Effect of Urtica dioica extract intake upon blood lipid profile in the rats

Aqueous (150 mg/kg/day) and to a lesser extent petroleum ether (20 mg/kg/day) extract of Urtica dioica given for 30 days to rats fed with normal or high-fat diet, improved the blood lipid profile. Significant decreases in total cholesterol, LDL cholesterol, LDL/HDL cholesterol ratio and plasma total apo B were observed. Assessment of GOT, GPT and LDH activities showed that no liver damage has occurred during the study period.     

Downregulation of DEK induces cell apoptosis via inhibition of NF-κB signaling pathway in gastric carcinoma SGC-7901 cells

AIM: To investigate the effect of DEK downregulation on the apoptosis of gastric carcinoma SGC-7901 cells, and to explore its associations with NF-κB signaling pathway and apoptosis related proteins. METHODS: SGC-7901 cells with different treatments were divided into 3 groups including untreated group, control siRNA group and DEK siRNA group. The expression of DEK at mRNA and protein levels in the SGC-7901 cells was detected by real-time PCR and Western blot. The cell apoptosis was examined by flow cytometry. Furthermore, the activities of caspase-3 and caspase-9 in the SGC-7901 cells were investigated by Caspase-Glo^®-3/9 kit. Finally, the expression of key regulatory protein p65 of NF-κB signaling pathway and apoptosis-related proteins Bcl-2 and Bax in the SGC-7901 cells was investigated by Western blot. RESULTS: Compared with untreated group and control siRNA group, the expression of DEK at mRNA and protein levels was significantly downregulated in DEK siRNA group (P<0.05). In addition, the ratios of early phase apoptosis and total apoptosis in DEK siRNA group were markedly higher than those in untreated group and control siRNA group (P<0.05). Most notably, the decrease in p65 and Bcl-2 proteins, increase in Bax protein and the increases of caspase-3 and caspase-9 activities were observed in DEK siRNA group. CONCLUSION: Downregulation of DEK mediates cell apoptosis of gastric carcinoma may be tightly associated with NF-κB signaling pathway.     

Protective effect of BNDF on vascular endothelial cells with H2O2-induced oxidative injury

AIM: To study the protective effect of brain-derived neurotrophic factor (BDNF) on vascular endothelial cells with H₂O₂-induced oxidative injury. METHODS: Human umbilical vein endothelial cells (HUVECs) were cultured in vitro, and the oxidation injury model of HUVECs was established by treatment with H₂O₂. The oxidatively injured HUVECs were cultured with different concentrations (1, 10 and 100 μg/L) of BDNF. At the same time, the control group (no injury), PBS treatment after H₂O₂ injury group and TrkB inhibitor group (with 100 μg/L BDNF and 1: 1 000 TrkB inhibitor) were also set up. The viability of the HUVECs was detected by MTT assay. The levels of LDH, MDA, SOD and GSH were measured. The releases of NO, ET-1 and ICAM-1 were analyzed by ELISA. The changes of ROS production and cell apoptosis were evaluated by flow cytometry. The protein levels of TrkB, p-TrkB, cleaved caspase-3, Bcl-2 and Bax were determined by Western blot. RESULTS: Compared with uninjured control group, in H₂O₂ oxidative injury plus PBS treatment group, the viability of the cells was decreased significantly, the LDH and MDA levels were increased significantly and the activities of SOD and GSH were decreased significantly. The NO secretion was decreased, and the ET-1 and ICAM-1 concentrations were increased significantly. The ROS content and apoptotic rate were increased significantly. The protein levels of cleaved caspase-3 and Bax were increased but Bcl-2 protein expression was decreased significantly. Compared with PBS treatment group, in H₂O₂-injured HUVECs treated with different concentrations of BDNF, the cell viability was gradually increased, the LDH and MDA levels were decreased and the activities of SOD and GSH were increased gradually. The secretion of NO was increased but ET-1 and ICAM-1 were decreased gradually. The ROS content and apoptotic rate were decreased significantly. The TrkB and p-TrkB levels were significantly increased significantly, the protein expression of cleaved-caspase 3 and Bax was decreased gradually and the Bcl-2 protein expression increased gradually. The role of BDNF was inhibited by TrkB inhibitor. CONCLUSION: BDNF protects HUVECs from oxidative injury by binding with TrkB to activate the BDNF-TrkB signaling pathways.     

Promoting effect of botulinum neurotoxin serotype A heavy chain on neuritogenesis in cultured Neuro-2a cells

AIM: To observe the neuritogenic actions of botulinum neurotoxin serotype A heavy chain (BoNT/A HC) on cultured Neuro-2a cells and to investigate the related signaling mechanisms for the effect of BoNT/A HC. METHODS: Neuro-2a cells were treated with different doses of BoNT/A HC (0.01, 0.1, 1 and 10 nmol/L), and then the cells were harvested at 24 h, 48 h and 72 h of BoNT/A HC exposure for detecting the neurite length and the percen-tage of the cells with neuronal processes by immunofluorescence staining. The most efficient dose of BoNT/A HC was chosen for exposure to Neuro-2a cells as the above. Whole cell protein was harvested at different time points for detecting the protein levels of phosphorylated ERK1/2 (p-ERK1/2) and phosphorylated Akt (p-Akt) by Western blot. RESULTS: Low doses of BoNT/A HC stimulated the neurite outgrowth, and increased the percentage of the cells with neurites compared with the negative controls (P<0.05), especially in the group with 1 nmol/L of BoNT/A HC treatment. Meanwhile, the phosphorylation of ERK1/2 and Akt was increased after treated with BoNT/A HC. There was an increasing tendency for the phosphorylation of ERK1/2 after the exposure of the cells to BoNT/A HC. The obvious increase in p-ERK1/2 was seen from 60 min to 5 h with 1 nmol/L of BoNT/A HC treatment (P< 0.05), and the increased protein level of p-Akt was mainly observed at 15 min and 60 min (P<0.05). CONCLUSION: BoNT/A HC stimulates the neuritogenesis. The neuritogenic mechanism of BoNT/A HC on Neuro-2a cells might be realized by activation of the phosphorylation of ERK1/2 and Akt.     

常山胡柚叶片DNA的抽提与分析

经反复实验，采用在抽提前加入一定量的抗氧化剂β－巯基乙醇，用冰冻的异丙醇来沉淀DNA，并增加氯仿／异戊醇抽提次数的所谓改良CTAB法，对常山胡柚叶片DNA抽提与分析，不仅成功提取到常山胡柚叶片DNA，而且所得的DNA浓度高、纯度好，20个试样的DNA苹均质量浓度为272.86μg/mL，平均每克鲜叶片可获DNA约82μg，纯度基本上都在1.4-1.8范围内，并经RAPD反应验证，完全能满足常规分子生物学分析的要求。     

Schisandrin B protects against solar irradiation-induced oxidative injury in BJ human fibroblasts

The effects of schisandrin B (Sch B) and its analogs on solar irradiation-induced oxidative injury were examined in BJ human fibroblasts. Sch B and schisandrin C (Sch C) increased cellular reduced glutathione (GSH) level and protected against solar irradiation-induced oxidative injury. The photoprotection was paralleled by decreases in the elastases-type protease activity and matrix-metalloproteinases-1 expression in solar-irradiated fibroblasts. The cytochrome P-450-mediated metabolism of Sch B or Sch C caused ROS production. The results suggest that by virtue of its pro-oxidant action and the subsequent glutathione antioxidant response, Sch B or Sch C may offer the prospect of preventing skin photo-aging.     

宁波检验检疫局多次截获非洲伞滑刃组线虫

2006年来,宁波出入境检验检疫局植检实验室曾多次从进境木质包装中首次截获并报道非洲伞滑刃组（africanus group）线虫,它们分别为非洲伞滑刃线虫（Bursaphelenchus africanus Braasch, Gu, Burgermeister, Brandstetter &; Metge, 2006）、伯氏伞滑刃线虫（B. burgermeisteri Braasch, Gu, &; Brandstetter, 2007）和欧斐切伞滑刃线虫（B. obeche Gu, Braasch, Zhen, Burgermeister &; Lin, 2008）。这些线虫均为作者最先截获。非洲伞滑刃组线虫的主要鉴定特征是：侧线4条;尾乳突7个（第3对和第4对靠近并位于交合伞起始处,第3对略位于第4对前并更靠近腹面）;交合刺较直,中部有横纹,冠状体愈合（基顶和喙突不明显）,远端无盘状突;后阴子宫囊约占肛阴距1 /2。目前尚无关于该组线虫媒介昆虫及致病性的报道。     

绿化工程主材“甲供”与“乙供”苗木模式的比较研究

主材供应方式是园林工程中受重视的环节。以恒大公司的几个园林工程为例,通过比较绿化工程苗木材料的"甲供"和"乙供"模式的利弊,归纳总结出适合不同要求的采购模式的方法,从而帮助业主更高效准确地作出选择,并使其选择的材料在达到预期绿化效果的同时,又能适当控制成本。     

拟松材线虫研究进展

松材线虫和拟松材线虫共同构成松材线虫复合群体,为松材线虫病的病原物。拟松材线虫危害过去没有引起足够重视,相关研究工作不如松材线虫细致。近年来,随着拟松材线虫致病性增强现象不断被报道,人们逐步加强了拟松材线虫研究。本文从拟松材线虫分类学特征、致病性研究及与松材线虫关系等角度对拟松材线虫研究进展进行综述,并展望未来可能的研究热点。     

非氧化性修复剂在恢复NF/RO膜出水水质的应用研究

随着膜系统运行至一定年限,加上膜系统长期超负荷运行和膜化学清洗的不及时、不规范,都将加快膜元件的老化,造成膜元件对离子、小分子有机物等物质的截留率有所下降。膜出水COD偏高,电导率升高、颜色偏黄已成为纳滤/反渗透(NF/RO)系统运行过程中出现较频繁的问题之一,严重影响着膜系统的出水水质和出水美观度。本试验选取长沙生活垃圾渗滤液处理厂出水水质差的反渗透/纳滤处理系统为分析对象,通过冲击性投加的方式将专用NR-MRA-1000型修复剂粘附于膜表面,并24 h长期运行。试验结果表明,膜系统添加NR-MRA-1000型修复剂且运行48 h后,呈现出膜出水色度明显降低,COD截留率上升以及出水电导率下降、膜运行压力上涨等产水特征,对膜产水通量没有显著影响;且膜修复剂试验运行60 d后,膜机组相关产水性能恢复至原来的标准。