Soil salinity is one of the most important environmental factors limiting plant growth and productivity in many regions in the world. Salt stress directly affects plant photosynthesis, which is an important physiologi...Soil salinity is one of the most important environmental factors limiting plant growth and productivity in many regions in the world. Salt stress directly affects plant photosynthesis, which is an important physiological process to limit plant growth and crop yield. But the effects of salt stress on the mechanism of the photosynthesis is still not clear. In this experiment, the salt tolerant plant Alhagi pseudalhagi was selected as the experiment material, and the salt sensitive plant Vigna radiata as the control, to explore the effects of salt stress on photosynthetic parameters of A. pseudalhagi. Plants were grown in a greenhouse,cultured with 1/2 Hoagland nutrient solution, treated by 0(control), 50, 100 or 200 s of mmol/L of NaCl solution for 12 d. Then,the chlorophyll contents, gas exchange parameters and chlorophyll a fluorescence in each treatment were measured. The results showed that under the salt stress simulated by 50 mmol/L NaCl, the net photosynthetic rate(Pn) and stomatal conductance(gs)of A. pseudalhagi were significantly increased compared with the control, while intercellular CO_2 concentration(Ci) was significantly decreased, Fv'/Fm', Fv/Fm and Fv/Fo were increased over time, but had no significant differences with the control ФPSⅡ,ETR and qP were significantly increased, and NPQ was significantly decreased. Under the salt stress simulated by 100 and 200mmol/L NaCl, Fv'/Fm', Fv/Fm, Fv/Fo, ФPSⅡ and qP of A. pseudalhagi were gradually decreased over time. In contrary, under the salt stress simulated by 50 and 100 mmol/L NaCl, the Pn, gs, Ci, Fv'/Fm', Fv/Fm, Fv/Fo, ФPSII, qP and ETR were all significantly decreased, while NPQ was significantly increased.展开更多
目的研究骆驼刺提取物(Alhagi pseudalhagi(M.B.)Desv.Extract,APE)对脂多糖诱导的大鼠小肠隐窝上皮细胞(Intestinal epithelial cell,IEC-6)损伤模型NLRP3炎症小体及相关细胞因子的影响。方法培养IEC-6细胞,将其分为空白组、模型组、AP...目的研究骆驼刺提取物(Alhagi pseudalhagi(M.B.)Desv.Extract,APE)对脂多糖诱导的大鼠小肠隐窝上皮细胞(Intestinal epithelial cell,IEC-6)损伤模型NLRP3炎症小体及相关细胞因子的影响。方法培养IEC-6细胞,将其分为空白组、模型组、APE低、中、高浓度组,用1.0μg/mL的脂多糖(Lipopolysaccharide,LPS)诱导建立细胞炎症损伤模型,APE(低、中、高浓度:15、25、35μg/mL)干预后采用CCK-8法检测细胞的存活率,通过ELISA试剂盒检测炎症因子IL-1β、IL-18、TNF-α的分泌水平。蛋白质印迹法(WB)检测核苷酸结合寡聚化结构域样受体蛋白3(Nucleotide-binding oligomerization domain-like receptor protein 3,NLRP3)炎症小体信号通路5个关键蛋白:NLRP3、半胱氨酸天冬氨酸蛋白酶1(Cystein-asparate protease-1,Caspase-l)、凋亡相关斑点样蛋白(Apoptosis-associated speck-like protein containing a CARD,ASC)及抗凋亡蛋白Bcl-2(Anti-apoptosis Protein Bcl-2)和Bcl-xl(Anti-apoptosis Protein Bcl-xl)表达。结果与空白组比较,模型组IEC-6细胞的存活率降低,NLRP3、Caspase-1、ASC蛋白表达水平升高,抗凋亡蛋白Bcl-2、Bcl-xl的表达水平降低,促炎因子IL-1β、IL-18和TNF-α的分泌水平升高,差异有统计学意义(P<0.05)。与模型组比较,APE低、中、高浓度组细胞存活率升高,35μg/mL APE组IEC-6细胞的NLRP3、Caspase-1、ASC蛋白相对表达水平降低,抗凋亡蛋白Bcl-2、Bcl-xl的表达水平升高,差异有统计学意义(P<0.05)。中、高浓度的APE能够抑制炎症因子分泌,25μg/mL APE对IL-1β、IL-18、TNF-α炎症因子分泌水平抑制率分别为31.60%、31.19%和31.09%(P<0.05)。结论骆驼刺提取物通过提高抗凋亡蛋白Bcl-2、Bcl-xl的表达水平,下调NLRP3炎症小体组成成分以及促炎因子IL-1β、IL-18和TNF-α分泌,从而抑制NLRP3炎症小体组装和激活,实现缓解LPS对IEC-6细胞的损伤。展开更多
基金Supported by China Agricultural University-Xinjiang Agricultural University Scientific Research Cooperation Fund Projects:Cloning and the Functional Analysis of Main Salinity and Water Stress Resistant Gene in Alhagi pseudoalhagiXinjiang Anjudan Biotechnology Co.,Ltd.(Anjudan Green Life 2016-001)
文摘Soil salinity is one of the most important environmental factors limiting plant growth and productivity in many regions in the world. Salt stress directly affects plant photosynthesis, which is an important physiological process to limit plant growth and crop yield. But the effects of salt stress on the mechanism of the photosynthesis is still not clear. In this experiment, the salt tolerant plant Alhagi pseudalhagi was selected as the experiment material, and the salt sensitive plant Vigna radiata as the control, to explore the effects of salt stress on photosynthetic parameters of A. pseudalhagi. Plants were grown in a greenhouse,cultured with 1/2 Hoagland nutrient solution, treated by 0(control), 50, 100 or 200 s of mmol/L of NaCl solution for 12 d. Then,the chlorophyll contents, gas exchange parameters and chlorophyll a fluorescence in each treatment were measured. The results showed that under the salt stress simulated by 50 mmol/L NaCl, the net photosynthetic rate(Pn) and stomatal conductance(gs)of A. pseudalhagi were significantly increased compared with the control, while intercellular CO_2 concentration(Ci) was significantly decreased, Fv'/Fm', Fv/Fm and Fv/Fo were increased over time, but had no significant differences with the control ФPSⅡ,ETR and qP were significantly increased, and NPQ was significantly decreased. Under the salt stress simulated by 100 and 200mmol/L NaCl, Fv'/Fm', Fv/Fm, Fv/Fo, ФPSⅡ and qP of A. pseudalhagi were gradually decreased over time. In contrary, under the salt stress simulated by 50 and 100 mmol/L NaCl, the Pn, gs, Ci, Fv'/Fm', Fv/Fm, Fv/Fo, ФPSII, qP and ETR were all significantly decreased, while NPQ was significantly increased.
文摘目的研究骆驼刺提取物(Alhagi pseudalhagi(M.B.)Desv.Extract,APE)对脂多糖诱导的大鼠小肠隐窝上皮细胞(Intestinal epithelial cell,IEC-6)损伤模型NLRP3炎症小体及相关细胞因子的影响。方法培养IEC-6细胞,将其分为空白组、模型组、APE低、中、高浓度组,用1.0μg/mL的脂多糖(Lipopolysaccharide,LPS)诱导建立细胞炎症损伤模型,APE(低、中、高浓度:15、25、35μg/mL)干预后采用CCK-8法检测细胞的存活率,通过ELISA试剂盒检测炎症因子IL-1β、IL-18、TNF-α的分泌水平。蛋白质印迹法(WB)检测核苷酸结合寡聚化结构域样受体蛋白3(Nucleotide-binding oligomerization domain-like receptor protein 3,NLRP3)炎症小体信号通路5个关键蛋白:NLRP3、半胱氨酸天冬氨酸蛋白酶1(Cystein-asparate protease-1,Caspase-l)、凋亡相关斑点样蛋白(Apoptosis-associated speck-like protein containing a CARD,ASC)及抗凋亡蛋白Bcl-2(Anti-apoptosis Protein Bcl-2)和Bcl-xl(Anti-apoptosis Protein Bcl-xl)表达。结果与空白组比较,模型组IEC-6细胞的存活率降低,NLRP3、Caspase-1、ASC蛋白表达水平升高,抗凋亡蛋白Bcl-2、Bcl-xl的表达水平降低,促炎因子IL-1β、IL-18和TNF-α的分泌水平升高,差异有统计学意义(P<0.05)。与模型组比较,APE低、中、高浓度组细胞存活率升高,35μg/mL APE组IEC-6细胞的NLRP3、Caspase-1、ASC蛋白相对表达水平降低,抗凋亡蛋白Bcl-2、Bcl-xl的表达水平升高,差异有统计学意义(P<0.05)。中、高浓度的APE能够抑制炎症因子分泌,25μg/mL APE对IL-1β、IL-18、TNF-α炎症因子分泌水平抑制率分别为31.60%、31.19%和31.09%(P<0.05)。结论骆驼刺提取物通过提高抗凋亡蛋白Bcl-2、Bcl-xl的表达水平,下调NLRP3炎症小体组成成分以及促炎因子IL-1β、IL-18和TNF-α分泌,从而抑制NLRP3炎症小体组装和激活,实现缓解LPS对IEC-6细胞的损伤。
