原卟啉原氧化酶抑制剂类除草剂进展概况

本文对近期开发的原卟啉氧化酶抑制剂按用途进行了简要的介绍。文中涉及原卟啉氧化酶抑制剂的化学结构、生物活性、登记与专利和开发公司等。     

Effect of feeding fermentable fiber on synthesis of total and mucosal protein in the intestine of the growing pig

In a previous study, a reduced efficiency of ileal digestible threonine (THR) use for body protein deposition was observed in growing pigs when pectin was included in the diet. This response was not due to increased physical endogenous ileal THR loss. Our aim was to explore the contribution of diet-induced increases in protein synthesis in the colon, especially mucins, to dietary THR requirements. Twelve barrows (21 kg mean BW) were fed either a cornstarch–soybean meal-based diet (Control) or Control with 12% pectin (Pectin). Pigs were given intravenously 1.5 mmol/kg BW of L-1-¹³C valine (40 mol%) to measure fractional and absolute synthesis rates (FSR, ASR, respectively) of mucosal and whole intestinal protein in the jejunum and colon. Dietary pectin inclusion increased plasma levels of glucose, isoleucine and glutamine (P < 0.05) but had no effect on insulin or urea nitrogen (P > 0.10). There were no differences in FSR and ASR of whole intestinal protein in jejunum and colon (P > 0.10). The FSR of mucosal proteins in colon, not in jejunum, was increased with dietary pectin supplementation (P < 0.05). Assuming mucosal protein mass is constant, these results imply that the higher protein synthesis in colon mucosa contributes to the reduced THR efficiency observed in pectin-supplemented diet.     

仔猪精氨酸的内源合成及其影响因素

由于精氨酸及其代谢产物具有广泛生物学作用,使得近年来研究者们在生理、生化和营养等方面对其作了大量的研究。母乳严重缺乏精氨酸,仔猪精氨酸内源合成对精氨酸的平衡起了重要作用,使得哺乳仔猪精氨酸的内源合成成为精氨酸营养的研究核心。通过对精氨酸内源合成路径和场所的了解,研究者们进一步研究了精氨酸内源合成的影响因素,主要有仔猪日龄、日粮中精氨酸的水平、乳酸盐和皮质醇的浓度等。本文就仔猪精氨酸内源合成的途径和场所、内源合成的量、影响因素以及精氨酸的需要量等进行了综述,重点阐述了精氨酸内源合成的影响因素。     

茚酮肟醚衍生物的合成与生物活性

通过傅－克反应及环化、肟化、成醚等反应,合成了10个未见文献报道的茚酮肟醚类化合物,其结构均经1H NMR、IR、LC/MS及元素分析确证。初步生物活性测试结果表明,所合成的化合物具有明显的杀菌活性或杀虫活性,如在100 mg/L时,化合物 V1 对小麦白粉病菌Erysiphe graminis 的抑制率为 95.6%, V5 对粘虫Mythimna separata的致死率为100%。     

N-(7-氟-3-氧-3,4-二氢-苯并噁嗪-6-基-)乙酰胺类化合物的合成及除草活性

为了寻找高效、安全的具有除草活性的新化合物,利用2-取代乙酰氯和2H苯并噁嗪-3-酮反应合成了9个N-(7-氟-3-氧-3,4-二氢苯并噁嗪-6-基-)乙酰胺类化合物,其结构经元素分析、IR、1H NMR确证。初步除草活性测试表明:在有效剂量75 g/hm2下,化合物 5d 芽后茎叶处理对刺苋Amaranthus spinosus等4种杂草显示出90%以上的抑制率。     

细菌耐药颉颃剂的研究现状及应用

作者介绍了具有颉颃细菌耐药性作用的物质的研究应用进展情况，包括灭活酶抑制剂、药物渗透促进剂、外输泵抑制剂、细菌生物被膜抑制剂、抗菌药物增强剂、耐药质粒消除剂等。     

Effect of NOS on podocytes in hyperlipidemia rats and the protection of simvastatin in podocyte damage

AIM: To investigate the possible effect of hyperlipidemia on golmerular podocytes,the nitric oxide synthase (NOS) availability and the synthesis of NOS in podocyte damage by hyperlipidemia,further to study the protective effect of simvastatin on podocytes.METHODS: 4 groups of Wistar rats were fed high fat diet for 18 weeks.Serum lipid,urinary protein excretion and renal pathological changes were detected.Immunohistochemistry was used to determine the expression of desmin.The expression of nNOS was detected by Western blotting.RESULTS: The level of serum lipid was increased significantly in hyperlipidemic group and treated group after 4 weeks (P<0.01) and was decreased significantly in simvastatin treated group compared with hyperlipidemic group (P<0.01).Podocyte injury was detected under electronic microscopy in hyperlipidemic group after 4 weeks,and the injury became more serious during the lasting time.The expression of desmin was increased in hyperlipidemic group after 4 weeks,and the level was significantly decreased in treated groups (P<0.01).The urinary protein excretion was increased significantly after 6 weeks (P<0.01),and the level was significantly lower in treated groups (P<0.01).The expression of nNOS was significantly decreased in hyperlipidemic and treated groups (P<0.01),and the level significantly decreased in simvastatin group (P<0.01).CONCLUSION: Hyperlipidemia induces podocyte injury.The injury seems to be associated with NO deficiency and decreased renal NOS activity.The injury can be relieved by simvastatin.     

Caspase 3 inhibitor Ac-DEVD-CHO attenuates 10-hydroxycamptothecin-induced activation of NF-κB in Bcap37 cells

AIM:To investigate the role of caspase 3 inhibitor Ac-DEVD-CHO in caspase 3 signaling pathway and NF-κB activation induced by 10-hydroxycamptothecin (HCPT) in human breast carcinoma cells. METHODS:The cell growth inhibition was measured by MTT assay. Agarose gel electrophoresis was performed for detecting cell apoptosis. Western blotting was used for determining protein expression. DIG-EMSA was conducted to measure the DNA-binding activation of NF-κB. RESULTS:Caspase 3 inhibitor Ac-DEVD-CHO attenuated HCPT-induced apoptosis in human breast carcinoma. Ac-DEVD-CHO also suppressed the degradation of caspase 3 and IκBα,and arrested the activation of NF-κB. CONCLUSION:Caspase 3 inhibitor Ac-DEVD-CHO regulates the activation of caspase 3 and NF-κB,and attenuates apoptosis in Bcap37 cell line induced by HCPT.     

N-取代苯并口恶嗪酮类化合物的合成及其生物活性

为寻求具有高生物活性的新农药化合物,以邻氨基苯酚为原料设计合成了N-取代的苯并口恶嗪酮类化合物18个,其化学结构经1H NMR及元素分析确证。初步的生物活性测试结果表明,部分化合物具有良好的除草活性,如化合物c3、c5、c6、c7和c8在浓度为100mg/L时对苋菜Ambrosia tricolorL inn.的抑制率达90%。