Ferroelectric HfO_(2)has attracted much attention owing to its superior ferroelectricity at an ultra-thin thickness and good compatibility with Si-based complementary metal-oxide-semiconductor(CMOS)technology.However,...Ferroelectric HfO_(2)has attracted much attention owing to its superior ferroelectricity at an ultra-thin thickness and good compatibility with Si-based complementary metal-oxide-semiconductor(CMOS)technology.However,the crystallization of polar orthorhombic phase(o-phase)HfO_(2)is less competitive,which greatly limits the ferroelectricity of the as-obtained ferroelectric HfO_(2)thin films.Fortunately,the crystallization of o-phase HfO_(2)can be thermodynamically modulated via interfacial stress engineering.In this paper,the growth of improved ferroelectric Al doped HfO_(2)(HfO_(2):Al)thin films on(111)-oriented Si substrate has been reported.Structural analysis has suggested that nonpolar monoclinic HfO_(2):Al grown on(111)-oriented Si substrate suffered from a strong compressive strain,which promoted the crystallization of(111)-oriented o-phase HfO_(2)in the as-grown HfO_(2):Al thin films.In addition,the in-plane lattice of(111)-oriented Si substrate matches well with that of(111)-oriented o-phase HfO_(2),which further thermally stabilizes the o-phase HfO_(2).Accordingly,an improved ferroelectricity with a remnant polarization(2P_(r))of 26.7C/cm^(2) has been obtained.The results shown in this work provide a simple way toward the preparation of improved ferroelectric HfO_(2)thin films.展开更多
Glycidol is a common lipid-derived foodborne toxicant mainly presents in refined oils and related foodstuffs.Vascular endothelial cells may be potential targets of the deleterious effects associated with glycidol expo...Glycidol is a common lipid-derived foodborne toxicant mainly presents in refined oils and related foodstuffs.Vascular endothelial cells may be potential targets of the deleterious effects associated with glycidol exposure.In human umbilical vein endothelial cells(HUVECs),we found that glycidol treatment promoted endothelialto-mesenchymal transition(EndMT)at a lower concentration(0.5 mmol/L),while induced apoptosis and inflammation at a higher concentration(1 mmol/L).These harmful effects were achieved by the activation of NF-κB/MAPK signaling pathway and were mediated by reactive oxygen species(ROS).In addition,the protective potential of 6-C-(E-2-fluorostyryl)naringenin(6-CEFN)against glycidol was evaluated and compared with naringenin.HUVECs pre-treated with 6-CEFN,but not naringenin,displayed resistance to endothelial dysfunction caused by glycidol.展开更多
【目的】探讨猪链球菌2型超氧化物歧化酶A(SodA)、硫氧还蛋白A(TrxA)和TrxC基因在调控氧化应激和参与致病过程中的生物学功能。【方法】比较猪链球菌2型3个突变菌株ΔSodA、ΔTrxA和ΔTrxC对抗应激能力和毒力的调控作用。通过应激存活试...【目的】探讨猪链球菌2型超氧化物歧化酶A(SodA)、硫氧还蛋白A(TrxA)和TrxC基因在调控氧化应激和参与致病过程中的生物学功能。【方法】比较猪链球菌2型3个突变菌株ΔSodA、ΔTrxA和ΔTrxC对抗应激能力和毒力的调控作用。通过应激存活试验,分别检测SodA、TrxA和TrxC基因对不同氧化应激处理(0.04%过氧化氢(H 2O 2)、10 mol/L百草枯(PQ))的抗氧化应激能力以及不同温度(4、43℃)的抗温度应激能力;将不同基因缺失株与猪肠道上皮细胞(IPEC-J2)、小鼠巨噬细胞(RAW264.7)共培养,探究3个基因对细胞黏附和抗吞噬功能的影响;通过小鼠攻毒试验,测定各组织载菌量和血清抗氧化酶与肝功能指标,探明SodA、TrxA和TrxC基因在抗氧化应激以及致病过程中的作用。【结果】抗应激试验结果显示,在不同氧化应激和不同温度应激条件下,ΔSodA和ΔTrxC菌株存活能力均极显著低于野生菌株(P<0.01),ΔTrxA菌株在43℃高温刺激下存活能力极显著低于野生菌株(P<0.01)。细胞黏附试验结果显示,SodA和TrxA基因缺失导致细菌黏附能力降低55%~65%,极显著低于野生菌株(P<0.01)。细胞抗吞噬试验结果显示,ΔSodA、ΔTrxC和ΔTrxA菌株在吞噬细胞中的存活率极显著或显著低于野生菌株(P<0.01;P<0.05)。动物攻毒试验结果显示,与野生菌株相比,ΔSodA、ΔTrxA和ΔTrxC菌株毒力均极显著下降(P<0.01);ΔSodA、ΔTrxA和ΔTrxC菌株组小鼠死亡率分别为10%、50%和20%,组织载菌量分别为3.6 lg CFU/g~4.4 lg CFU/g、4.2 lg CFU/g~5.1 lg CFU/g和3.1 lg CFU/g~4.1 lg CFU/g;野生菌株组小鼠死亡率为90%,组织载菌量为6.4 lg CFU/g~7.8 lg CFU/g。小鼠感染ΔSodA、ΔTrxC和ΔTrxA菌株后血清中超氧化物歧化酶(SOD)、过氧化氢酶(CAT)活性和总抗氧化能力(T-AOC)极显著高于野生菌株(P<0.01),天门冬氨酸转氨酶(AST)、谷丙转氨酶(ALT)和碱性磷酸酶(ALP)活性极显著低于野生菌株(P<0.01)。【结论】猪链球菌2型SodA和TrxC基因通过中和菌体内超氧根离子和维持蛋白稳态对抗氧化应激引起的损伤,从而介导细菌毒力,而TrxA可能作为一个调控基因参与抗氧化应激反应。展开更多
Aging is an inevitable biological phenomenon that involves a multitude of physiological alterations.Dietary interventions are being considered as potential strategies for delaying age-related dysfunction.Unsaponifiabl...Aging is an inevitable biological phenomenon that involves a multitude of physiological alterations.Dietary interventions are being considered as potential strategies for delaying age-related dysfunction.Unsaponifiable matter(USM),a composition of highly active ingredients found in walnut oil,has demonstrated antioxidant effects.This study aims to explore the neuroprotective effects of USM on d-galactose-treated C57BL/6 mice and elucidate its underlying mechanism,which was validated in PC12 cells treated with d-galactose.The results of behavioral tests demonstrated that USM significantly improved cognitive deficits associated with aging.The morphological analysis demonstrated that USM effectively alleviated hippocampal neuronal damage,synaptic impairment,and mitochondrial dysfunction induced by d-galactose.Furthermore,USM significantly increases the antioxidant enzymes activity while reducing the malondialdehyde and reactive oxygen species levels.The results suggest that USM can mitigate age-related symptoms caused by d-galactose by activating the nuclear factor erythroid-2-related factor 2 signaling pathway,which enhances the expression of antioxidant enzymes,restore redox balance,and improves synaptic and mitochondrial functions.This has a positive on improving cognition and memory disorders in elderly mice.展开更多
Theaflavins from black tea effectively improve insulin secretion in obesity and diabetes,but the molecular mechanisms are unclear.Here,the palmitic acid(PA)-induced pancreaticβ-TC-6 cells and high fat-/high glucose-i...Theaflavins from black tea effectively improve insulin secretion in obesity and diabetes,but the molecular mechanisms are unclear.Here,the palmitic acid(PA)-induced pancreaticβ-TC-6 cells and high fat-/high glucose-induced zebrafish were used.The effects of theaflavin-3,3'-digallate(TF3)on glucolipotoxicityinduced insulin secretion dysfunction,ferroptosis and endoplasmic reticulum(ER)stress were investigated by a variety of molecular biological approaches,inductively coupled plasma-mass spectrometry(ICP-MS),transmission electron microscopy(TEM)and widely targeted metabolomics analysis.TF3 was found to potently inhibit glucolipotoxicity-induced insulin secretion dysfunction and ferroptosis inβ-TC-6 cells and zebrafish,with increasing glutathione peroxidase 4(GPX4)expression,suppressing lipid peroxidation and iron accumulation and protecting mitochondria.Additionally,TF3 attenuated ER stress by regulating 3 unfolded protein response(UPR)pathways inβ-TC-6 cells,and significantly modulated linoleic acid metabolism and L-kynurenine signalling in zebrafish.The expression of sarcoplasmic/endoplasmic reticulum calcium ATPase 2(SERCA2)was obviously enhanced by TF3.Thapsigargin,a SERCA2 inhibitor,remarkably reversed the effects of TF3 on insulin production,ferroptosis,ER stress and the kynurenine signalling.Together,this work revealed the critical role of SERCA2 in ferroptosis regulation,and demonstrated TF3 targeted SERCA2 to inhibit ER stress and ferropto sis,thereby protectingβ-cell secretory function from glucolipotoxicity.展开更多
基金Research Fund of Guangdong-Hong Kong-Macao Joint Laboratory for Intelligent Micro-Nano Optoelectronic Tech-nology,China(Grant No.2020B1212030010)Project of Faculty of Agricultural Equipment of Jiangsu University (Grant No. NZXB20210202) are acknowledged。
文摘Ferroelectric HfO_(2)has attracted much attention owing to its superior ferroelectricity at an ultra-thin thickness and good compatibility with Si-based complementary metal-oxide-semiconductor(CMOS)technology.However,the crystallization of polar orthorhombic phase(o-phase)HfO_(2)is less competitive,which greatly limits the ferroelectricity of the as-obtained ferroelectric HfO_(2)thin films.Fortunately,the crystallization of o-phase HfO_(2)can be thermodynamically modulated via interfacial stress engineering.In this paper,the growth of improved ferroelectric Al doped HfO_(2)(HfO_(2):Al)thin films on(111)-oriented Si substrate has been reported.Structural analysis has suggested that nonpolar monoclinic HfO_(2):Al grown on(111)-oriented Si substrate suffered from a strong compressive strain,which promoted the crystallization of(111)-oriented o-phase HfO_(2)in the as-grown HfO_(2):Al thin films.In addition,the in-plane lattice of(111)-oriented Si substrate matches well with that of(111)-oriented o-phase HfO_(2),which further thermally stabilizes the o-phase HfO_(2).Accordingly,an improved ferroelectricity with a remnant polarization(2P_(r))of 26.7C/cm^(2) has been obtained.The results shown in this work provide a simple way toward the preparation of improved ferroelectric HfO_(2)thin films.
基金supported by the National Key R&D Program of China(2021YFD2100103)the National Natural Science Foundation of China(32101935).
文摘Glycidol is a common lipid-derived foodborne toxicant mainly presents in refined oils and related foodstuffs.Vascular endothelial cells may be potential targets of the deleterious effects associated with glycidol exposure.In human umbilical vein endothelial cells(HUVECs),we found that glycidol treatment promoted endothelialto-mesenchymal transition(EndMT)at a lower concentration(0.5 mmol/L),while induced apoptosis and inflammation at a higher concentration(1 mmol/L).These harmful effects were achieved by the activation of NF-κB/MAPK signaling pathway and were mediated by reactive oxygen species(ROS).In addition,the protective potential of 6-C-(E-2-fluorostyryl)naringenin(6-CEFN)against glycidol was evaluated and compared with naringenin.HUVECs pre-treated with 6-CEFN,but not naringenin,displayed resistance to endothelial dysfunction caused by glycidol.
文摘【目的】探讨猪链球菌2型超氧化物歧化酶A(SodA)、硫氧还蛋白A(TrxA)和TrxC基因在调控氧化应激和参与致病过程中的生物学功能。【方法】比较猪链球菌2型3个突变菌株ΔSodA、ΔTrxA和ΔTrxC对抗应激能力和毒力的调控作用。通过应激存活试验,分别检测SodA、TrxA和TrxC基因对不同氧化应激处理(0.04%过氧化氢(H 2O 2)、10 mol/L百草枯(PQ))的抗氧化应激能力以及不同温度(4、43℃)的抗温度应激能力;将不同基因缺失株与猪肠道上皮细胞(IPEC-J2)、小鼠巨噬细胞(RAW264.7)共培养,探究3个基因对细胞黏附和抗吞噬功能的影响;通过小鼠攻毒试验,测定各组织载菌量和血清抗氧化酶与肝功能指标,探明SodA、TrxA和TrxC基因在抗氧化应激以及致病过程中的作用。【结果】抗应激试验结果显示,在不同氧化应激和不同温度应激条件下,ΔSodA和ΔTrxC菌株存活能力均极显著低于野生菌株(P<0.01),ΔTrxA菌株在43℃高温刺激下存活能力极显著低于野生菌株(P<0.01)。细胞黏附试验结果显示,SodA和TrxA基因缺失导致细菌黏附能力降低55%~65%,极显著低于野生菌株(P<0.01)。细胞抗吞噬试验结果显示,ΔSodA、ΔTrxC和ΔTrxA菌株在吞噬细胞中的存活率极显著或显著低于野生菌株(P<0.01;P<0.05)。动物攻毒试验结果显示,与野生菌株相比,ΔSodA、ΔTrxA和ΔTrxC菌株毒力均极显著下降(P<0.01);ΔSodA、ΔTrxA和ΔTrxC菌株组小鼠死亡率分别为10%、50%和20%,组织载菌量分别为3.6 lg CFU/g~4.4 lg CFU/g、4.2 lg CFU/g~5.1 lg CFU/g和3.1 lg CFU/g~4.1 lg CFU/g;野生菌株组小鼠死亡率为90%,组织载菌量为6.4 lg CFU/g~7.8 lg CFU/g。小鼠感染ΔSodA、ΔTrxC和ΔTrxA菌株后血清中超氧化物歧化酶(SOD)、过氧化氢酶(CAT)活性和总抗氧化能力(T-AOC)极显著高于野生菌株(P<0.01),天门冬氨酸转氨酶(AST)、谷丙转氨酶(ALT)和碱性磷酸酶(ALP)活性极显著低于野生菌株(P<0.01)。【结论】猪链球菌2型SodA和TrxC基因通过中和菌体内超氧根离子和维持蛋白稳态对抗氧化应激引起的损伤,从而介导细菌毒力,而TrxA可能作为一个调控基因参与抗氧化应激反应。
基金supported by the National Key Research and Development Program(2022YFD1600402)Hebei Provincial Major Science and Technology Achievement Transformation Project(21287101Z)Hebei Provincial Innovation and Entrepreneurship Team Project(215A7102D)。
文摘Aging is an inevitable biological phenomenon that involves a multitude of physiological alterations.Dietary interventions are being considered as potential strategies for delaying age-related dysfunction.Unsaponifiable matter(USM),a composition of highly active ingredients found in walnut oil,has demonstrated antioxidant effects.This study aims to explore the neuroprotective effects of USM on d-galactose-treated C57BL/6 mice and elucidate its underlying mechanism,which was validated in PC12 cells treated with d-galactose.The results of behavioral tests demonstrated that USM significantly improved cognitive deficits associated with aging.The morphological analysis demonstrated that USM effectively alleviated hippocampal neuronal damage,synaptic impairment,and mitochondrial dysfunction induced by d-galactose.Furthermore,USM significantly increases the antioxidant enzymes activity while reducing the malondialdehyde and reactive oxygen species levels.The results suggest that USM can mitigate age-related symptoms caused by d-galactose by activating the nuclear factor erythroid-2-related factor 2 signaling pathway,which enhances the expression of antioxidant enzymes,restore redox balance,and improves synaptic and mitochondrial functions.This has a positive on improving cognition and memory disorders in elderly mice.
基金supported by National Natural Science Foundation of China(32272303)Natural Science Foundation of Zhejiang Province,China(LY21C200010)。
文摘Theaflavins from black tea effectively improve insulin secretion in obesity and diabetes,but the molecular mechanisms are unclear.Here,the palmitic acid(PA)-induced pancreaticβ-TC-6 cells and high fat-/high glucose-induced zebrafish were used.The effects of theaflavin-3,3'-digallate(TF3)on glucolipotoxicityinduced insulin secretion dysfunction,ferroptosis and endoplasmic reticulum(ER)stress were investigated by a variety of molecular biological approaches,inductively coupled plasma-mass spectrometry(ICP-MS),transmission electron microscopy(TEM)and widely targeted metabolomics analysis.TF3 was found to potently inhibit glucolipotoxicity-induced insulin secretion dysfunction and ferroptosis inβ-TC-6 cells and zebrafish,with increasing glutathione peroxidase 4(GPX4)expression,suppressing lipid peroxidation and iron accumulation and protecting mitochondria.Additionally,TF3 attenuated ER stress by regulating 3 unfolded protein response(UPR)pathways inβ-TC-6 cells,and significantly modulated linoleic acid metabolism and L-kynurenine signalling in zebrafish.The expression of sarcoplasmic/endoplasmic reticulum calcium ATPase 2(SERCA2)was obviously enhanced by TF3.Thapsigargin,a SERCA2 inhibitor,remarkably reversed the effects of TF3 on insulin production,ferroptosis,ER stress and the kynurenine signalling.Together,this work revealed the critical role of SERCA2 in ferroptosis regulation,and demonstrated TF3 targeted SERCA2 to inhibit ER stress and ferropto sis,thereby protectingβ-cell secretory function from glucolipotoxicity.
