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1.
培养大鼠胰岛素瘤细胞(INS-1),以四氧嘧啶损伤细胞,培养液中加入不同浓度的AMP-1,MTT法测定细胞存活率,PI荧光染色观测凋亡细胞密度,流式细胞术法检测细胞凋亡率,Western blot法检测蛋白bcl-2和bax的表达。结果表明,AMP-1浓度在50 mg·L~(-1)至500 mg·L~(-1)之间,均可提高受四氧嘧啶损伤的INS-1细胞的存活率,其中浓度为400 mg·L~(-1)时存活率最高;凋亡细胞密度,随AMP-1浓度的增大而降低;AXN+AMP-1组INS-1细胞凋亡率均低于四氧嘧啶组;Western blot法检测显示bcl-2蛋白表达量升高,bax蛋白表达量降低。AMP-1对四氧嘧啶诱导大鼠INS-1细胞凋亡具有明显的拮抗作用,其作用机制可能是通过对线粒体途径中bcl-2和bax蛋白表达的调控而抑制了细胞的凋亡。 相似文献
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以诱导表达方式制备的新型昆虫源抗菌肽(AMP-17)为研究对象,采用平板扩散法和倍比稀释法测定其对多株食品腐败微生物的抑菌活性,将200 μg·mL-1山梨酸钾、50 μg·mL-1和100 μg·mL-1的抗菌肽AMP-17喷淋后的草莓4℃冰箱中贮藏,研究草莓贮藏期间品质指标和理化指标,以期为草莓的防腐保鲜提供参考依据.结果 表明:抗菌肽AMP-17对黑曲霉菌、黄曲霉菌等真菌的MIC值(最低抑菌浓度)为50 μg·mL-1,MBC值(最低杀菌浓度)为100 μg·mL-1,对细菌抑制作用不明显.在4℃贮藏条件下,50 μg·mL-1和100 μg·mL-1的抗菌肽AMP-17可显著降低由于真菌污染导致的草莓腐烂,延缓草莓维生素C含量、可滴定酸含量的降低,同时能够抑制草莓总糖含量的升高,在色泽、外观以及气味等感官指标评分显著(P＜0.05)高于200 μg·mL-1山梨酸钾处理组和空白组. 相似文献
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以酿酒酵母(Saccharomyces cerevisiae)细胞经紫外辐射和过氧化氢溶液处理后的存活率为指标,考察苇蘑(Hygrophoropsis sp.)子实体提取物的抗辐射和抗氧化能力。结果表明:在紫外辐射120 s的条件下,苇蘑子实体乙醇提取物添加量为4%时,酿酒酵母细胞的存活率可达54.1%,添加4%苇蘑子实体水提取物后,酿酒酵母细胞存活率为43.9%;对照组(不添加苇蘑子实体提取物)的存活率为4.6%;在140 mmol/L过氧化氢溶液处理下,苇蘑子实体水提取物浓度在0.5%~2.5%时,酿酒酵母细胞存活率从11.4%增加到47.4%;而苇蘑子实体水提取物浓度超过2.5%时,细胞存活率反而降低。在相同的过氧化氢处理时间下,添加1%苇蘑子实体提取物后,酿酒酵母细胞的存活率均显著高于对照组。 相似文献
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以拟南芥为试验材料,向培养基中添加不同浓度的NaCl模拟盐胁迫、不同比例的PEG-6000模拟水势胁迫,观察并记录种子萌发率、幼苗根长、幼苗存活率等生理指标,检测幼苗中丙二醛(MDA)含量,研究了盐胁迫和水势胁迫对拟南芥种子萌发及幼苗生长的影响,以期明确盐胁迫程度和水势影响拟南芥植株生理状态的规律,为水势和盐胁迫处理提供依据。结果表明:当NaCl浓度等于及高于150 mmol·L-1时,幼苗平均根长为5.2 mm,显著低于对照组(24.8 mm);幼苗平均存活率为52.1%,显著低于对照组(98.1%)。当水势等于及低于-0.7 MPa时,幼苗无侧根生长,平均存活率为89.2%,显著低于对照组(98.7%),由此可知,NaCl浓度150 mmol·L-1和水势-0.7 MPa是拟南芥胁迫处理的阈值,当NaCl浓度高于150 mmol·L-1,或水势低于-0.7 MPa时,拟南芥种子萌发及幼苗生长被明显抑制。 相似文献
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以山杏叶水提物为试材,以脂多糖(Lipopolysaccharides,LPS)诱导的小鼠单核巨噬细胞RAW264.7为炎症模型,通过CCK8法、Griess试剂法、酶联免疫吸附法(ELISA)和RT-PCR法检测山杏叶水提物处理后细胞存活率的变化和炎症相关因子的分泌表达情况,研究了山杏叶水提物对LPS诱导的RAW264.7细胞炎症模型的抗炎作用。结果表明:山杏叶水提物在0.5~2.0 mg·mL~(-1)浓度范围内与1μg·mL~(-1) LPS共培养时,对RAW264.7细胞的增殖无明显影响;LPS处理可显著提升细胞NO和IL-6的分泌量,但山杏叶水提物能够有效抑制NO的释放和IL-6的产生;而在基因水平,水提物的处理可显著抑制炎症因子IL~(-1)2p40、COX-2、IL-6和TNF-α的mRNA表达,且具有浓度依赖性。 相似文献
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通过转录组测序探究不同浓度(0、1%、2%和4%)外源葡萄糖对‘红地球’葡萄试管苗糖代谢和光合作用的影响。结果表明,2%葡萄糖处理下试管苗生长最好,其次是4%和1%处理,不添加葡萄糖的生长最弱。4个浓度下测序共获得了21.53 Gb Clean Data,Q30碱基百分比在89.49%以上。各样品与参考基因组的比对效率在68.31%～73.71%之间。单核苷酸多态性(Single Nucleotide Polymorphisms,SNP)的转换效率为64.73%～66.76%,颠换在33.24%～35.27%之间,且发生A?G和C?T突变类型最多。可变剪切类型中主要发生的是第一和最后一个外显子剪切事件。通过设定筛选差异基因的阈值,共获得了3 272个差异基因,包括下调基因2 826个和上调基因446个。在COG注释分类中,1%、2%和4%葡萄糖处理与0对照比对,分别注释到了1 449、846和597个差异基因,且大多数注释到除一般功能预测外,都是与转录相关的基因。对叶片碳代谢相关酶进行测定发现,蔗糖合成酶(SS)和葡萄糖6磷酸脱氢酶(G6PDH)活性随着葡萄糖处理浓度增加均表现出先减小后增加的趋势,且SS在4%葡萄糖处理中活性最高,而G6PDH在0对照中最高,中性转化酶(NI)和蔗糖磷酸合成酶(SPS)具有相同的变化趋势,两者的活性峰均出现在2%葡萄糖处理。经qRT-PCR验证,14个基因中有12个基因的表达趋势与转录测序结果一致,表明不同浓度葡萄糖通过影响叶片中碳代谢相关基因的表达来提高‘红地球’葡萄试管苗的生长。 相似文献
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JIA Jin-song XU Shi-rong JIA Cun-rong MA Jie MA Wei-dong YAO Yin-rong WANG Yi SHI Cui-ying 《园艺学报》2004,20(2):228-233
目的:探讨脂质体转染细胞周期素B1(cyclinB1)反义脱氧寡核苷酸(ASON)对HL60细胞增殖调控的作用。方法:用针对cyclinB1mRNA5’端编码区起始密码子(ATG/AUG)的ASON,通过脂质体导入HL60细胞共培养后,用流式细胞术(FCM)和RT-PCR分别检测cyclinB1蛋白和mRNA的表达水平,电镜和原位细胞凋亡检测法(POD)、FCM及DNA凝胶电泳法检测细胞凋亡。结果:CyclinB1ASON组与SON及空白对照组相比,ASON能特异地抑制cyclinB1蛋白及mRNA水平的表达,当ASON的浓度达到一定程度时,HL60细胞的增殖及集落形成率均明显受抑制,出现细胞凋亡,并且此作用随ASON浓度的升高而增强。结论:CyclinB1的特异ASON能封闭其蛋白及mRNA的表达水平,可剂量依赖性地抑制白血病细胞增殖,诱导细胞凋亡。 相似文献
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不同浓度营养液对番茄无土栽培幼苗生长的影响 总被引：1，自引：0，他引：1
为研究不同浓度营养液对番茄幼苗生长的影响,以ND1558番茄为供试材料,以Hoagland-Arnon配方工作液为标准浓度(1.0C),设置6个营养液浓度(0.5C、2.5C、5.0C、7.5C、10.0C、12.5C)对番茄幼苗进行处理。结果表明:5.0C以下浓度对番茄幼苗抑制作用不明显;10.0C以上浓度处理的番茄幼苗抑制作用明显,但是定植后难以恢复生长;对幼苗株型调控较佳的组合为先用7.5C的营养液处理、再恢复正常浓度,该处理对番茄后期长势及产量有一定的促进作用。 相似文献
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应用RT-PCR技术,研究了国产巴西蘑菇多糖(ABPS)对几种细胞刺激因子(CSF)基因表达的影响。研究结果表明,人粒．单祖细胞克隆刺激因子(GM-CSF)和白细胞介素2(IL-2)扩增片段分别在255bp和500bp处出现明显的条带,而小鼠骨髓基质细胞表达的GM-CSF则在369bp处出现一条带。揭示国产巴西蘑菇多糖有诱导人脐血单个核细胞和小鼠骨髓基质细胞表达GM—CSF和IL-2的作用,其浓度范围为1～6μg／mL,最佳浓度为1μg／mL,从而证实了国产巴西蘑菇多糖促进粒一单祖细胞生成和调节动物机体免疫功能的分子机理。 相似文献
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蜜环菌菌索多糖对小鼠血糖及急性毒性作用研究 总被引：12，自引：3，他引：12
本文研究了蜜环菌菌索多糖AMP - 1和AMP - 2组分对小鼠血糖及其急性毒性作用。结果表明 :AMP - 1能使正常小鼠的糖耐量增强 ;AMP - 1、AMP - 2均能抑制四氧啶糖尿病小鼠血糖升高 ;AMP - 2能显著降低四氧啶糖尿病小鼠的血糖 ;AMP - 1、AMP - 2 (灌胃剂量为 10g/kg/d)对供试小鼠无毒性作用 ,内脏器官均正常无损 相似文献
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AIM: To differentiate bone marrow mesenchymal stem cells (BMSCs) into functional insulin-producing cells to produce sufficient pancreatic islet cells for transplantation. METHODS: Recombinant adenovirus vectors carrying PDX1 and NKX6.1 genes were constructed and the bone marrow mesenchymal stem cells were infected by the recombinant adenovirus combined with several cytokines for differentiation. The expressions of PDX1, NKX6.1 and insulin and C-peptide in the differentiated bone marrow mesenchymal stem cells were detected by RT-PCR and Western blotting. After the differentiated bone marrow mesenchymal stem cells were transplanted into subrenal capsule of diabetic mice, cell morphology of the grafts as well as their secretion of insulin and C-peptide were detected. Besides, regulating capacities of grafts on the blood glucose level of the diabetic mice were also detected. RESULTS: BMSCs induced by recombinant adenovirus (pAdxsi-CMV-PDX1/CMV-NKX6.1) and several cytokines showed positive dithizone staining and the expressions of β-cell related molecule such as insulin and glucose transporter 2 were detected by RT-PCR, which showed a sustaining and stable expression. The similar results were showed by Western blotting, immunohistochemical staining and indirect immunofluorescence. The insulin secretions in the cells stimulated with glucose at concentrations of 5.5 and 25 mmol/L in the experimental group were (1 240.4±109.3) mU/L and (3 539.8±245.1) mU/L, respectively, and were significantly higher than those in control group. Moreover, transplantation of the cells to STZ mice in treatment group made serum glucose recover to normal level. CONCLUSION: PDX1 and NKX6.1 gene-modified bone marrow mesenchymal stem cells differentiate into insulin-producing cells in vitro. When these cells transplanted into STZ induced diabetic mice, their serum glucose could return to the normal level and they could live well. Thus this is a promising method for diabetes treatment. 相似文献
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ZHANG Li-na HOU Le-le LIU Zu-lin LI Ping-gan HUANG Si-qi MENG Zhe OU Hui JIANG Zhuan-nan LIANG Li-yang 《园艺学报》2019,35(12):2150-2155
AIM: To establish rat insulinoma INS-1 cell iron overload model, and to study the effect of iron overload on the viability, insulin secretion, mitochondrial defect and oxidative stress change in the INS-1 cells. METHODS:INS-1 cells were cultured with ferric ammonium citrate (FAC) at different concentrations (0, 5, 10, 20, 40, 80, 160 and 320 μmol/L). Labile iron pool (LIP) were calculated by detecting calcein-AM fluorescence in 24 h, 48 h and 72 h. The cell viability was measured by CCK8 assay. Iron overload model was established by screening for the best combination to ensure both high LIP level and cell viability. Reactive oxygen species (ROS) level was further analyzed by flow cytometry after fluorescent probe staining. The function of insulin secretion was measured by ELISA. The mitochondrial membrane potential was detected by JC-1 kit, and the mitochondrial changes were observed by transmission electron microscopy. RESULTS: Intracellular LIP levels were significantly increased in FAC groups in a concentration-dependent manner (P<0.05). The viability of INS-1 cells was suppressed with increasing FAC concentration or culture time (P<0.05). The highest LIP level and cell viability over 50% were observed with the condition of exposure to FAC for 48 h, indicating that INS-1 cell iron overload model was established. With the increase in the FAC concentrations, the insulin secretion was also increased and then decreased, and that in 160 and 320 mol/L groups showed statistical difference compared with control group (P<0.05). The ROS level was significantly increased by FAC exposure as compared with control group (P<0.05). Mitochondrial membrane potential was decreased with the increase in the iron concentration (P<0.05). After iron overload, the mitochondria of INS-1 cells were swollen, the internal cristae were expanded, and the normal structure was lost. With the increase in the FAC concentration, the mitochondrial structure was destroyed more obviously. CONCLUSION: Co-culture of INS-1 cells with FAC for 48 h successfully establish the iron overload model. Iron overload significantly damages mitochondrial structure and increases intracellular ROS level. The viability of pancreatic β cells is sensitive to iron, even lower doses of iron can damage β cells. The insulin secretion is reduced when the number of β cells is decreased to a certain extent. 相似文献
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WU Hui-ling 《园艺学报》2014,30(12):2213-2218
AIM: To explore the protective effects of berberine （Ber） on islet beta cells and related possible mechanisms. METHODS: The injury of INS-1 cells was induced by treatment with alloxan (Axn). Berverine was then given at serial concentrations. The cells were divided into control group (Con), injury group (Axn), low-dose berberine group (LBer), medium-dose berberine group (MBer) and high-dose berberine group (HBer). Flow cytometry was employed to detect the apoptosis. The activation of PTEN/PI3K/Akt and HNF-1α/PDX-1 pathways and the protein level of cleaved caspase-3 were evaluated by Western blotting. The insulin releases under normal or high-glucose stimulation were measured by ELISA. RESULTS: Compared with Con group, the apoptotic rate increased significantly in Axn group. Berberine treatment reduced the apoptotic rate in LBer group, MBer group and HBer group in a concentration-dependent manner. Compared with Con group, the protein levels of PTEN and cleaved caspase-3 increased, while PI3K and phosphorylation of Akt decreased significantly in Axn group. However, this effect was reversed by berberine in a concentration-dependent manner. Compared with Con group, the activation of HNF-1α/PDX-1 signaling pathway was inhibited in Axn group but recovered by berberine administration. The abilities of releasing insulin under normal or high-glucose stimulation were impaired in Axn group but recovered by berberine treatment in LBer group, MBer group and HBer group in a concentration-dependent manner.CONCLUSION: Berberine shows protective effects against alloxan-induced damage in beta cells by inhibiting apoptosis and recovering insulin secretion, thus attenuating the activation of PTEN/PI3K/Akt and HNF-1α/PDX-1 signaling pathways. 相似文献
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AIM:To investigate the mechanism of palmitic acid inhibiting the proliferation of rat pancreatic β cell line INS-1. METHODS:INS-1 cells were treated with palmitic acid in time or concentration gradient experiments. The expression of Frizzled-2 (Fzd-2) and receptor tyrosine kinase-like orphan receptor 2 (Ror-2) at mRNA and protein levels was detected by RT-qPCR and Western blot. Interaction of Wnt5a with Fzd-2 or Ror-2 in INS-1 cells treated with palmitic acid was determined by the method of direct co-immunoprecipitation. The proliferation rates of the cells were measured by EdU assay after transfected with siRNA-Fzd-2 or siRNA-Ror-2. RESULTS:Fzd-2 and Ror-2 were up-regulated in INS-1 cells stimulated with palmitic acid at both mRNA and protein levels. Palmitic acid promoted Wnt5a to recruit receptors Fzd-2 and Ror-2. Silencing the expression of Fzd-2 or Ror-2 weakened the inhibitory effect of palmitic acid on INS-1 cell proliferation (P<0.05). CONCLUSION:Palmitic acid inhibits the proliferation of INS-1 cells via up-regulating the expression of Fzd-2 and Ror-2, as well as promoting Wnt5a to recruit these receptors. 相似文献
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LU Chun-li HU Dong-hui CHU Jia-cheng ZHOU Xia-li CHEN Wei-wei SUN Ming-jin 《园艺学报》2018,34(11):1963-1967
AIM: To investigate the effect of angiotensin (1-7)[Ang (1-7)] on palmitic acid (PA)-induced injury of Min6 cells and the potential protective mechanisms of autophagy. METHODS: Cultured Min6 cells were divided into 7 groups:control group, PA group, PA+Ang(1-7) group, PA+Ang(1-7)+A779 group, PA+Ang(1-7)+rapamycin group, Ang(1-7) group and A779 group. The function of Min6 cells was detected by glucose-stimulated insulin release test. Intracellular reactive oxygen species (ROS) production was measured by ROS assay kit. Apoptosis was analyzed by flow cytometry with Annexin V/PI staining. Autophagy-related proteins were determined by Western blot. RESULTS: Compared with control group, the secretion of insulin from Min6 cells in PA group was significantly decreased (P<0.05), and the apoptotic rate was increased (P<0.05). The ratio of LC3-Ⅱ/LC3-I was significantly increased (P<0.05). Compared with PA group, the insulin secretion in PA+Ang(1-7) group was increased (P<0.05). The intracellular ROS level and the A779 and LC3-Ⅱ/LC3-I were significantly decreased (P<0.05). This protective effect of Ang(1-7) was partially blocked by A779 and rapamycin. CONCLUSION: Ang(1-7) attenuates PA-induced Min6 cell injury, and its protective mechanism may be related to inhibiting the activity of autophagy. 相似文献
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AIM: To investigate the effect of high glucose toxicity on JNK pathway and cell function of INS-1 cells.METHODS: Cultured INS-1 cells with or without IGF-1 exposure, were treated with glucose at 3 concentrations (5.6 mmol/L, 11.2 mmol/L and 33.3mmol/L), respectively. MTT was used to measure the cell viability. Apoptosis was determined by immuno-fluorescence and flow-cytometry analysis. The serine 270 phosphorylation of IRS and phosphorylation of JNK in INS-1 cells were detected in the presence or absence of SP600125 treatment.RESULTS: The cell viability decreased and apoptosis increased with elevated glucose concentrations. The percentage of apoptosis cells was 11.3% in 5.6 G group, 12.7% in 11.2 G group and 28.2% in 33.3 G group. There was remarkable increase in apoptosis in 33.3 G group with a 2.49-fold increase to the cells in the basal 5.6 mmol/L glucose. High glucose activated the serine 270 phosphorylation of IRS correlates with JNK phosphorylation in INS-1 cells. Using Western blotting analysis, the levels of JNK phosphorylation were 3.33 fold increased and serine 270 phosphorylation of IRS was 1.17 fold increased in 33.3 G group compared to 11.2 G group (P<0.01). IGF-1 treatment inhibited phosphorylation of JNK and IRS. SP600125 treatment completely blocked JNK phosphorylation in 11.2 G group and reduced JNK phosphorylation by 90% in 33.3 G group. In addition, SP600125 treatment partly reduced serine 270 phosphorylation of IRS by 88.3% in 11.2 G group and 80% in 33.3 G group, the viability of INS-1 cells increased and the apoptosis decreased.CONCLUSION: The toxicity of chronic high glucose, which inhibits the cells viability and induces the cell apoptosis, might be related to suppress IRS signal by activating the JNK pathway. Blocking the JNK pathway might relieve the effect of glucose toxicity to the β cell function by improving the IRS signal pathway. 相似文献
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AIM: To induce mouse induced pluripotent stem cells (iPSCs) to differentiate into insulin-producing cells (IPCs) by a new 3-step method, and to detect the efficiency and maturity for the treatment of diabetic mice. METHODS: We constructed iPSCs from mouse embryonic fibroblasts of male C57/C mouse by piggyBac transposon, then induced the iPSCs into IPCs by a 3-step method. The cell morphological change was traced by microscopy during the process of differentiation. The expression of mRNA and protein associated with islet β cell development was determined by real-time PCR and immunofluorescence staining. Flow cytometry was used to analysis the efficiency of differentiation. Insulin and C-peptide secretions of IPCs in response to glucose at high (25 mmol/L) or low (5.5 mmol/L) level were measured by ELISA. The IPCs were transplanted into the capsul of left kidney in the male C57/C diabetic mouse model. Blood glucose was continuously monitored for 28 day, serum insulin was tested by ELISA in different stages. The glucose tolerance test was performed on the 28th day, and the left kidney was excised. RESULTS: IPCs were obtained from mouse iPSCs by the 3-step method. The cells expressed the marker genes (Pdx1, Ngn3, Pax6 and Ins2) and proteins (Pdx1, Nkx6.1 and insulin) of β cells. The glucose stimulation induced the secretion of insulin and C-peptide. The efficiency of differentiation was 28% detected by flow cytometry. After transplantation of IPCs to the diabetic mice, the blood glucose was decreased to normal level on the 3rd day,and serum insulin level and the ability of regulating glucose were improved. IPCs were still alive after 28 d of transplantation by pathological observation. CONCLUSION: iPSCs is efficiently induced into IPCs by a 3-step method , and the induction time is shortened significantly. The hyperglycemia of diabetes mice is reversed after transplanting IPCs to same sex inbred strain mice. 相似文献
19.
AIM：To establish the animal model of insulinoma and to analyze the properties of insulinoma for further study. METHODS：The hormone-releasing ability of rat insulinoma cell line INS-1 was detected in vitro. INS-1 cells were transplanted into the left kidney capsule of nude mice. The islets of the animals were destroyed by intraperitoneal injection of streptozocin (STZ) 3 d before transplantation or 2 weeks after transplantation. The venous blood was sampled, and the level of blood glucose less than 2.8 mmol/L was defined as successful establishment of insulinoma model. Different irritants were given to the model animals, and the changes of blood glucose and insulin content in serum were observed. The pancreatic tissues and the renal tissues in the injecting sites were taken from all mice for detecting insulin and glucagon by immunohistochemical staining. RESULTS：Insulinoma cells expressed insulin and glucagon at the same time. The blood glucose was less than 2.8 mmol/L 3 to 4 weeks after inoculation of INS-1 cells. Apparent tumor formed in the left kidneys where INS-1 cells were transplanted and the tumor diameters were more than 1 cm. The level of blood glucose transiently increased to higher than the normal level in the mice with tumor cell transplantation after intraperitoneal injection of STZ, and then decreased gradually and returned to less than 2.8 mmol/L after 2 weeks. The level of blood glucose in the normal nude mice after administration of STZ increased significantly. After transplantation of INS-1 cells, the level of blood glucose decreased gradually, and returned to less than 2.8 mmol/L after 4 weeks. After stimulated with high glucose, the blood glucose levels in the mice with 3 methods to establish the insulinoma models showed lower glucose peaks than that in the normal control mice. After stimulated with high glucose plus arginine or acetylcholine in the normal animals, the blood glucose peak was lower than that in the normal animals only stimulated with high glucose, and rapidly recovered to the normal level. However, the levels of blood glucose in the mice with 3 methods to establish the insulinoma models under the same stimulations were significantly higher than that in the mice only stimulated with high glucose. After stimulated with high glucose plus norepinephrine, the blood glucose peak time in the normal animals delayed, and the blood glucose level declined slowly. After stimulated with high glucose plus norepinephrine, the levels of blood glucose in the mice with 3 methods to establish the insulinoma models increased as compared with that in the mice only stimulated with high glucose. Compared with normal control group, serum insulin in insulinoma mice increased significantly. CONCLUSION：The insulinoma animal model is successfully established by transplantation of INS-1 cells into the renal capsule of nude mice. The insulinoma cells express both insulin and glucagon, and are not easily damaged by STZ. 相似文献