氨基化硅胶固定化葡萄糖氧化酶的研究

利用溶胶-凝胶技术,以四甲氧基硅（TMOS）和γ-氨丙基甲基二甲氧基硅烷（APMDMOS）为前驱体制成了一种功能化的材料——氨基化硅胶.并以戊二醛为交联剂,利用该氨基化硅胶为载体对葡萄糖氧化酶（GOD）进行交联固定化,研究了TMOS用量、戊二醛浓度、给酶量、温度和pH值等因素对固定化GOD活力的影响,并考察了固定化GOD的热稳定性和贮存稳定性.红外光谱验证了氨基化硅胶交联固定化GOD的可行性.确定出了优化的固定化条件：TMOS用量为10%,戊二醛的浓度2.0%,给酶量1 600 U,最适pH和最适温度分别为5.2和32℃.固定化GOD具有良好的热稳定性和贮存稳定性.     

白花龙胆花抗炎作用研究

为了研究白花龙胆花的抗炎作用,本文对白花龙胆花水提物和70%乙醇提取物的抗炎活性进行了试验,并测定了水提物和70%乙醇提物中龙胆苦苷的含量.试验采用二甲苯所致小鼠急性耳肿胀试验和二甲苯所致小鼠腹部毛细管通透性试验.将昆明种小白鼠分为7组,分别为空白对照组,白花龙胆花水提物高、中、低剂量组和70%乙醇提取物高、中、低剂量组,灌胃(ig)给药14 d后,用二甲苯分别于小鼠右耳及腹部致炎.测定左右耳重量,计算肿胀度及肿胀抑制率,测定吸光值.结果表明:白花龙胆花水提物和乙醇提取物的中、高剂量组对于二甲苯所致的小鼠急性耳肿胀和小鼠腹部毛细管通透性都有显著的抑制作用.从而表明:白花龙胆花具有显著的抗炎疗效.     

向日葵花盘水溶性多糖提取工艺及抗氧化研究

目的:研究了向日葵花盘中水溶性粗多糖的提取工艺及抗氧化性能.方法:采用单因素试验和L_9(3~4)正交试验设计,对多糖提取工艺进行优化,并采用Fenton体系和邻苯三酚自氧化法评价了该提取物的体外抗氧化能力.结果:优化工艺条件为:提取温度95℃、料液比1:20、提取时间4h,向日葵水溶性粗多糖得率为9.73%,其中温度是影响粗多糖提取的重要因素.结论:结果表明向日葵水溶性粗多糖有较好的抗氧化活性.     

Novel roles for protein kinase Cdelta-dependent signaling pathways in acute hypoxic stress-induced autophagy

Macroautophagy, a tightly orchestrated intracellular process for bulk degradation of cytoplasmic proteins or organelles, is believed to be essential for cell survival or death in response to stress conditions. Recent observations indicate that autophagy is an adaptive response in cells subjected to prolonged hypoxia. However, the signaling mechanisms that activate autophagy under acute hypoxic stress are not clearly understood. In this study, we show that acute hypoxic stress by treatment with 1% O(2) or desferroxamine, a hypoxia-mimetic agent, of cells renders a rapid induction of LC3-II level changes and green fluorescent protein-LC3 puncta accumulation, hallmarks of autophagic processing, and that this process involves protein kinase Cdelta (PKCdelta), and occurs prior to the induction of BNIP3 (Bcl-2/adenovirus E1B 19-kDa interacting protein 3). Interestingly, hypoxic stress leads to a rapid and transient activation of JNK in Pa-4 or mouse embryo fibroblast cells. Acute hypoxic stress-induced changes in LC3-II level and JNK activation are attenuated in Pa-4 cells by dominant negative PKCdeltaKD or in mouse embryo fibroblast/PKCdelta-null cells. Intriguingly, the requirement of PKCdelta is not apparent for starvation-induced autophagy. The importance of PKCdelta in hypoxic stress-induced adaptive responses is further supported by our findings that inhibition of PKCdelta-facilitated autophagy by 3-methyladenine or Atg5 knock-out renders a greater prevalence of cell death following prolonged desferroxamine treatment, whereas PKCdelta- or JNK1-deficient cells exhibit resistance to extended hypoxic exposure. These results uncover dual roles of PKCdelta-dependent signaling in the cell fate determination upon hypoxic exposure.     

Activation of the JNK signaling pathway: breaking the brake on apoptosis

The JNK signaling pathway is involved in regulation of many cellular events, including growth control, transformation and programmed cell death (apoptosis). The role of JNK activation in apoptosis is highly controversial, being suggested to have a pro-apoptotic, anti-apoptotic or no role in this process. It appears that the JNK pathway functions in a cell-type and stimulus-dependent manner and its different components can sometimes play opposing roles in apoptosis. Recent studies reveal that the effect of JNK activation on apoptosis depends on the activity of other signaling pathways like the NF-kappaB pathway. Here we propose a model that can explain how activation of the JNK pathway "breaks the brake" on apoptosis, thereby regulating, but not initiating the apoptotic process.     

钉螺在枫杨防护林和芦林分布密度的比较研究

通过对长江外滩枫杨防护林和芦林钉螺分布密度的调查比较,结果表明：枫杨林钉螺分布密度明显低于芦林;两种群落钉螺分布密度不同程度受长江洪泛的影响;两种群落中４种抑制钉螺的植物对钉螺分布密度的影响相似。     

Cyclic AMP inhibits p38 activation via CREB-induced dynein light chain

The mitogen-activated protein kinase p38 plays a critical role in inflammation, cell cycle progression, differentiation, and apoptosis. The activity of p38 is stimulated by a variety of extracellular stimuli, such as the proinflammatory cytokine tumor necrosis factor alpha (TNF-alpha), and subjected to regulation by other intracellular signaling pathways, including the cyclic AMP (cAMP) pathway. Yet the underlying mechanism by which cAMP inhibits p38 activation is unknown. Here we show that the induction of dynein light chain (DLC) by cAMP response element-binding protein (CREB) is required for cAMP-mediated inhibition of p38 activation. cAMP inhibits p38 activation via the protein kinase A-CREB pathway. The inhibition is mediated by the CREB target gene Dlc, whose protein product, DLC, interferes with the formation of the MKK3/6-p38 complex, thereby suppressing p38 phosphorylation activation by MKK3/6. The inhibition of p38 activation by cAMP leads to suppression of NF-kappaB activity and promotion of apoptosis in response to TNF-alpha. Thus, our results identify DLC as a novel inhibitor of the p38 pathway and provide a molecular mechanism by which cAMP suppresses p38 activation and promotes apoptosis.