神经介素B及其受体NMBR参与抗A型流感病毒H1N1亚型感染的信号通路

NMB/NMBR通过调节A型流感病毒（IAV/H1N1/PR8）感染诱导的细胞因子表达而参与抗IAV的先天性免疫反应。为探究其发挥抗IAV/H1N1感染的信号通路，本文用PR8和WSN毒株分别感染MLE-12细胞和小鼠，用NF-κB抑制剂BAY11-7028单独或联合NMB处理MLE-12细胞，小鼠后腿肌内注射NMB和NMBRA，采用RT-PCR和qRT-PCR分析NMB、NMBR、IL-6、IFN-α和NP基因表达变化，采用Western blot分析NMB、NMBR、P65/p-P65、IκBα和NP蛋白表达的变化。结果显示，BAY11-7028可促使PR8和WSN感染的MLE-12细胞中NMB、NMBR、IL-6和IFN-α基因表达水平均下降和NP基因表达水平上升，并降低NMB、NMBR和p-P65蛋白表达水平和提升IκBα和NP蛋白表达水平。然而，NMB联合BAY 11-7028诱导PR8或WSN感染后的细胞中IL-6和NP表达出现极显著下降和IFN-α显著上升。此外，NMB抑制PR8和WSN感染的小鼠肺组织内p-P65和NP蛋白表达水平和促进IκBα蛋白表达水平；NMBRA联合NMB抵消NMB对PR8或WSN感染后的这些蛋白表达水平的调节作用。综上表明，NMB/NMBR通过调节PR8和WSN感染的MLE-12细胞和小鼠体内的NF-κB信号通路上P65蛋白磷酸化和IκBα的表达，进而影响下游细胞因子IL-6和IFN-α基因的表达，从而发挥抗IAV/H1N1感染的先天性免疫应答反应。     

膜联蛋白B1在猪囊尾蚴免疫逃避作用的研究进展

膜联蛋白是一类有效的内源性调节蛋白,在Ca²⁺存在的条件下与膜磷脂结合,参与细胞活动的多种功能,其与肿瘤发生、自身免疫性疾病、病毒和寄生虫感染等密切相关。作为膜联蛋白家族成员Annexin B1具有独特的氨基酸残基结构,与不同种属的寄生虫入侵特异性宿主密切相关。本文主要阐述了膜联蛋白的种类及膜联蛋白B1在猪囊尾蚴感染宿主机体过程中免疫逃避的作用,旨在探索其猪囊尾蚴感染的免疫逃避机制。深入对膜联蛋白B1和囊尾蚴之间相互关系的进一步了解,以及膜联蛋白B1在寄生虫免疫中更深入的研究,对寄生虫免疫逃避的生物学意义和寄生虫病诊断治疗提供了相关的策略。     

黄曲霉毒素B1、玉米赤霉烯酮和呕吐毒素的累加细胞毒性研究

由于饲料中多种霉菌毒素并存的几率比较高，本研究以仔猪肠上皮细胞（IPEC-J2）为模型，研究黄曲霉毒素B1（AFB1）、玉米赤霉烯酮（ZEA）和呕吐毒素（DON）的叠加细胞毒性。细胞毒性试验选用AFB1、ZEA和DON三种毒素作为响应面Box-Behnke设计的三个因素，以AFB1：10、20、30 μg/L，ZEA：150、300、450 μg/L，DON：500、1000、1500 μg/L作为Box-Behnke设计的三个编码水平。利用响应面设计构建得到17组复合霉菌毒素组合，以其对IPEC-J2细胞活力的影响作为参考指标，得到对细胞损伤程度最高和最低的霉菌毒素添加比例。结果表明：经方程预测后，得到细胞活力最低（霉菌毒素毒性最高）的AFB1、ZEA和DON组合为30、150 μg/L和1500 μg/L，经测定细胞活力为32.32%|得到细胞活力最高（霉菌毒素毒性最低）的AFB1、ZEA和DON组合为10、150 μg/L和600 μg/L，经测定细胞活力为53.01%。该结果为多种霉菌毒素叠加毒性的研究提供了依据。 [关键词] IPEC-J2细胞|黄曲霉毒素B1|玉米赤霉烯酮|呕吐毒素|细胞毒性     

硼肥用量对玉米生长发育及产量的影响

以郑单958和豫单606为试验材料,采用盆栽试验方法,探索不同硼肥用量对玉米产量及生长发育的影响。结果表明,施用适量硼肥可促进玉米生长发育,显著提高叶面积指数,使植株干物质积累量增加,同时硼肥能够促进干物质向果穗运输。施用硼肥能够促进玉米穗分化,使雌雄间隔期缩短,显著提高花丝数和花丝生长速率,进而增加穗粒数。施用硼肥显著提高玉米产量,且不同用量对其影响不同,3.33 mg/kg土壤硼肥处理的效果最为显著,郑单958和豫单606分别较不施硼肥处理增产14.3%和17.4%;施用量为13.3 mg/kg时郑单958增产3.5%;豫单606产生中毒症状,产量较对照降低4.4%。     

Up-regulation of miR-181a attenuates releases of CSE-induced pro-inflammatory factors and expression of collagen IV,fibronectin and α-SMA in human bronchial epithelial cells

AIM: To investigate the effect and potential mechanism of microRNA-181a (miR-181a) on cigarette smoke extract (CSE)-induced the productions of pro-inflammatory factors and the expression of collagen IV, fibronectin and α-smooth muscle actin (α-SMA) in human bronchial epithelial cells (HBECs). METHODS: CSE-induced miR-181a expression was detected by RT-qPCR in the HBECs. After tansfected with miR-181a mimic, the releases of tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), IL-6 and transforming growth factor-β1 (TGF-β1) were measured by ELISA, the protein expression of collagen IV, fibronectin and α-SMA was determined by Western blot. The activation of NF-κB/TGF-β1/Smad3 pathway was also evaluated by Western blot. RESULTS: CSE increased the levels of TNF-α, IL-1β, IL-6 and TGF-β1 and the expression of collagen IV, fibronectin and α-SMA, and decreased the expression of miR-181a in the HBECs (P<0.05). However, transfected with miR-181a mimic partially prevented the releases of TNF-α, IL-1β, IL-6 and TGF-β1, and inhibited the expression of collagen IV, fibronectin and α-SMA (P<0.05). Additionally, the activation of NF-κB/TGF-β1/Smad3 evoked by CSE was attenuated after transfected with miR-181a mimic. CONCLUSION: Up-regulation of miR-181a prevents the releases of CSE-induced pro-inflammatory factors and expression of collagen IV, fibronectin and α-SMA in the HBECs, and its mechanism may be related to the inhibition of NF-κB/TGF-β1/Smad3 pathway.     

FAM3C activates Akt to promote viability of oral squamous-cell carcinoma cells

AIM: To investigate the expression and roles of family with sequence similarity 3, member C (FAM3C) in oral squamous-cell carcinoma cells. METHODS: The mRNA and protein expression levels of FAM3C in dysplastic oral keratinocyte (DOK) and oral squamous-cell carcinoma WSU-HN6 cells were detected by RT-qPCR and Western blot. The WSU-HN6 cells were treated with siFAM3C or FAM3C antibody. After 24, 48 and 72 h, the viability of WSU-HN6 cells was measured by CCK-8 assay, and the activation of protein kinase B (Akt) was detected by Western blot. Adenovirus was used to mediate over-expression of FAM3C in the DOK cells. The DOK cell viability was measured by CCK-8 assay after adenovirus infection for 24, 48 and 72 h, and the activation of Akt was detected by Western blot. RESULTS: Compared with the DOK cells, the mRNA and protein levels of FAM3C were significantly increased in the WSU-HN6 cells (P<0.05). The viability of WSU-HN6 cells transfected with siFAM3C was significantly inhibited at 48 h and 72 h (P<0.05). siFAM3C treatment inhibited the activation of Akt (P<0.05). FAM3C antibody treatment also suppressed the viability of the WSU-HN6 cells at 48 h and 72 h and the activation of Akt (P<0.05). Over-expression of FAM3C in the DOK cells promoted the cell viability at 48 h and 72 h and activated Akt (P<0.05). CONCLUSION: FAM3C might promote oral squamous-cell carcinoma cell growth by activating Akt.     

PPARγ mediates effects of diosgenin on proliferation and apoptosis in human glioblastoma U87MG cells

AIM:To investigate the effect of diosgenin (Dio) on the proliferation, apoptosis and expression of peroxisome proliferator-activated receptor γ (PPARγ) in human glioblastoma U87MG cells and its possible mechanism. METHODS:Human astrocytes (HA) and U87MG cells were cultured in vitro and treated with Dio (0, 10, 20, 30, 40 and 50 μmol/L) and GW9662 (5 μmol/L) for 48 h, and then the cell viability was detected by CCK-8 assay. Cell colony formation assay was used to assess the proliferation potential. Flow cytometry was used to analyze the cell cycle distribution and apoptosis. The mRNA expression level of PPARγ was measured by RT-PCR. Western blot was used to determine the protein levels of PPARγ, cyclin D1, cyclin E1, Bcl-2 and Bax. RESULTS:Dio had no significant influence on the viabi-lity of HA (P>0.05). However, Dio remarkably reduced the viability of U87MG cells in a dose-dependent manner (P<0.05) with IC₅₀ of 24.31 μmol/L. Meanwhile, Dio remarkably diminished colony formation ability (P<0.05), induced G₀/G₁ phase arrest of the cell cycle and apoptosis (P<0.05), up-regulated the expression of PPARγ at mRNA and protein levels, increased the protein level of Bax (P<0.05), and down-regulated the protein levels of cyclin D1, cyclin E1 and Bcl-2 (P<0.05) in a dose-dependent manner. However, these effects induced by Dio were inhibited by GW9662 (P<0.05), a specific inhibitor of PPARγ. CONCLUSION:Dio may inhibit proliferation and induce apoptosis in human glioblastoma U87MG cells most likely via up-regulating the expression of PPARγ, and then down-regulating the protein levels of cyclin D1, cyclin E1 and Bcl-2, and up-regulating the protein level of Bax.     

天维菌素酰化衍生物的合成及杀虫杀螨活性

以天维菌素B、天维菌素B单糖苷和天维菌素B苷元为原料,经选择性C-5羟基保护,在C-13、C-4′和C-4″位引入不同酰基基团,合成了3个系列共23个天维菌素B酰化衍生物,并通过1H NMR、13C NMR和高分辨质谱对所有目标化合物的结构进行了表征。生物活性测定结果表明,所有衍生物对小菜蛾Plutella xylostella、朱砂叶螨Tetranychus cinnabarinus以及松材线虫Bursaphelenchus xylophilus均表现出不同程度的毒杀活性,其中天维菌素B C-4″位衍生物的活性优于C-4′位衍生物及13位衍生物。化合物8e对小菜蛾和松材线虫的毒杀活性最优,LC50值分别为9.2 mg/L和0.42 mg/L,化合物8b对朱砂叶螨的毒性最高,LC50值为0.0019 mg/L,均优于对照药天维菌素B。