高温对茶树叶片光合及抗逆特性的影响和恢复*3     

韩冬  杨菲  杨再强  金志凤 《中国农业气象》2016,(3):297-306

以4个茶树品种福鼎大白茶、鸠坑、龙井43和乌牛早7a生植株为研究对象,采用人工气候箱模拟高温（35℃和40℃）处理6、12、18、24、48h,取出后置于人工气候箱中（25℃）恢复3、6、9d,以未经高温处理置于人工气候箱中（温度25℃）的各品种茶树为对照（CK）,测定茶树叶片的最大净光合速率、荧光参数、抗氧化酶活性以及细胞伤害率。结果表明：高温胁迫显著抑制了茶树的最大净光合速率（Pnmax）和最大光化学效率（Fv/Fm）,处理时间越长、温度越高,Pnmax和Fv/Fm下降越快,除35℃处理的福鼎大白茶外,其它3种茶树经过高温处理后,在恢复期间其Fv/Fm无法恢复至正常水平;茶树叶片的SOD酶活性在高温处理的前12h迅速上升,随着处理时间的延长,其活性降低;叶片MDA含量的平均值在高温处理第48小时达到最大,恢复期间缓慢下降;随着处理温度的升高和处理时间的延长,各茶树叶片的细胞伤害率均呈增加趋势。4种茶树耐热性的强弱由高到低依次为福鼎大白茶＞乌牛早＞鸠坑＞龙井43。  相似文献   

棉花盐害的控制技术及其机理   总被引：18，自引：5，他引：18  

代建龙  董合忠  段留生 《棉花学报》2010,22(5):486-492

棉花是耐盐作物,但土壤耕层中积累过多的盐离子会通过离子毒害、渗透胁迫和引起营养失衡等机制导致盐害。控制棉花盐害的途径主要有两条,一是提高棉花自身的耐盐性,另一方面是躲避或减轻盐胁迫。本文评述了提高棉花耐盐性和躲避或减轻盐胁迫的途径、原理和方法,提出在工程措施改良盐碱地的基础上,综合运用适宜品种、水肥运筹、种子处理及地膜覆盖和诱导根区盐分差异分布等农艺措施是现阶段控制盐碱地棉花盐害的有效途径。  相似文献   

滴灌土壤湿润区对棉花生长及产量的影响研究   总被引：2，自引：0，他引：2  

丁浩  李明思  孙浩 《灌溉排水学报》2009,28(3)

针对棉花作物,以桶栽试验为基础,通过控制滴头流量得到不同宽度的土壤湿润区,观测了棉花相应的生长状况及产量。试验结果表明,棉花的生长发育和产量与滴灌土壤湿润区的大小密切相关,宽的土壤湿润区可以使棉花的生长发育提前,其株高、叶面积、产量都比窄的土壤湿润区条件下的棉花相应指标高;宽的土壤湿润区下的棉花叶面积衰老速度比窄的土壤湿润区下的棉花叶面积衰老速度慢。另外,随着土壤湿润区变宽,土壤耗水深度变浅,棉花单铃重、衣分和单株产量增加,但单株铃数减少。  相似文献   

单线圈径向流磁流变阀优化设计与性能分析     

胡国良  李林森  胡安琪  喻理梵 《农业机械学报》2019,50(7):417-426

针对磁流变阀通过改变内部结构提高压降而导致阀体积增大、内部通道易阻塞的问题,在不改变普通单线圈径向流磁流变阀内部基本结构及外观尺寸的基础上,对单线圈径向流磁流变阀压降与压降可调系数进行了多目标优化,设计了一种带有隔磁套筒的单线圈径向流磁流变阀,并阐述了其工作原理,基于Bingham模型推导了其压降数学模型。采用有限元法建立了磁流变阀二维仿真模型,观察径向圆盘阻尼间隙处磁感应强度分布规律,建立约束条件,分析了磁流变阀关键部件尺寸对剪切屈服应力与压降等相关性能的影响。运用ANSYS零阶和一阶优化工具对磁流变阀进行几何尺寸参数优化,并对优化前后磁流变阀有效阻尼间隙处的平均磁感应强度,以及进出口压降进行仿真对比分析。在磁流变阀动态性能测试平台上,对优化前后磁流变阀压降性能进行实验测试对比,实验结果表明,当励磁电流为1. 8 A时,优化前磁流变阀压降为1. 84 MPa,优化后磁流变阀压降为2. 58 MPa,增加了40. 22%;优化前磁流变阀压降可调系数为7. 94,优化后压降可调系数为10. 07,增加了26. 83%;不同负载对磁流变阀压降效果影响不大。  相似文献   

二苯胺处理对鸭梨果实冷害的影响   总被引：2，自引：0，他引：2  

赵瑞平  王云峰  李育峰 《北方园艺》2009,(6)

研究了贮前二苯胺（DPA）处理对在低温条件下（0℃）贮藏鸭梨果实的果心褐变及生理变化的影响。结果表明：急骤降温（0℃）可产生严重的早期果心褐变,贮前二苯胺处理在一定条件下可减轻鸭梨果实的早期褐变,贮藏60 d时DPA处理果实的褐变指数为0.233,而对照为0.417;同时DPA处理可降低果实的乙烯释放量、抑制多酚氧化酶活性、保持果实酚类物质含量,对丙二醛（MDA）含量和果实相对电导率也有一定影响。  相似文献   

Changes of mitogen-activated protein kinases signal transduction pathway in ischemia/reperfusion injury     

CAI Qi  LI Xiao-mei  WANG Hai-yan 《园艺学报》2000,16(12):1335-1337

  相似文献   

The protection of the hepatic ischemic preconditioning is concerned with the NO/ET-1 system     

LU Ping  CHEN Dao-da  TIAN Yuan  ZHANG Jing-hui  WU Yi-hua 《园艺学报》2000,16(10):901-905

AIM: To study the relationship between the disturbance of nitric oxide/endothelin-1(NO/ET-1) and hepatic ischemia/reperfusion(I/R) injury as well as the regulation of NO/ET-1 system by hepatic ischemic preconditioning(IPC). METHODS: The changes of NO/ET-1 system and their relationship with hepatic I/R injury were compared between I/R group and IPC+I/R group in a rat hepatic I/R model. Two hours after reperfusion, the liver tissues were detected by RT-PCR to see whether there was inducible nitric oxide synthase (iNOS) mRNA expression. RESULTS:In the acute phase of hepatic reperfusion, the ratio of NO/ET-1 was reduced, which was due to a significant reduction of NO₂^-/NO₃^- (the metabolic product of NO) and significant elevation of ET-1 in the blood plasma. The content of ALT, AST, LDH and TNF-α in blood plasma, and of MDA in liver tissue were increased but ATP in liver tissue was reduced, the hepatic damage was deteriorated. The protection of the hepatic IPC was concerned with the elevation of the ratio of NO/ET-1 caused by the elevation of NO₂^-/NO₃^-, and reduction of ET-1 as well. There was no iNOS mRNA detected in the liver tissues.CONCLUSION: Hepatic I/R injury is related to the disturbance of NO/ET-1. The protection of the hepatic IPC in the acute phase might be conducted by its regulation of NO/ET-1 system. The cNOS rather than the iNOS generated the NO in this situation.  相似文献   

Effects of oxidative stress and inflammatory response on kidney injury in mice with hyperthyroidism     

JIN Bei-fang  LU Qin-zhen  ZHANG Yan  CUI Ya-lan  QIANG Zheng  LIAO Man-xi  TAN Hui-yuan  LIU Fang 《园艺学报》2000,36(9):1625-1630

AIM To explore the effects of oxidative stress and inflammatory response on kidney injury induced by hyperthyroidism in mice. METHODS Forty male Kunming mice were randomly divided into control group （n=20） and L-thyroxine （T4） group （n=20）. The mice in T4 group were intraperitoneally injected with T4 diluent at a dose of 1 mg/kg to induce hyperthyroidism, and those in control group were injected with normal saline of the same volume. After 7 weeks, the mice were weighed and dissected, the kidneys were removed and weighed, and the length of tibia was also measured. The activity of superoxide dismutase （SOD） and the content of malondialdehyde （MDA） in the kidney tissues were detected. The pathological changes of the kidney tissues were observed by HE staining. The levels of 4-hydroxynonenal （4-HNE）-modified proteins, interleukin-1 receptor-associated kinase 1 （IRAK1） and tumor necrosis factor receptor-related factor 6 （TRAF6） were determined by Western blot and immunohistochemistry. RESULTS Compared with control group, the body weight of the mice was decreased, while the kidney size and weight were increased significantly in T4 group. In addition, the ratios of kidney weight/body weight and kidney weight/tibia length were also increased （P<0.05）. In T4 group, the renal tubules were enlarged, and the epithelial cells of renal tubules were swollen and exfoliated, with vacuolar degeneration. Furthermore, reduced SOD activity, and increased MDA content and 4-HNE-modified proteins were found in T4 group, all of which were related to oxidative stress （P<0.05）. The levels of inflammation-related proteins IRAK1 and TRAF6 were significantly increased in T4 group （P<0.05）. CONCLUSION Excessive T4 may lead to kidney hypertrophy and injury in mice, and the mechanism may be related to oxidative stress and inflammatory response.  相似文献   

Curcumin attenuates rat lung ischemia/reperfusion injury by interfering with autophagy     

QIAN Wei  LOU Guo-qiang  ZHOU Zhuo-lin  WANG Jia  LIU Xiu-jie  HAO Mao-lin  WANG Wan-tie 《园艺学报》2000,36(11):2056-2061

AIM To investigate the role of curcumin （CUR） in lung ischemia/reperfusion （I/R） injury （LIRI） and its relationship with autophagy. METHODS 40 SD rats were randomly divided into sham operation （sham） group, I/R group, solvent （DMSO） group, CUR group and CUR+rapamycin （CUR-Rap） group. The rats were intraperitoneally injected with normal saline, DMSO, CUR or CUR+Rap before operation. After the rat LIRI model was established, the lung tissues were taken to measure W/D, TLW, IAR, and the contents of SOD and MDA were also measured to indicate the oxidative stress level. Light and electron microscopes were used to observed the morphology and ultrastrucure of lung tissues. The expression levels of autophagy-related proteins were determined by Western blot to evaluate autophagy levels. RESULTS Compared with sham group, wet weight/dry weight （W/D）, total lung water （TLW）, injured alveoli rate（IAR） and malondialdehyde （MDA） content in all other groups were increased, superoxide dismutase （SOD） activity was decreased, the levels of autophagy were increased （P<0.05）, and lung tissue injury and cell ultrastructural damage were aggravated in CUR group. Compared with DMSO group, W/D, TLW and IAR and MDA content were decreased, SOD activity was decreased, autophagy levels were also decreased （P<0.05）, and lung tissue and cell ultrastructural damage were attenuated. Compared with CUR group, W/D, TLW, IAR and MDA content were increased, SOD activity declined, the autophagy levels were increased （P<0.05）, and damage of lung tissues and cells were more serious in CUR-Rap group. CONCLUSION Curcumin attenuates the lung I/R injury in rats, and its mechanism may be related to the reduction of oxidative stress and the inhibition of autophagy.  相似文献   

Involvement of TLR4/NLRP3 inflammasome in contrast medium-induced inflammation and injury in renal tubular epithelial cells     

LIN Yan  LIN Jia-qiong  XIE Chu-li  GUAN Xiao-feng  TAN Xue-xian  HUANG Ze-na 《园艺学报》2017,33(12):2252-2258

AIM: To investigate whether Toll-like receptor 4 (TLR4) and Nod-like receptor protein 3 (NLRP3) inflammasome were involved in contrast medium (CM)-induced inflammation and injury in renal tubular epithelial cells. METHODS: Iopromide was used to injure NRK-52E cells in the study. The cell viability was measured by CCK-8 assay. The protein levels of TLR4, NLRP3, apoptosis-associated speckle-like protein (ASC), caspase-1 and cleaved caspase-3 were determined by Western blot. The releases of interleukin (IL)-1β and IL-18 were detected by ELISA. The apoptotic rate was evaluated by Hoechst staining, and mitochondrial membrane potential (MMP) was analyzed by JC-1 staining. siRNA was transfected into the NRK-52E cells to silence NLRP3 expression. RESULTS: CM decreased the viability of NRK-52E cells (P<0.05). CM also elevated the protein levels of cleaved caspase-3, TLR4, NLRP3, IL-1β and IL-18 (P<0.05). Silencing NLRP3 attenuated CM-induced releases of inflammatory cytokines. Moreover, treatment with TLR4 inhibitor TAK-242 or knockdown of NLRP3 by siRNA transfection both attenuated cell apoptosis and loss of MMP caused by CM. CONCLUSION: TLR4/NLRP3 inflammasome takes part in the pathogenesis of CM-induced acute kidney injury, and mediates CM-induced injury and inflammation in renal tubular epithelial cells.  相似文献