY灌胃2.5-3.5 h,小鼠的胃排空率均达68.9％以上,血浆中抗体浓度亦相应达高峰。该抗体腹腔注射或提前灌胃均能极显著延长眼镜蛇和蝰蛇毒中毒小鼠的存活时间（P<0.01）,同等剂量的双价抗蛇毒IgY提高眼镜蛇伤小鼠存活率优于蝰蛇伤,而灌胃有效剂量约为腹腔注射的10倍。结论：双价抗蛇毒IgY经2种给药途径（注射、口服）均能有效保护动物免受眼镜蛇毒和蝰蛇毒的攻击。     

眼镜蛇伤大鼠多项指标动态变化与抗蛇毒血清的时效关系

目的: 观察蛇伤后大鼠生化血气分析及病理等动态变化,探讨其与抗蛇毒血清使用时效性的关系,为优化眼镜蛇伤的临床治疗方案提供实验依据。方法: SD大鼠注入2-4 LD₅₀舟山眼镜蛇毒造模,于注毒后不同时段(20-140 min)分别进行血液生化、血气分析、肌组织病理等检测及注入抗眼镜蛇毒血清(40-120 min,血清/蛇毒:125 kU/g)对上述指标的影响。结果: 大鼠注入4 LD₅₀蛇毒20 min后二氧化碳总量(TCO₂)、剩余碱(BE)及酸碱度(pH)逐渐下降;而心酶、肝酶及胆红素明显上升,于60及120 min各出现1个峰值,与0 min相比有显著差异(P<0.05);心肌、骨骼肌于40 min时点出现广泛浊肿变性、凝固性坏死及炎症细胞浸润。注入2 LD₅₀蛇毒动物的心酶、肝酶及胆红素指标变化趋势与4 LD₅₀剂量组相似,但其峰值出现时间相对延迟且峰值较低。在心酶出现第1个峰值前施予抗血清,蛇伤大鼠的保护率可达60%以上;但第2个峰值后施予抗血清的疗效不显著。结论: 眼镜蛇伤后的心酶、肝酶等相关指标呈双峰变化规律,第2个峰值前为使用抗血清的有效时段。     

The Protective Effect of Vipera Raddei Venom on Peripheral Nerve Damage

Acute experiments were performed on spinal rats to study the protective actions of Vipera raddei venom after section of the sciatic nerve. Individual spike activity was recorded from interneurons and motoneurons in the lumbar segment of the spinal cord, induced by stimulation of the sciatic nerve and the extensor (gastrocnemius) and flexor (peroneus communis) nerves on the lesioned and symmetrical intact sides in controls and after daily injections of venom for four weeks. In animals not treated with Vipera raddei venom, the lesioned side lacked interneuron and motoneuron responses to stimulation of the extensor and flexor nerves of the distal stump, though these were present on stimulation of the contralateral side; responses were the inverse of this on the intact side, due to the failure of the proximal and distal stumps to fuse, as also demonstrated by atrophy of the distal stump of the sciatic nerve and the absence of movement activity in the lesioned limb. Treatment with Vipera raddei venom led to restoration, by four weeks, of interneuron and motoneuron responses on the lesioned side on stimulation of the ipsilateral nerves and on the intact side by stimulation of the contralateral nerves; this is the result of apparent fusion of the proximal and distal stumps of the lesioned nerve. Further evidence for this was hypertrophy of the distal stump and restoration of movement activity in the lesioned limb. These results show that Vipera raddei venom has potential for use in regenerating damaged peripheral nerves. __________ Translated from Rossiiskii Fiziologicheskii Zhurnal imeni I. M. Sechenova, Vol. 90, No. 12, pp. 1441–1456, December, 2004.     

The Protective Effect of Recombinant FomA-expressing Lactobacillus acidophilus Against Periodontal Infection

A number of studies have shown that the outer membrane protein FomA found in Fusobacterium nucleatum demonstrates great potential as an immune target for combating periodontitis. Lactobacillus acidophilus is a useful antigen delivery vehicle for mucosal immunisation, and previous studies by our group have shown that L. acidophilus acts as a protective factor in periodontal health. In this study, making use of the immunogenicity of FomA and the probiotic properties of L. acidophilus, we constructed a recombinant form of L. acidophilus expressing the FomA protein and detected the FomA-specific IgG in the serum and sIgA in the saliva of mice through oral administration with the recombinant strains. When serum containing FomA-specific antibodies was incubated with the F. nucleatum in vitro, the number of Porphyromonas gingivalis cells that coaggregated with the F. nucleatum cells was significantly reduced. Furthermore, a mouse gum abscess model was successfully generated, and the range of gingival abscesses in the immune mice was relatively limited compared with the control group. The level of IL-1β in the serum and local gum tissues of the immune mice was consistently lower than in the control group. Our findings indicated that oral administration of the recombinant L. acidophilus reduced the risk of periodontal infection with P. gingivalis and F. nucleatum.     

Pharmaco-Modulations of Induced Edema and Vascular Permeability Changes by Vipera lebetina Venom: Inflammatory Mechanisms

The inflammatory response induced by Vipera lebetina venom (VLV) in the mice hind paw was evaluated by paw edema value and vascular permeability changes. The edema was produced in a dose- and time-dependent manner. This response was maximal within 2 h and disappeared after 24 h The minimum edema-forming dose was estimated at 0.8 μg/20 g body weight. Microscopic examination confirmed that VLV also induces skin structure alterations with collagen fiber dissociation and polynuclear infiltration, which is characteristic of edema formation. The induced edema with VLV (1 μg/paw) could be due to the release of pharmacological active substances at the site of injection. Histamine, serotonine, and arachidonate metabolites may play important roles in the vasoactive and edematic effect of VLV since pretreatment of mice with cromoglycate, cyproheptadine, ibuprofen, loratidine, and indomethacin significantly reduced the edema formation (77, 63, 57, 45, and 43 %, respectively). The obtained results demonstrate that the induced edema and vasodilatation by this venom may be triggered and maintained by different pharmacological mechanisms, since cromoglycate and cyproheptadine were the most active inhibitors of the edema. The relationships between histamine and serotonin release from mast cells and arachidonate metabolites activation could be the main step in edema-forming and the induced vasodilatation by the venom.     

胰岛素对大鼠心肌缺血再灌注损伤保护作用及机制研究

目的 探讨胰岛素对大鼠缺血再灌注损伤心肌的保护作用及其保护机制。方法 结扎SD大鼠左冠状动脉前降支（LAD）．建立大鼠缺血再灌注模型，将48只SD雄性大鼠随机分组为：缺血再灌注对照组（18只），假手术组（12只），胰岛素处理组（18只），分别给予生理盐水、冠脉穿线（不结扎）、胰岛素干预。在再灌注结束后，检测心肌组织中丙二醛（MDA）含量、血清中乳酸脱氢酶（LDH）活性、心肌梗死范围（IS／AAR％）及心肌细胞凋亡指数（AI），并进行组间比较。结果 与缺血再灌注对照组相比，胰岛素处理组可明显降低MDA（P〈0．05）、LDH值（P〈0．01），减少心肌IS／AAR％和AI（P〈0．01）。结论 胰岛素对大鼠再灌注心肌损伤具有保护作用，其保护机制可能与抑制细胞凋亡及抗氧自由基作用有关。     

Piperine Augments the Protective Effect of Curcumin Against Lipopolysaccharide-Induced Neurobehavioral and Neurochemical Deficits in Mice

The aim of the present study was to investigate the protective effects of curcumin alone and in combination with piperine against lipopolysaccharide (LPS)-induced neurobehavioral and neurochemical deficits in the mice hippocampus. Mice were treated with curcumin (100, 200, and 400 mg/kg, p.o.) and piperine (20 mg/kg, p.o.) for 7 days followed by LPS (0.83 mg/kg, i.p.) administration. Animals exhibited anxiety and depressive-like phenotype after 3 and 24 h of LPS exposure, respectively. LPS administration increased the oxido-nitrosative stress as evident by elevated levels of malondialdehyde, nitrite, and depletion of glutathione level in the hippocampus. Furthermore, we found raised level of pro-inflammatory cytokines (IL-1β and TNF-α) in the hippocampus of LPS-treated mice. Pretreatment with curcumin alleviated LPS-induced neurobehavioral and neurochemical deficits. Furthermore, co-administration of curcumin with piperine significantly potentiated the neuroprotective effect of curcumin. These results demonstrate that piperine enhanced the neuroprotective effect of curcumin against LPS-induced neurobehavioral and neurochemical deficits.     

云南中缅边境蚊科昆虫群落的研究

为调查和了解云南省瑞丽市中缅边境蚊虫多样性状况,应用灯诱法和采集幼虫法对瑞丽市中缅边境上高丽村和周边方圆4 km原始森林内的蚊虫的优势种组成、蚊虫群落结构的集中性指数、多样性指数和均匀度指数进行分析.结果显示,在居民区共采获蚊虫3 305只,共5属13种,隶属于蚊科Culicidae中的伊蚊属Aedes、库蚊属Cule...     

瘦素对血管内皮细胞ECV-304缺氧/复氧损伤的保护作用

探讨外源性瘦素（Leptin）对血管内皮细胞ECV-304缺氧／复氧（H／R）损伤保护作用及其作用机制。建立人脐静脉（ECV．304）内皮细胞缺影复氧损伤模型,观察不同的缺氧和复氧时间对内皮细胞的损伤作用。设立正常对照组、损伤组、干预组,每组6例;利用试剂盒测定乳酸脱氢酶、丙二醛和超氧化物歧化酶的释放量;四唑盐比色法（MTT）测定血管内皮细胞的存活率。结果显示,单纯缺氧组和缺彰复氧组均可见细胞变圆、收缩、脱落;细胞死亡率较正常组增加;细胞上清中丙二醛（MDA）与乳酸脱氢酶（LDH）含量增加,超氧化物歧化酶（SOD）含量降低;缺氧／复氧组较单纯缺氧组损伤更加明显,与正常培养组相比具有显著意义（P〈0．05）。Leptin晚期预处理后,细胞形态基本上保持正常,上述检测指标与缺氧／复氧组相比有显著意义（P〈0．05）。并且50μg／L Leptin的保护作用最为明显。表明Leptin对ECV-304细胞缺氧／复氧损伤的保护作用具有剂量依赖性。     

The Protective Role of Per2 Against Carbon Tetrachloride-Induced Hepatotoxicity

Period 2 (Per2) is a key component of the core clock oscillator and is involved in regulating a number of different biological processes and pathways. Here we report that Per2 plays a protective role in carbon tetrachloride (CCl₄)-induced hepatotoxicity via the modulation of uncoupling protein-2 (Ucp2) gene expression in mice. Hepatic injury after acute CCl₄ injection was monitored in both wild-type and Per2-null mice. At the 12-hour time point after CCl₄ treatment, many more vacuolations were observed in the liver tissues of Per2-null mice whereas fatty tissue degeneration primarily occurred in the liver tissues of wide-type mice. Serum alanine and aspartate aminotransferase activities were elevated in Per2-null mice compared with wide-type mice at 24 hours after CCl₄ treatment, which was in agreement with the observation of significantly larger areas of centrilobular necrosis in the livers of Per2-null mice. A deficit of the Per2 gene enhanced Ucp2 gene expression levels in the liver. As a consequence, intracellular levels of ATP markedly decreased in the liver, allowing increased production of toxic CCl₄ derivatives. The absence of Per2 expression caused a dramatic elevation of Clock expression and influenced Ucp2 through a mechanism that involved a Clock-controlled PPAR-α signal transduction pathway. Our studies suggest that the Per2 gene functions in hepatocyte protection from chemical toxicants via the regulation of hepatic Ucp2 gene expression levels.