Plant phenolic acids are good sources of antioxidants and sinapic acid(SA)is one of them that can be applied in protein-based food system.However,little research is available regarding interactions between almond prot...Plant phenolic acids are good sources of antioxidants and sinapic acid(SA)is one of them that can be applied in protein-based food system.However,little research is available regarding interactions between almond protein(AP)and SA.In this study,structure-affinity interaction between SA and AP,structure and antioxidant activity of proteins were investigated.Different mathematical models showed that Ka of binding SA and AP were 3.27×10^4 L/mol and 3.08×10^4 L/mol.CD(Circular dichroism)spectroscopy and FT-IR(Fourier transform infrared)spectroscopy showed that the amount of random coil andα-helix decreased whileβ-sheet increased in AP-SA complex.In combination,the interaction model of AP-SA complex was static quenching and attributed to hydrophobic interaction.Further,AP-SA complex exerted better DPPH radical scavenging ability(36.97±0.78%),ABTS+radical scavenging ability(47.26±0.45%),and higher ORAC value(2.41±0.23 M trolox/g)compared to AP.In the further,SA can be applied in protein matrix to improve film stability,gel strength and restraining fat oxidation degradation.展开更多
Cerebral ischemia and the aftermath of reperfusion form a hypoxic/hyperoxic sequence of events that can trigger DNA damage in neurons of central nervous system. Neuronal apoptosis will happen without immediate DNA rep...Cerebral ischemia and the aftermath of reperfusion form a hypoxic/hyperoxic sequence of events that can trigger DNA damage in neurons of central nervous system. Neuronal apoptosis will happen without immediate DNA repair. APE/Ref-1 is a multifunctional protein involoved in DNA base excision repair pathway and in redox reguiation of DNA-binding activity of AP-1 family members, which may play an important role in protection of postischemic neuronal damage.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 the National Key Research and Development Program of China (2016YFD0401401)The Technological innovation project of Hubei Province (2017ABA142)+2 种基金The Science and Technology Plan Project of Tibet Autonomous Region (XZ201901NA04)The Science and Technology Plan Project of Hunan Science (2017NK2212)The Agricultural Science and Technology Innovation Project of Chinese Academy of Agricultural Sciences (CAAS-ASTIP-2016-OCRI)
文摘Plant phenolic acids are good sources of antioxidants and sinapic acid(SA)is one of them that can be applied in protein-based food system.However,little research is available regarding interactions between almond protein(AP)and SA.In this study,structure-affinity interaction between SA and AP,structure and antioxidant activity of proteins were investigated.Different mathematical models showed that Ka of binding SA and AP were 3.27×10^4 L/mol and 3.08×10^4 L/mol.CD(Circular dichroism)spectroscopy and FT-IR(Fourier transform infrared)spectroscopy showed that the amount of random coil andα-helix decreased whileβ-sheet increased in AP-SA complex.In combination,the interaction model of AP-SA complex was static quenching and attributed to hydrophobic interaction.Further,AP-SA complex exerted better DPPH radical scavenging ability(36.97±0.78%),ABTS+radical scavenging ability(47.26±0.45%),and higher ORAC value(2.41±0.23 M trolox/g)compared to AP.In the further,SA can be applied in protein matrix to improve film stability,gel strength and restraining fat oxidation degradation.
文摘Cerebral ischemia and the aftermath of reperfusion form a hypoxic/hyperoxic sequence of events that can trigger DNA damage in neurons of central nervous system. Neuronal apoptosis will happen without immediate DNA repair. APE/Ref-1 is a multifunctional protein involoved in DNA base excision repair pathway and in redox reguiation of DNA-binding activity of AP-1 family members, which may play an important role in protection of postischemic neuronal damage.
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。
