外源5-氨基乙酰丙酸对低温胁迫下茶树叶片光合及生理特性的影响

通过对陕茶1号（耐低温型）和金牡丹（低温敏感型）2个茶树品种在冬季自然低温胁迫下喷施不同浓度（0、10、30、50 mg·L^-1）的外源5-氨基乙酰丙酸（5-aminolevulinic acid,ALA）,探究外源ALA对低温胁迫下茶树叶片光合荧光特性及生理特性的调控作用。结果表明,适宜浓度的外源ALA对低温胁迫下茶树叶片净光合速率、气孔导度、胞间CO₂浓度、蒸腾速率、PSⅡ最大光化学效率及PSⅡ潜在活性具有促进作用,能够提高水浸出物、咖啡碱、游离氨基酸、儿茶素类物质、茶氨酸、可溶性糖、可溶性蛋白等生理活性物质含量的累积;外源ALA能够提高低温胁迫下茶树光合作用的能力并改善茶叶品质,其中50 mg·L^-1的ALA处理能有效提高陕茶1号应对低温胁迫的能力,10 mg·L^-1和30 mg·L^-1的外源ALA对金牡丹应对低温胁迫具有较好的缓解效用。     

不同氮肥处理下高温胁迫对夏玉米产量及叶片超微构造的影响

以郑单958为材料,研究高温胁迫对夏玉米产量及叶片超微构造的影响。结果表明,高温处理缩短夏玉米的生育天数,降低夏玉米产量及叶绿素含量。随氮肥增加,高温处理对玉米产量的影响先降低后升高(在310.5 kg/hm^2氮肥下,高温处理玉米产量的降低达到27.2%、31.1%)。高温处理较对照维管束鞘细胞变大,高温处理维管束鞘细胞内的叶绿体出现淀粉粒,对照处理维管束鞘细胞内的叶绿体没有出现淀粉粒。高温线粒体及细胞核(被)膜开始解离,对照处理线粒体及细胞核(被)膜完整,说明高温条件下,玉米对氮的耐受力降低。高温处理叶绿体数、叶绿体基粒数减少及基粒片层数减少,叶绿体面积及叶绿体长/宽比值变小,高温处理较对照线粒体数先增加后减少。高温处理与对照叶肉细胞叶绿体内均未发现淀粉粒。     

玉米受精和早期子粒发育过程及逆境胁迫对其影响

玉米受精及子粒发育早期是决定穗粒数及粒重的重要时期,也是对环境变化相对较敏感的阶段。受精极核需要经历游离核、细胞化和细胞分化3个阶段形成胚乳,受精卵同样需要一系列的分裂分化形成最终的胚。玉米受精前极易遭受不良环境的影响,导致性器官发育不正常,影响花粉或花丝活力间接影响玉米受精过程。受精过程中的环境胁迫会通过阻碍花粉与花丝的识别、减缓花粉管在花丝中的延伸速率影响受精过程。子粒发育早期主要是受精极核分裂分化形成胚乳、受精卵分裂分化形成胚的过程,该阶段遭受环境胁迫下,胚乳细胞分裂受阻影响子粒库容。研究表明,逆境胁迫条件下,玉米的受精及子粒早期发育过程与碳水化合物的代谢以及激素的合成密切相关。     

玉米热激蛋白ZmHSP70-12基因的克隆及表达分析

热激蛋白70(HSP70)是原核和真核细胞中普遍存在的一种高度保守的分子伴侣。从玉米中克隆1个HSP70家族成员。该基因cDNA序列全长为1 992 bp,开放阅读框为2 352 bp,编码663个氨基酸,蛋白质分子量约75.0 kD。蛋白结构预测及同源比对分析表明,该基因编码蛋白含ATPase位点和HSP70保守结构域,与拟南芥AtHSP70-12序列高度相似,命名为ZmHSP70-12。蛋白亚细胞定位显示,ZmHSP70-12蛋白在内质网中表达。实时荧光定量PCR分析表明,ZmHSP70-12对非生物胁迫高温、干旱均具有明显的应答反应,推测ZmHSP70-12是玉米中与胁迫逆境相关的基因。     

盐胁迫下外源功能微生物调控水稻生长特征研究

以高产水稻品种中浙优1号为材料,设置2个盐胁迫处理(S0,正常生长条件;S1,盐逆境,3g NaCl/kg干土)和2个微生物处理(M0,对照;MM,荧光假单胞菌与巴西固氮螺菌共同接种水稻根际环境),研究了盐胁迫下外源功能微生物对水稻生长特征的影响。结果表明,与S0处理相比,S1处理下水稻植株生育期严重滞后,干物质积累量以及产量构成因子显著降低;与S1M0处理相比,S1MM处理可显著提高水稻剑叶光合速率、地上部干物质量以及产量构成因子。可见,荧光假单胞菌与巴西固氮螺菌进入稻田土壤可缓解盐逆境对水稻生长的抑制作用,提升水稻叶片光合能力、耐盐性能,并显著提高水稻分蘖能力和结实率,增加千粒重,进而增加水稻产量。     

外源亚精胺对盐胁迫下甜菜生长及养分吸收的影响

为了探究外源亚精胺是否具有缓解甜菜盐害作用,采用霍兰营养液室内水培方法,测定了280mmol/L NaCl胁迫条件下,喷施0.25 mmol/L外源亚精胺后,耐盐‘T510’和盐敏感‘210’甜菜品系幼苗生长、生理及其体内N、P、K养分含量的变化情况。结果发现,盐胁迫下(Na处理),除MDA和P素含量升高外,两品系甜菜幼苗的叶片相对含水量、叶面积、叶绿素含量、幼苗生物量及N、K养分含量指标均明显降低;与Na处理比,喷施亚精胺的盐胁迫处理,除MDA和P素含量降低外,其它指标明显增加,两品系甜菜幼苗生长和养分吸收状况明显改善;外源亚精胺对耐盐‘T510’品系的调节作用大于‘210’品系。因此外源亚精胺能有效缓解盐胁迫对甜菜生长的伤害,对耐盐品系的调节效果更佳。     

Role of chlorogenic acid in endothelial dysfunction in db/db mice

AIM: To explore the effects of chlorogenic acid (CGA) on endothelial dysfunction in db/db mice and the possible mechanism. METHODS: Male db/db mice (n=12) were divided into control group and CGA group, with 6 mice in each group. The mice in CGA group were treated with diet containing 0.02% CGA, while the mice in control group were given normal diet only. The observation period was 12 weeks. Fasting blood glucose level, tail blood pressure and the body weight were analyzed each week. At the end of the 12th week, the mice were anesthetized and blood was taken from carotid artery. The plasma levels of heme oxygenase-1 (HO-1), catalase (CAT), NAD(P)H dehydrogenase quinone 1 (NQO1) and glutathione peroxidase-1 (GPx-1) were measured by ELISA. The mouse aortas were isolated, and the superoxide anion and nitric oxide (NO) levels were measured by DHE and DAF-2 DA staining, respectively. Wire Myograph System was used to detect the vasorelaxation of db/db mouse aorta. The protein levels of peroxisome proliferator-activated receptor α (PPARα), nuclear factor E2-related factor 2 (Nrf2), phosphorylated AMP-activated protein kinase (p-AMPK), phosphorylated endothelial NO synthase (p-eNOS), P22^phox and P47^phox were determined by Western blot. RESULTS: Dietary CGA decreased fasting blood glucose and body weight in db/db mice as compared with control group (P<0.01 or P<0.05). The plasma levels of HO-1, CAT, NQO1 and GPx-1 in CGA group were higher than those in control group (P<0.01 or P<0.05). Administration of CGA for 12 weeks attenuated superoxide anion level, increased NO level in the mouse endothelium and improved endothelium-dependent relaxation of the db/db mouse aorta. CGA also increased the protein levels of PPARα, Nrf2, p-AMPK and p-eNOS, and decreased P22^phox and P47^phox levels (P<0.01). CONCLUSION: Dietary CGA improves db/db mouse endothelium-dependent relaxation. This effect may be related to the increases in the levels of antioxidant molecules PPARα, Nrf2 and p-AMPK, and the up-regulation of antioxidant capacity, thus decreasing the oxidative stress, promoting eNOS phosphorylation, and increasing NO level.     

大豆PHD家族蛋白的全基因组鉴定及表达特征分析

PHD（Plant Homeodomain Finger）基因家族编码一类锌指转录因子,广泛参与植物的生长发育和逆境应答过程。通过全基因组鉴定获得了95个大豆PHD家族蛋白。通过共线性分析、进化树构建、基因结构和功能结构域鉴定、GO注释分析、不同组织间和非生物胁迫下表达分析等,获得了大豆PHD家族基因复制、家族进化、保守结构域及基因表达等信息。结果表明,大豆PHD基因在家族进化、基因结构和保守结构域上存在较大变异,可能参与Zn ²⁺结合、DNA结合及表观遗传调控等分子过程,参与调控植物生长发育和逆境应答。这些结果为进一步研究大豆PHD家族在生长发育和逆境应答中的生物学功能提供重要线索。     

NRF2 attenuates oxidative stress and lysosomal dysfunction in doxorubicin-induced H9C2 cells

AIM:To study the effect of nuclear factor E2-related factor 2 (NRF2) on oxidative stress injury and lysosomal dysfunction in doxorubicin (DOX)-induced rat myocardial H9C2 cells. METHODS:The H9C2 cells were treated with DOX. The expression of NRF2 at mRNA and protein levels was determined by real-time PCR and Western blot. The H9C2 cells stably over-expressing NRF2 were established by lentiviral infection. Real-time PCR and Western blot were used to identify the efficiency of over-expression. After DOX treatment, the cell viability was measured by CCK-8 assay, the activity of lactate dehydrogenase (LDH), superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) and catalase (CAT), and the content of malondialdehyde (MDA) in the cell supernatant were detected. FITC-dextran was used to analyze lysosomal pH, and the protein expression of lysosomal-associated membrane protein 1 (LAMP1) and cathepsin B was determined by Western blot.RESULTS:The expression of NRF2 at mRNA and protein levels in DOX-treated H9C2 cells was significantly decreased (P<0.05). Over-expression of NRF2 significantly up-regulated the mRNA and protein expression of NRF2 in DOX-treated H9C2 cells (P<0.05). After DOX treatment, the cell viability was decreased, and LDH activity was increased. The activity of SOD, GSH-Px and CAT was decreased, and the content of MDA was increased (P<0.05). The lysosomal pH was increased, and the protein expression of LAMP1 and cathepsin B decreased (P<0.05). Over-expression of NRF2 increased the cell viability, decreased LDH activity, increased the activity of SOD, GSH-Px and CAT, and decreased the content of MDA in cell supernatant (P<0.05). Over-expression of NRF2 also decreased the lysosomal pH, and increased the protein expression of LAMP1 and cathepsin B (P<0.05). CONCLUSION:DOX inhibits the expression of NRF2 in the myocardial H9C2 cells. Over-expression of NRF2 attenuates oxidative stress and lysosomal dysfunction in the H9C2 cells induced by DOX.