白藜芦醇通过调控HIF-1α/NOX4/ROS通路抑制低氧诱导的大鼠肺动脉平滑肌细胞氧化应激与增殖

本文旨在明确白藜芦醇对低氧诱导的肺动脉平滑肌细胞(pulmonary artery smooth muscle cells, PASMCs)氧化应激与增殖的作用及分子机制。体外分离培养原代大鼠PASMCs,采用不同浓度的白藜芦醇(10、20和40μmol/L)或NADPH氧化酶(NADPH oxidases, NOXs)抑制剂VAS2870 (10μmol/L)预处理0.5 h,然后将细胞置于常氧(21%O_2, 5%CO_2)或低氧(2%O_2, 5%CO_2)中培养24h。采用CCK-8法和增殖细胞核抗原(proliferatingcellnuclearantigen,PCNA)的表达水平检测细胞增殖,用DCFH-DA测定细胞内活性氧(reactive oxygen species, ROS)的生成,用real-time RT-PCR和Western blot检测NOX1、NOX4和低氧诱导因子-1α(hypoxia inducible factor 1α, HIF-1α)的表达水平,通过小干扰RNAs (small interference RNAs, siRNAs)特异性沉默Hif-1α和Nox4后确定相关信号通路。结果显示,白藜芦醇和VAS2870均能显著抑制低氧诱导的大鼠PASMCs细胞增殖和ROS生成,同时白藜芦醇还能有效阻止低氧诱导的HIF-1α蛋白的聚集和NOX4的表达上调,而对NOX1没有明显的影响。沉默Hif-1α或Nox4后,低氧诱导的大鼠PASMCs细胞增殖和ROS累积均显著降低,且能被白藜芦醇进一步抑制。上述结果提示,白藜芦醇可能通过阻断HIF-1α/NOX4/ROS信号通路抑制低氧诱导的大鼠PASMCs氧化应激和增殖。     

稻飞虱卵期寄生蜂稻虱缨小蜂引诱剂的筛选与田间试验(英文)

植食性昆虫的天敌能够利用虫害诱导的挥发物进行有效的寄主或猎物定位。为了开发稻飞虱卵期天敌稻虱缨小蜂Anagrus nilaparvatae Pang et Wang的引诱剂,分别在室内和室外检测了多种褐飞虱诱导的水稻挥发物组分对褐飞虱卵期天敌稻虱缨小蜂的引诱作用。Y型嗅觉仪实验结果表明,5种单一化合物,Z-3-己烯乙酸酯,1-戊烯基-3-醇,Z-3-己烯醛,芳樟醇和水杨酸甲酯,以及3种混合物,水杨酸甲酯+Z-3-己烯醛,Z-3-己烯醛+Z-3-己烯乙酸酯+芳樟醇,水杨酸甲酯+Z-3-己烯醛+Z-3-己烯乙酸酯+芳樟醇,对稻虱缨小蜂具有明显引诱作用。田间试验表明,3种单一化合物,Z-3-己烯乙酸酯,Z-3-己烯醛和芳樟醇,以及一种混合物,水杨酸甲酯+Z-3-己烯醛+Z-3-己烯乙酸酯+芳樟醇,能明显提高稻虱缨小蜂对褐飞虱卵的寄生作用。这些结果对于改善褐飞虱治理具有重要的意义。     

猪多能性干细胞研究进展与前瞻北大核心CSCD

多能干细胞具有能够分化为多种特定细胞类型的能力,主要包括胚胎干细胞、胚胎生殖细胞和诱导多能干细胞。猪因其在免疫学、形态学和生理结构上与人有着诸多类似的特点,正逐渐成为人类异种移植、细胞治疗和再生医学研究的理想生物学模型。然而,目前对猪多能干细胞的来源、特征及机制认识的不足直接阻碍了该研究领域的发展。因此,将对猪多能性干细胞的种类、鉴定标准、研究进展、亟待解决的问题进行详细地阐述,并在此基础上对猪多能性干细胞的研究进行了展望,希望为该研究领域的科研人员提供参考。     

多顺反子质粒重编程人脂肪干细胞为诱导多能干细胞

为建立多顺反子质粒载体转染技术获得人脂肪干细胞(adipose stem cells,ASCs)来源的诱导多能干细胞(induced pluripotency stem cells,iPSCs),应用2A元件连接Oct4/Sox2/KLF4/c-Myc四因子基因,构建为单一开放阅读框的多顺反子质粒载体．使用该质粒对ASCs进行转染及重编程为iPSC．采用形态学观察、特异性抗体免疫荧光鉴定、体外拟胚体诱导分化和体内畸胎瘤形成等方法进行鉴定．结果显示,ASCs成功重编程为iPSCs,具有与人胚胎干细胞相似的形态学及多向分化潜能;通过拟胚体和畸胎瘤实验证实iPSCs能在体内外分化成三胚层细胞;DNA印迹实验显示质粒载体序列未整合至iPSCs基因组中．因此,通过多顺反子质粒载体重编程技术成功建立的人iPSCs具有多向分化潜能,可减免发生插入突变和免疫排斥问题,为iPSCs在遗传性或退行性疾病的治疗奠定了实验基础．     

植物细胞工程技术生产紫杉醇研究进展

紫杉醇是一种二萜类生物碱,主要从红豆杉树皮中分离提取。目前采用植物细胞工程技术是提高紫杉醇产率、保护稀缺资源红豆杉、解决紫杉醇药源紧缺的一种最有效方法。该文对近十年来国内外有关采用植物细胞工程技术生产紫杉醇的研究进展,包括红豆杉细胞系的建立、悬浮培养条件的研究、生物反应器培养以及紫杉醇合成代谢调控方面的最新研究进展进行综述。并重点论述了前体、诱导子和代谢支路抑制剂对红豆杉细胞悬浮培养生产紫杉醇的影响,为植物细胞工程技术生产紫杉醇提供借鉴和参考。     

Tetanic contraction induces enhancement of fatigability and sarcomeric damage in atrophic skeletal muscle and its underlying molecular mechanisms

Muscle unloading due to long-term exposure of weightlessness or simulated weightlessness causes atrophy, loss of functional capacity, impaired locomotor coordination, and decreased resistance to fatigue in the antigravity muscles of the lower limbs. Besides reducing astronauts＇ mobility in space and on returning to a gravity environment, the molecular mechanisms for the adaptation of skeletal muscle to unloading also play an important medical role in conditions such as disuse and paralysis. The tail-suspended rat model was used to simulate the effects of weightlessness on skeletal muscles and to induce muscle unloading in the rat hindlimb. Our series studies have shown that the maximum of twitch tension and the twitch duration decreased significantly in the atrophic soleus muscles, the maximal tension of high-frequency tetanic contraction was significantly reduced in 2-week unloaded soleus muscles, however, the fatigability of high- frequency tetanic contraction increased after one week of unloading. The maximal isometric tension of intermittent tetanic contraction at optimal stimulating frequency did not alter in 1- and 2-week unloaded soleus, but significantly decreased in 4-week unloaded soleus. The 1-week unloaded soleus, but not extensor digitorum Iongus （EDL）, was more susceptible to fatigue during intermittent tetanic contraction than the synchronous controls. The changes in K＋ channel characteristics may increase the fatigability during high-frequency tetanic contraction in atrophic soleus muscles. High fatigability of intermittent tetanic contraction may be involved in enhanced activity of sarcoplasmic reticulum Ca2＋-ATPase （SERCA） and switching from slow to fast isoform of myosin heavy chain, tropomyosin, troponin I and T subunit in atrophic soleus muscles. Unloaded soleus muscle also showed a decreased protein level of neuronal nitric oxide synthase （nNOS）, and the reduction in nNOS-derived NO increased frequency of calcium sparks and elevated intracellular resting Ca2＋ concentration （[Ca2＋]i） in unloaded soleus muscles. High [Ca2＋]i activated calpain-1 which induced a higher degradation of desmin. Desmin degradation may loose connections between adjacent myofibrils and further misaligned Z-disc during repeated tetanic contractions. Passive stretch in unloaded muscle could preserve the stability of sarcoplasmic reticulum Ca2＋ release channels by means of keeping nNOS activity, and decrease the enhanced protein level and activity of calpain to control levels in unloaded soleus muscles. Therefore, passive stretch restored normal appearance of Z-disc and resisted in part atrophy of unloaded soleus muscles. The above results indicate that enhanced fatigability of high-frequency tetanic contraction is associated to the alteration in K＋ channel characteristics, and elevated SERCA activity and slow to fast transition of myosin heavy chain （MHC） isoforms increases fatigability of intermittent tetanic contraction in atrophic soleus muscle. The sarcomeric damage induced by tetanic contraction can be retarded by stretch in atrophic soleus muscles.     

疫苗诱导的Th17细胞是长期保护表型稳定的记忆亚群

Th17细胞在免疫介导的保护中,越来越多地被认为是重要的辅助性T细胞亚群,特别是对通过黏膜入侵的病原体。在许多情况下,这与通过接种疫苗诱导的Th17细胞记忆是高度相关的。据报道,     

陕西省烟草灰霉病病原及云芝多糖对其防治研究

采用形态学观察和分子鉴定方法对2011年在陕西省发生的一种烟草未知病害的病原菌进行鉴定。从病叶组织分离纯化得到病原菌,通过致病性测定以及人工接种后再分离病菌,证明编号LJL007的菌株为该病的致病菌。依据病原菌的形态学和培养特征,将菌株LJL007鉴定为灰葡萄孢Botrytis cinerea Pers.,其有性型为富氏葡萄孢盘菌Botryotinia fuckeliana Whetzel。通过核糖体DNAITS序列分析,分离菌株LJL007序列(登录号:HM17900)与富氏葡萄孢盘菌序列(登录号:HM849615)同源性达100%,进一步证明该病原菌是灰葡萄孢Botrytis cinerea。云芝多糖在离体条件下,对灰葡萄孢的菌丝生长和孢子萌发均无直接抑制作用。云芝多糖对烟草灰霉病有较好预防保护作用,其预防效果可达56.29%。云芝多糖可显著提高烟草体内几丁质酶和β-1,3-葡聚糖酶活性,其活性峰值分别比对照提高56.89%和429.83%,说明云芝多糖可诱导植物产生抗病性。     

Jagged-1/Notch3 signaling transduction pathway is involved in apelin-13-induced vascular smooth muscle cells proliferation

The apelin/apelin receptor （APJ, apelin-angiotensin receptor-like 1） system is a newly deorphanized G protein- coupled receptor system. Both apelin and APJ that are important regulatory factors are expressed in the cardio- vascular system. Our previous studies demonstrated that apelin-13 significantly stimulated vascular smooth muscle cell （VSMC） proliferation. In this paper, our data sug- gested that the Jagged-l/Notch3 signaling transduction pathway is involved in apelin-13-induced VSMC prolifer- ation by promoting the expression of Cyclin D1. Results indicated that apelin-13 stimulates the proliferation of VSMC and the expression of Jagged-1 and Notch3 in con- centration- and time-dependent manners. The increased expression of Jagged-1 and Notch3 induced by apelin-13 could be abolished by extracellular signal-regulated protein kinase （ERK） blockade. PD98059 （ERK inhibitor） can inhibit the activation of Jagged-I/Notch3 induced by apelin- 13. Down-regulation of Notch3 using small interfering RNA inhibits the expression of Cyclin DI and prevents apelin- 13-induced VSMC proliferation. In conclusion, Jagged-I/ Notch3 signaling transduction pathway is involved in VSMC proliferation induced by apelin-13.     

Gene expression profiles of sodium-dependent vitamin C transporters in mice after alcohol consumption

Alcoholic liver disease （ALD） is a serious fiver problem in western countries. Our previous study has demonstrated that vitamin C plays a protective role in ALD. The vitamin C homeostasis is tightly regulated by sodium-dependent vitamin C transporters （SVCTs） 1 and 2. But the role of two SVCTs in ALD is less understood. In this study, we exam- ined the expression patterns of two SVCTs in mice after alcohol consumption. Our results suggested that alcohol con- sumption obviously increased the expression of two SVCTs in liver and SVCT1 in kidney and intestine, which is important for vitamin C absorption. Vitamin C supplement increased the sera vitamin C content and ameliorated the symptom of ALD. Intestinal absorption and renal re-absorption mediated by SVCTI are key factors to increase the sera vitamin C content after alcohol consumption. We proposed that both reactive oxygen species and low vitamin C concentration regulate the expression of SVCTs, and the protective role of vitamin C is mediated by suppressing the stability of hypoxia-inducible factor-loL. Thus, our study is significant for the understanding of vitamin C homeostasis in ALD and for better use of other antioxidants in ALD therapy.