玉米粉淀粉含量近红外模型建立与优化     

韩洁楠  王美娟  赵训超  鲁鑫  周志强  李明顺  张德贵  郝转芳  翁建峰  雍洪军  李新海 《玉米科学》2020,28(6):81-87

以230份玉米自交系为样本,采用旋光法与一阶导数及去一条直线的光谱预处理法,构建玉米粉样淀粉含量的近红外分析（NIRS）模型。研究标明,该模型可显著提高子粒淀粉含量预测的准确性。该模型的定标标准偏差（RMSEE）、交叉验证标准偏差（RMSECV）、外部验证标准偏差（RMSEP）、定标相关系数（R_cal²）、交叉验证相关系数（R_cv²）、外部验证相关系数（R_cv²）分别为0.609、0.722、0.738、0.909、0.864和0.854。建立的玉米粉样NIRS模型可将预测值与化学值偏差控制在1.7%内,能够准确定量分析玉米子粒淀粉含量,应用于育种材料早期筛选及群体水平粗淀粉分析。  相似文献   

不同春玉米品种茎秆显微结构对抗折强度的响应     

蒋傲男  闫静琦  卢海博  赵海超  黄智鸿 《玉米科学》2020,28(5):53-59

以冀西北寒旱区9个春玉米品种为研究对象,通过测定玉米基部第3节抗折强度,利用光学显微镜观察其茎节显微结构,对维管束各项显微指标与节折强度进行相关分析,研究春玉米节折强度与茎秆显微结构之间的关系。结果表明,不同春玉米品种间节折强度达显著水平。对各品种维管束显微指标进行统计分析表明,维管束鞘厚度和表皮细胞厚度变异系数最大,分别达到34.8%和23.2%;茎节维管束数目增多不利于节折强度的提高(r=-0.945**,r=-0.927**),维管束平均面积、韧皮部面积增大有利于节折强度的增加(r=0.831*,r=0.799*;r=0.733*,r=0.786*)。通径分析表明,维管束数目对节折强度的直接效应最大,表皮细胞厚度次之,维管束最大面积、维管束鞘厚度、韧皮部面积等指标也通过维管束数目对茎折强度起间接作用。参试品种中,京农科728、纪元108维管束数目较少,维管束平均面积、韧皮部面积较大,茎折强度较高,抗倒伏性优于其他品种。  相似文献   

新疆春小麦育成品种耐热性评价     

张金波  王小波  严勇亮  肖菁  彭惠茹  丛花 《麦类作物学报》2020,40(9):1055-1063

为筛选出耐热性好的小麦种质材料,通过开花期至成熟期人工模拟高温胁迫环境,以千粒重热感指数为主要评价指标,评价了新疆近30年来审定的春小麦品种的相对耐热性,并分析了高温胁迫对小麦籽粒蛋白质、湿面筋含量的影响。结果表明,与自然生长相比,高温胁迫条件下新疆春小麦育成品种的千粒重、籽粒宽度的变化均达到了极显著水平（P<0.01）,籽粒长度变化不显著(P>0.05),不同品种间耐热性存在很大差异。综合三年千粒重热感指数（HSI）分析,耐热性相对较好的品种有17个,连续三年HSI＜1的品种有11个,其中新春37号、新春2号、新春38号在高温胁迫条下千粒重变化较小,产量较稳定,为强耐热品种;对高温敏感品种有26个,连续三年HSI≥1的品种有13个,其中新春13号、新春18号、新春33号耐热性相对较弱。高温胁迫影响小麦籽粒的品质,其中13.95%的品种蛋白质含量降低,6.98%的品种湿面筋含量降低,其他品种高温胁迫后籽粒蛋白质、湿面筋含量均较自然生长有所提高。  相似文献   

水分和盐胁迫下小麦种子萌发相关性状的QTL定位     

王秀华  于鸿翔  潘香逾  赵岩  李斯深 《麦类作物学报》2020,40(10):1157-1165

小麦萌发期对水分和盐胁迫敏感,对该时期水分和盐胁迫下种子萌发性状进行QTL定位具有重要的意义。本研究以小麦“泰农18×临麦6号” RIL群体为材料,以20%PEG-6000溶液和100 mmol·L^-1 NaCl溶液分别模拟水分和盐胁迫环境,对种子萌发期10个性状进行了QTL定位。结果表明,在正常、水分胁迫和盐胁迫3种不同处理下各性状变异较大。相关分析表明,抗旱和耐盐可能是两个独立遗传的性状,胚芽鞘长可以作为节水抗旱的鉴定指标。3种处理下共检测到10个萌发相关性状的103个QTL,其中,17个为相对高频QTL（RHF-QTL）,分布在7条染色体（1A、3A、3B、4B、7A、7B和7D）上,平均贡献率为7.55%~15.97%。这些RHF-QTL形成4个QTL簇（QTL cluster,QC）,分布在3A、7A和7D染色体上。其中,7A染色体上的QC2包括3个RHF-QTLs（ QSdw-7A.1、 QGf-7A.1和 QGi-7A.1）,均与小麦耐盐性相关;7D染色体上的QC3包括2个RHF-QTLs（ QGi-7D.1、 QGdrc-7D.1）,均与小麦节水抗旱性相关。这2个QCs增加效应均来自母本泰农18。本研究获得的RHF-QTLs和QCs,可为小麦萌发期节水抗旱和耐盐分子标记辅助选择提供理论和技术支持。  相似文献   

Effects of calpain-2 and autophagy-related protein 5 on hepatocyte apoptosis induced by endoplasmic reticulum stress     

CHEN Yu-si  HAN Bing  ZHENG Lu  CAI Shuang  TANG Lei  YANG Yi  GUO Yi-xin  LIANG Cai  ZHAO Jin-you  YANG Ting  YANG Qin  XIE Ru-jia 《园艺学报》2020,36(5):847-853

AIMTo investigate the effects of calpain-2 and autophagy-related protein 5 (Atg5) on apoptosis of BRL-3A rat normal liver cells during endoplasmic reticulum stress (ERS) induced by dithiothreitol (DTT). METH?ODS: BRL-3A cells were treated with DTT at 2.0 mmol/L for 0, 6, 12 and 24 h to induce ERS. Real-time cell analysis (RTCA) was used to measure the effect of DTT on BRL-3A cell proliferation. Apoptosis and cell cycle distribution were analyzed by flow cytometry. The mRNA expression of calpain-2 and Atg5 was detected by real-time PCR. The protein levels of calpain-2, Atg5, Atg7, Atg12 and microtubule-associated protein 1 light chain 3 (LC3) were determined by Western blot. The interaction between calpain-2 and Atg5 was investigated by co-immunoprecipitation (Co-IP). RESULTSThe proliferation of BRL-3A cells treated with DTT was significantly inhibited. The apoptosis of BRL-3A cells was significantly increased after DTT treatment for 6, 12 and 24 h as compared with 0 h group (P<0.05). The cell cycle was arrested in G₁ phase after DTT treatment (P<0.05). After DTT treatment for 6, 12 and 24 h, the mRNA expression of calpain-2 and Atg5 in the BRL-3A cells was significantly increased as compared with 0 h group (P<0.05). The protein levels of calpain-2, Atg12 and Atg7 in the cells treated with DTT for 6, 12 and 24 h were significantly higher than those in 0 h group, and the ratio of LC3-II/LC3-I was also significantly higher than that in 0 h group, while Atg5 expression was significantly lower than that in 0 h group (P<0.05). The results of Co-IP found that the anti-calpain-2 antibody precipitated Atg5 protein from the cell lysates, and the anti-Atg5 antibody also precipitated calpain-2 from the cell lysates, which confirmed the interaction between calpain-2 and Atg5. CONCLUSION Calpain-2 may participate in ERS-induced hepatocyte apoptosis by interacting with Atg5.  相似文献   

Roles of protein phosphatase 4 in down-regulation of eNOS Ser633 phosphorylation induced by palmitic acid in human umbilical vein endotheli?al cells     

QIN Si  ZHANG Qian  WANG Jing-jie  YU Min  LUO Yan-bei  DING Jing  LU De-qin 《园艺学报》2020,36(5):803-809

AIMTo investigate the roles of protein phosphatase 4 (PP4) in down-regulation of endothelial nitric oxide synthase (eNOS) Ser633 phosphorylation induced by palmitic acid (PA). METHODSHuman umbilical vein endothelial cells (HUVECs) were treated with PA at 25 μmol/L, 50 μmol/L, 100 μmol/L and 200μmol/L for 36 h, or treated with PA at 100 μmol/L for 12 h, 24 h, 36 h and 48 h. Protein phosphatase 2A (PP2A) family inhibitor fostriecin (FST, 20 nmol/L) or okadaic acid (OA, 5 nmol/L) was selected to pretreat the HUVECs for 30 min. Protein phosphatase 4 catalytic subunit (PP4c) siRNA or protein phosphatase 2A catalytic subunit (PP2Ac) siRNA was transfected into the HUVECs. The protein expression levels of of eNOS, PP4c and PP2Ac, as well as the level of eNOS Ser633 phosphorylation, were detected by Western blot. The intracellular nitric oxide (NO) content was measured by DAF-FM DA. RESULTS(1) Compared with control group, the levels of eNOS Ser633 phosphorylation were decreased in PA groups in which the HUVECs were treated with 25 μmol/L, 50 μmol/L, 100 μmol/L and 200 μmol/L PA for 36 h (P<0.05) and 100 μmol/L PA for 24 h, 36 h and 48 h (P<0.05). No significant difference in the level of total eNOS protein expression among all the groups was observed. (2) Compared with control group, both FST and OA pretreatment reversed the reduction of eNOS Ser633 phosphorylation (P<0.05) and the decrease in intracellular NO content (P<0.05) induced by PA. No significant difference in the level of total eNOS protein expression among all the groups was observed. (3) Compared with si-Control group, the PP4c protein expression was significantly reduced (P<0.05), while the level of eNOS Ser633 phosphorylation was significantly increased in si-PP4c group (P<0.05). Although the levels of PP2Ac protein expression declined significantly (P<0.05), the level of eNOS Ser633 phosphorylation remained unchanged in si-PP2Ac group. No significant differencein the level of total eNOS protein expression among all the groups was found. CONCLUSION PA significantly reduces the level of eNOS Ser633 phosphorylation and the content of NO in the HUVECs, which may be due to PA inducing the activation of the PP2A family member PP4 rather than PP2A.  相似文献   

Effect of Linc00152 targeting miR-376c-3p on viability,apoptosis and radiosensitivity of cervical cancer cells     

LIU Xiao-juan  WANG Jing  ZHANG Juan  GAO Yue-yue  WANG Hong 《园艺学报》2020,36(1):67-74

AIM: To investigate the effect of Linc00152 on the viability, apoptosis and radiosensitivity of cervical cancer cells. METHODS: RT-qPCR was used to detect the expression levels of Linc00152 and microRNA-376c-3p(miR-376c-3p) in human cervical cancer HeLa cells and SiHa cells, and normal cervical Ect1/E6E7 cells. The cervical cancer HeLa cells with low Linc00152 expression or miR-376c-3p over-expression were established. MTT assay, flow cytometry, colony formation assay and Western blot were used to determine the cell viability, apoptosis, radiosensitivity and related protein expression. The dual-luciferase reporter assay was used to verify the regulatory relationship between Linc00152 and miR-376c-3p in the HeLa cells. RESULTS: Compared with the Ect1/E6E7 cells, Linc00152 was up-regulated in the HeLa cells and SiHa cells, and miR-376c-3p was down-regulated (P < 0.05). Low expression of Linc00152 or over-expression of miR-376c-3p inhibited the viability of HeLa cells, induced apoptosis, enhanced the radiosensitivity, inhibited the protein expression of cyclin D and Bcl-2, and promoted the protein expression of P21 and Bax (P < 0.05). Linc00152 negatively regulated miR-376c-3p expression in the HeLa cells, and inhibition of miR-376c-3p expression reversed the effect of low expression of Linc00152 on HeLa cell viability, apoptosis and radiosensitivity. CONCLUSION: Linc00152 is highly expressed in the cervical cancer cells. Linc00152 affects the viability, apoptosis and radiosensitivity of HeLa cells by targeting miR-376c-3p, which is a potential diagnosis and treatment target for cervical cancer.  相似文献   

MRTF-A induces autophagy to attenuate cerebral cortical nerve cell injury in rats with cerebral ischemia-reperfusion     

LI Xiang  ZHANG Ling  JIA Yue  LI Zhen  ZHAO Yu-jie  MA Lan  LI Rui-wen  LI Li  CAO Xiao-lu 《园艺学报》2020,36(4):673-680

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Role of PERK pathway in morphine-induced myocardial protection of H9c2 cells     

ZHAO Miao  HAN Ya-ru  HE Yi-fei  FU Yu  LIU Yu-lin  XI Jin-kun  HE Yong-gui 《园艺学报》2020,36(1):9-16

AIM: To explore whether morphine protects oxidative stress-damaged myocardial cells by inhibiting the PERK pathway to reduce endoplasmic reticulum stress and prevent mitochondrial permeability transition pore (mPTP) opening. METHODS: Rat myocardial H9c2 cells were cultured to establish an oxidative stress model, and then randomly divided into control group, H₂O₂ group, H₂O₂+morphine group, H₂O₂+morphine+PERK pathway inhibitor GSK2656157 group, morphine group and GSK2656157 group. Immunohistochemical method was used to detect the effects of morphine on expression of glucose-regulated protein (GRP) 78 and GRP94 induced by oxidative stress. The protein levels of PERK signaling pathway-related molecules were determined by Western blot. Confocal microscopy was used to observe the effects of morphine on mPTP opening and endoplasmic reticulum induced by oxidative stress. Cellular toxicity was detected by lactate dehydrogenase (LDH) kit and cell viability was measured by MTT assay. RESULTS: Compared with control group, GRP78 and GRP94 proteins in H₂O₂ group were strongly expressed, and the brown-yellow particles were significantly increased, but morphine significantly inhibited this process. Compared with control group, the phosphorylation of PERK was significantly reduced with GSK2656157 treatment at different concentrations, among which 2 μmol/L had the most significant effect (P < 0.05). Oxidative stress significantly increased the protein levels of GRP78, GRP94, p-PERK and CHOP, but significantly decreased p-GSK-3β level. These changes were inhibited by morphine, and the effects of morphine were further enhanced by GSK2656157 (P < 0.05). Compared with control group, oxidative stress significantly reduced the fluorescence intensity of mitochondrial TMRE and ER-Tracker Red. Morphine significantly inhibited this effect even when mitochondrial membrane potential was reduced, mPTP was open, and endoplasmic reticulum was damaged, while GSK2656157 further enhanced the effect of morphine (P < 0.05). Compared with control group, H₂O₂ significantly increased cellular toxicity and decreased the cell viability. Morphine inhibited this effect and GSK2656157 significantly enhanced the effect of morphine (P < 0.05). CONCLUSION: Morphine protects cardiac H9c2 cells under oxidative condition by inhibiting endoplasmic reticulum stress through PERK pathway and preventing the mPTP opening via GSK-3β inactivation.  相似文献   

Soluble Klotho protein suppresses THP-1-derived foam cell formation     

LIU Wei  LI Lin  LIU Jia-ni  SHI Jing  HONG Tian  CHEN Xiu-juan 《园艺学报》2020,36(5):816-821

AIMTo investigate the role of soluble Klotho protein in THP-1-derived foam cell formation. METHODSTHP-1 monocytes were induced into macrophages by treatment with 160 nmol/L phorbol myristate acetate for 48 h, and then were divided into 6 groups: negative control group (THP-1-derived macrophages), positive control group [THP-1-derived foam cells induced by oxidized low-density lipoprotein (ox-LDL) for 48 h], and 25, 50, 100 and 200 μg/L soluble Klotho protein groups (THP-1-derived macrophages pretreated with soluble Klotho protein at the indicat?ed concentraions for 2 h and then induced by ox-LDL for 48 h). Lipid droplets in cytoplasm were observed by oil red O staining. The cholesterol outflow rate was detected by scintillation counting technique. The content of intracellular total cholesterol, free cholesterol and cholesterol ester was detected by enzyme fluorescence analysis. The expression of acyl-coenzyme A:cholesterol acyltransferase 1 （ACAT1） and ATP-binding cassette transport?er A1 (ABCA1) at mRNA and protein levels was determined by RT-qPCR and Western blot, respectively. RESULTSOil red O staining and lipid mass quantification showed that THP-1-derived foam cell formation was dose-dependently suppressed by soluble Klotho protein. The cholesterol efflux rate of THP-1-derived foam cells was increased by soluble Klotho protein in a dose-dependent manner (P<0.05). In addition, soluble Klotho protein decreased the expression of ACAT1 and increased the expression of ABCA1 in a dose-dependent manner (P<0.05). CONCLUSION The soluble Klotho protein inhibits THP-1-derived foam cell formation in a dose-dependent manner by down-regulating the expression of ACAT1 and up-regulating the expression of ABCA1.  相似文献