东北三省大豆种质品质性状鉴评与综合分析

根据目标性状有的放矢的选配杂交亲本是提高优异品质组成品种的选择效率的基本前提。本研究对东北三省102份大豆种质资源的蛋白、氨基酸组分、油份及脂肪酸组分进行测定,通过遗传多样性、主成分和聚类分析,对其进行表型鉴定及基因型分类以综合评价种质品质特性。结果表明:东北三省大豆种质油份及脂肪酸组分变异较丰富,遗传多样性程度较高。根据主成分分析筛选到9个主成分进行聚类分析,通过聚类分析将供试种质资源分为5类。第I类群蛋白含量较高、油份含量偏低,第II类群蛋白、油份含量均居中,第III类群油份含量较高、蛋白含量偏低,第IV类群高油,第V类群高蛋白,类群间的氨基酸、脂肪酸组分各有差异。需根据育种目标在群体间选配亲本,以提高品质育种的效率。     

靖粳26号的特征特性及高产栽培技术

靖粳26号系由云南省曲靖市农业科学院选育的优质粳稻新品种,具有良好的丰产性和优异的抗逆性,是一个适应性较广的优质、高产、耐寒、多抗粳稻新品种。     

Mechanism of quercetin improving rat coronary artery myogenic response under high glucose

AIM: To investigate the mechanism of quercetin improving rat coronary artery myogenic response under high glucose (HG) by measuring muscle tension of coronary arterial ring and recording voltage-gated K⁺ channel (Kv) current of coronary artery smooth muscle cells by whole cell patch clamp. METHODS: The coronary rings from the normal SD rats were acutely isolated, and then divided into 6 groups: (1) control group; (2) HG group; (3) HG+low dose (3 μmol/L) of quercetin group; (4) HG+moderate dose (10 μmol/L) of quercetin group; (5) HG+high dose (30 μmol/L) of quercetin group; (6) HG+C6303 (PKC inhibitor)+high dose of quercetin group. Determinations of coronary artery response to vasoconstrictor (60 mmol/L KCl or 0.1 mmol/L U46619) or vasodilator (ACh at 10^-9~10^-5 mol/L) were performed, and the percentage of coronary ring tension was calculated using the contraction as 100% caused by 60 mmol/L KCl. The rat coronary artery smooth muscle cells were acutely isolated for recording the Kv current using whole cell patch clamp. RESULTS: Compared with control group, the contraction amplitudes to 60 mmol/L KCl or 0.1 mmol/L U46619 were significantly increased under HG incubation. Quercetin intervention concentration-dependently reduced the coronary artery contraction amplitude. Incubation of PKC specific inhibitor C6303 attenuated the effect of quercetin. Compared with control group, the diastolic amplitude to ACh decreased significantly in HG group, and quercetin intervention concentration-dependently increased the coronary artery diastolic amplitude. Incubation of PKC specific inhibitor C6303 attenuated the effect of quercetin. Compared with control group, HG incubation inhibited Kv current of coronary artery vascular smooth muscle cells significantly, and quercetin intervention attenuated the inhibitory effect of HG on Kv current intensity. Incubation of PKC specific inhibitor C6303 attenuated the effect of quercetin. CONCLUSION: Quercetin has a protective effect on myogenic response of coronary artery under HG and the effects is related to the increase in Kv current and the activation of PKC in vascular smooth muscle cells.     

Kernel vitreousness and protein content: Relationship,interaction and synergistic effects on durum wheat quality

Four sets of durum samples were used in this study to further understand the interrelationships among hard vitreous kernels (HVK), protein content, and pigment concentration, with a focus on the interaction and synergistic effects of protein content and vitreousness on durum quality. HVK level increases with higher protein content in the range of 9.5–12.5%, but this relationship is less evident in durum samples with high protein content (12.5–14.5%). Both protein content and kernel vitreousness can significantly affect durum milling quality. White starchy kernels (WSK) in low protein durum have a very detrimental impact on milling and pasta processing quality, but high protein content can mitigate the adverse impact of WSK on durum quality. Although protein content plays a dominant role, higher HVK might contribute positively to pasta firmness. There was no significant difference in yellow pigment content between HVK and WSK. However, pigment loss from semolina to dough was higher for WSK than HVK. Despite the difference in protein content, HVK and WSK have little difference in gluten strength. The monomeric protein was preferentially accumulated in HVK. The glutenin proteins of HVK and WSK were similar in the ratios of 1Bx/1By and HMW/LMW-GS.     

玉米大斑病菌StSNF1的基因组定位、蛋白质结构预测及表达分析

为了明确StSNF1在玉米大斑病菌基因组中的位置,解析该基因编码蛋白的结构特征,探究该基因在侵染寄主的不同时期、分生孢子萌发侵染过程中以及不同碳源培养下的表达情况。结果表明,该基因ID号为008026214,全长3 046 bp,位于scaffold_17负链的97 793-100 838位置。StSNF1与玉米圆斑病菌SNF1同源关系较近,由877个氨基酸残基编码而成。StSNF1蛋白具有氮端的蛋白激酶结构域、氮端的碳代谢产物去阻遏蛋白激酶结构域和碳端的激酶相关结构域。在蛋白激酶结构域内,具有ATP结合位点和丝氨酸/苏氨酸活性位点。Real-time PCR结果表明,StSNF1在侵染后期高表达,72 h表达量最高;StSNF1在分生孢子萌发24 h时(即侵入丝形成时期)表达量最高;StSNF1在蔗糖为单一碳源的培养基中表达量最高,果胶培养基次之。综上所述,StSNF1与侵染寄主和碳源利用密切相关,在侵染后期发挥作用,利用寄主细胞内的非发酵型碳源进行次级侵染。     

miR-140-3p inhibits viability,invasion and migration of non-small-cell lung cancer A549 cells by targeting PD-L1

AIM: To explore the target relationship between microRNA-140-3p (miR-140-3p) and programmed cell death ligand 1 (PD-L1) and their effect on the viability, migration and invasion of non-small-cell lung cancer A549 cells.METHODS: RT-qPCR was used to detect the miR-140-3p expression in HLF-1, A549 and H1299 cells, and then the A549 cells with the most significant difference were selected as the subsequent research object. TargetScan software and dual-luciferase reporter assay were performed to predict and confirm the target relationship between miR-140-3p and PD-L1. RT-qPCR and Western blot were used to determine the effects of miR-140-3p mimic and inhibitor on PD-L1 expression level. MTT assay was used to detect the viability of A549 cells. Transwell assay was performed to detect the migration and invasion abilities of the A549 cells.RESULTS: miR-140-3p was significantly down-regulated in the A549 cells and H1299 cells (P<0.05). Transfection with miR-140-3p mimic decreased the expression of PD-L1 and inhibited the viability, migration and invasion of the A549 cells. Transfection with pcDNA3.0-PD-L1 reversed the inhibitory effect of miR-140-3p on the viability, migration and invasion of the A549 cells.CONCLUSION: miR-140-3p inhibits the viability, migration and invasion of A549 cells by targeting PD-L1.     

Ethanol extract from Cortex Albiziae attenuates mouse acute liver injury induced by carbon tetrachloride via modulation of NF-κB pathway

AIM:To investigate the protective effect of ethanol extract from Cortex Albiziae on acute liver injury, and to explore its possible mechanism. METHODS:Acute liver injury in mice was induced by single intraperitoneal injection of 25% carbon tetrachloride (olive oil solubilization). The effective parts of ethanol extract from Cortex Albizziae against acute liver injury were screened. The pathological changes of the liver tissues were examined by pathological sections with HE staining. The activity of total superoxide dismutase (T-SOD) and the content of malondialdehyde (MDA) of the liver tissues were detected, the serum levels of interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) were mea-sured by ELISA, and the protein expression levels of NF-κB p65, Bcl-2 and Bax in the liver cells of the mice in each group were determined by Western blot. RESULTS:Compared with model group, the serum levels of AST and ALT in low-dose n-butanol phase of ethanol extract from Cortex Albiziae (AB-L, 4 mg·kg^-1·d^-1) group and high-dose n-butanol phase of ethanol extract from Cortex Albiziae (AB-H, 8 mg·kg^-1·d^-1) group were significantly decreased. The necrosis extent and degree of the hepatocytes and infiltration of inflammatory cells were significantly lower than that in model group. Compared with model group, the serum levels of TNF-α and IL-6 in AB-H group and AB-L group were significantly decreased (P<0.05). The protein level of NF-κB p65 in the nuclei of mouse liver cells in AB-H group and AB-L group were also decreased significantly (P<0.05). Compared with model group, the protein expression of Bax was decreased, the protein expression of Bcl-2 was increased, and the Bcl-2/Bax ratio was increased in AB-L group and AB-H group. CONCLUSION:The n-butanol phase of ethanol extract from Cortex Albiziae may protect the liver by reducing the activation of NF-κB p65, inhibiting the excessive release of inflammatory cytokines IL-6 and TNF-α, and decreasing hepatocyte apoptosis via regulating Bcl-2 and Bax expression.     

Role of cytokeratin 8 on changes of intestinal epithelial permeability induced by corticotropin-releasing factor

AIM: To investigate the role of cytokeratin 8 (CK8) on the change of intercellular permeability of intestinal epithelial cells induced by corticotropin-releasing factor (CRF). METHODS: The expression levels of CRF receptor 1 (CRFR1) and CRFR2 on human colon adenocarcinoma HT29 cell surface were determined by immunofluorescence staining. After treatment with 100 nmol/L CRF for 72 h, the translocation of FITC-labelled dextran was measured in a Transwell chamber. The structural changes of tight junctions were observed under transmission electron microscope. The expression levels of CK8, and tight junction proteins ZO-1 and occludin were determined by Western blot. The activity of protein kinase C (PKC) was detected by ELISA. Furthermore, the effects of CRF on intestinal epithelial permeability were examined in CK8-silencing HT29 cells, which were constructed by infection with sh-CK8 lentivirus. RESULTS: CRF treatment increased the permeability of FITC-labelled dextran (P<0.05), caused the opening of tight junctions, and induced increased fluorescence intensity of CK8. The expression levels of occludin and ZO-1 were down-regulated (P<0.05). PKC activity was decreased at 1 h after CRF treatment (P<0.05). CRF-induced increase in the permeability and down-regulation of occludin were not blocked by CK8 silencing. Nevertheless,CK8 silencing blocked the effects of CRF regarding the decrease in the expression levels of ZO-1 and the increase in PKC activity (P<0.05). CONCLUSION: CK8 may be involved in CRF-induced increase in intestinal epithelial permeability by inhibiting the activity of PKC, and there may be other signaling pathways involved.     

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.