目的:通过对C3H10T1/2细胞分化为成熟棕色脂肪细胞的培养、诱导分化及鉴定,深入探讨棕色脂肪细胞的生物学特性,为人类棕色脂肪细胞的相关研究提供实验参考与理论依据。方法:C3H10T1/2细胞经细胞接种、培养及诱导分化处理,利用光学显微...目的:通过对C3H10T1/2细胞分化为成熟棕色脂肪细胞的培养、诱导分化及鉴定,深入探讨棕色脂肪细胞的生物学特性,为人类棕色脂肪细胞的相关研究提供实验参考与理论依据。方法:C3H10T1/2细胞经细胞接种、培养及诱导分化处理,利用光学显微镜观察细胞形态变化,并通过油红O染色、免疫荧光法、线粒体探针法以及线粒体电镜技术对分化细胞进行鉴定分析。结果:未分化的C3H10T1/2细胞形态多样,具有突触伸展特征;分化后的细胞逐渐变为圆形或椭圆形,形成环形脂滴;未分化组细胞形态无明显变化。油红O染色显示,未分化组细胞基本无染色,而分化组中约90%的细胞红染,脂滴分布于细胞核周围,吸光度值显著升高(P<0.05)。分化组解偶联蛋白1(uncoupling protein 1,UCP1)、过氧化物酶体增殖激活受体γ(peroxisome proliferator-activated receptorγ,PPARγ)辅激活因子1α(PPARγco-activator-1α,PGC-1α)、PPARγ和转录因子PRDM16的相对荧光强度和蛋白表达量显著高于未分化组(P<0.05),且线粒体活性增强。结论:本研究成功诱导C3H10T1/2细胞分化为成熟棕色脂肪细胞,结合细胞形态观察、关键蛋白表达检测及线粒体功能分析进行综合评估,证实了细胞的有效分化及成熟棕色脂肪细胞的功能特性。展开更多
A ternary composite of TiO2 and a SiO2-Al2O3 aerogel with good photocatalytic activity was prepared by a simple sol-gel method with TiO2 nanoparticles and SiO2-Al2O3 aerogels derived from industrial fly ash.The struct...A ternary composite of TiO2 and a SiO2-Al2O3 aerogel with good photocatalytic activity was prepared by a simple sol-gel method with TiO2 nanoparticles and SiO2-Al2O3 aerogels derived from industrial fly ash.The structural features of the TiO2/SiO2-Al2O3 aerogel composite were investigated by X-ray powder diffraction,Fourier transform infrared spectroscopy,transmission electron microscopy,gas adsorption measurements and diffuse reflectance UV-visible spectroscopy.The optimal conditions for photocatalytic degradation of 2-sec-butyl-4,6-dinitrophenol（DNBP],included an initial DNBP concentration of 0.167 mmol/L at pH = 4.86 with a catalyst concentration of 6 g/L,under visible light irradiation for 5 h.A plausible mechanism is proposed for the photocatalytic degradation of DNBP.Our composite showed higher photocatalytic activity for DNBP degradation than that of pure TiO2.This indicates that this material can serve as an efficient photocatalyst for degradation of hazardous organic pollutants in wastewater.展开更多
In order to explore the reaction mechanism of Fe^3＋ and the mineralization effect of the micropollutant, Fe^3＋ assisted photocatalytic oxidation of sulfadiazine （SD） in the TiO2 suspended solution is investigated....In order to explore the reaction mechanism of Fe^3＋ and the mineralization effect of the micropollutant, Fe^3＋ assisted photocatalytic oxidation of sulfadiazine （SD） in the TiO2 suspended solution is investigated. The effect of Fe^3＋ participation, the degradation kinetics of SD, the effect of SD mineralization and the possible mechanism of Fe^3＋ participation in TiO2 suspension are analyzed by adding FeCl3, taking samples at a given time and determining the SD concentration. Results indicate that the degradation of SD catalyzed by TiO2/ Fe^3＋ is faster than that catalyzed by TiO2 or Fe^3＋ separately. The photocatalytic degradation of SD follows the pseudo-first- order kinetics model in a range of 20 to 80 mg/L of initial concentration. The mineralization rate of SD can be enhanced by the addition of Fe^3＋ in the TiO2 suspended solution. The mechanism of the rapid degradation of SD is proposed, which indicates that Fe^3＋ adsorbed on the surface of TiO2 particles acts as an electron acceptor. The amount of recombining electronhole pairs decreases, and the amount of hydroxyl radicals increases. The increased hydroxyl radical strengthens the degradation of SD in the TiO2/Fe^3＋ suspended solution.展开更多
Pathological cardiac hypertrophy is an early and significant cardiac structural characteristic that contributes to the onset and progression of heart failure(HF).Its mainly structural feature is the abnormally enlarge...Pathological cardiac hypertrophy is an early and significant cardiac structural characteristic that contributes to the onset and progression of heart failure(HF).Its mainly structural feature is the abnormally enlarged cardiomyocyte.Effective intervention targets for abnormally enlarged cardiomyocyte remain to be identified.Previous studies have shown that the cellular shape and size can be regulated by the actin related protein 2/3(Arp2/3)complex,which is an actin-binding protein complex involved in the actin nucleation and assembly.However,the roles of the Arp2/3 complex in cardiomyocyte hypertrophy remain unknown.Here our study identifies its novel roles in the occurrence and development of cardiomyocyte hypertrophy.We found that mRNA levels of all subunits from the Arp2/3 complex are significantly upregulated(P<0.05)in the angiotensin Ⅱ(Ang Ⅱ)-induced neonatal rat primary and H9c2 cardiomyocyte hypertrophy.Further studies showed that siRNA-directed ARPC 2 silencing inhibits the reactivation of fetal genes and enlargement of cardiomyocyte area induced by Ang Ⅱ in neonatal rat primary cardiomyocytes(NRCMs)and H9c2 cells(P<0.05).In addition,the upstream activators of the Arp2/3 complex including SH3 protein interacting with Nck,90 kD(SPIN90)and Ras-related C3 botulinum toxin substrate 1(Rac1)/WASp family Verprolin-homologous protein-2(WAVE-2)are upregulated(P<0.05)in Ang Ⅱ-induced neonatal rat primary and H9c2 cardiomyocyte hypertrophy,indicating the excessive activation of the Arp2/3 complex.We further show that CK666,a specific Arp2/3 complex inhibitor,prevents the reactivation of fetal genes and the enlargement of cardiomyocyte area induced by Ang Ⅱ in NRCMs and H9c2 cells(P<0.05).Our results reveal that the Arp2/3 complex plays a crucial role in Ang Ⅱ-induced cardiomyocyte hypertrophy,which is beneficial to further studies about the molecular mechanisms by which the Arp2/3 complex regulates pathological cardiac hypertrophy.展开更多
文摘目的:通过对C3H10T1/2细胞分化为成熟棕色脂肪细胞的培养、诱导分化及鉴定,深入探讨棕色脂肪细胞的生物学特性,为人类棕色脂肪细胞的相关研究提供实验参考与理论依据。方法:C3H10T1/2细胞经细胞接种、培养及诱导分化处理,利用光学显微镜观察细胞形态变化,并通过油红O染色、免疫荧光法、线粒体探针法以及线粒体电镜技术对分化细胞进行鉴定分析。结果:未分化的C3H10T1/2细胞形态多样,具有突触伸展特征;分化后的细胞逐渐变为圆形或椭圆形,形成环形脂滴;未分化组细胞形态无明显变化。油红O染色显示,未分化组细胞基本无染色,而分化组中约90%的细胞红染,脂滴分布于细胞核周围,吸光度值显著升高(P<0.05)。分化组解偶联蛋白1(uncoupling protein 1,UCP1)、过氧化物酶体增殖激活受体γ(peroxisome proliferator-activated receptorγ,PPARγ)辅激活因子1α(PPARγco-activator-1α,PGC-1α)、PPARγ和转录因子PRDM16的相对荧光强度和蛋白表达量显著高于未分化组(P<0.05),且线粒体活性增强。结论:本研究成功诱导C3H10T1/2细胞分化为成熟棕色脂肪细胞,结合细胞形态观察、关键蛋白表达检测及线粒体功能分析进行综合评估,证实了细胞的有效分化及成熟棕色脂肪细胞的功能特性。
基金supported by the National Natural Science Foundation of China(21377018)the Natural Science Foundation of Liaoning Province of China(2013020116)the Fundamental Research Funds for the Central Universities(DUT15ZD240)~~
文摘A ternary composite of TiO2 and a SiO2-Al2O3 aerogel with good photocatalytic activity was prepared by a simple sol-gel method with TiO2 nanoparticles and SiO2-Al2O3 aerogels derived from industrial fly ash.The structural features of the TiO2/SiO2-Al2O3 aerogel composite were investigated by X-ray powder diffraction,Fourier transform infrared spectroscopy,transmission electron microscopy,gas adsorption measurements and diffuse reflectance UV-visible spectroscopy.The optimal conditions for photocatalytic degradation of 2-sec-butyl-4,6-dinitrophenol（DNBP],included an initial DNBP concentration of 0.167 mmol/L at pH = 4.86 with a catalyst concentration of 6 g/L,under visible light irradiation for 5 h.A plausible mechanism is proposed for the photocatalytic degradation of DNBP.Our composite showed higher photocatalytic activity for DNBP degradation than that of pure TiO2.This indicates that this material can serve as an efficient photocatalyst for degradation of hazardous organic pollutants in wastewater.
基金The Priority Academic Program Development of Jiangsu Higher Education Institutions (No. 1105007001 )the Ph. D. Programs Foundation of Ministry of Education of China (No. 20100092120018)the Natural Science Foundation of Jiangsu Province (No. BK2009453)
文摘In order to explore the reaction mechanism of Fe^3＋ and the mineralization effect of the micropollutant, Fe^3＋ assisted photocatalytic oxidation of sulfadiazine （SD） in the TiO2 suspended solution is investigated. The effect of Fe^3＋ participation, the degradation kinetics of SD, the effect of SD mineralization and the possible mechanism of Fe^3＋ participation in TiO2 suspension are analyzed by adding FeCl3, taking samples at a given time and determining the SD concentration. Results indicate that the degradation of SD catalyzed by TiO2/ Fe^3＋ is faster than that catalyzed by TiO2 or Fe^3＋ separately. The photocatalytic degradation of SD follows the pseudo-first- order kinetics model in a range of 20 to 80 mg/L of initial concentration. The mineralization rate of SD can be enhanced by the addition of Fe^3＋ in the TiO2 suspended solution. The mechanism of the rapid degradation of SD is proposed, which indicates that Fe^3＋ adsorbed on the surface of TiO2 particles acts as an electron acceptor. The amount of recombining electronhole pairs decreases, and the amount of hydroxyl radicals increases. The increased hydroxyl radical strengthens the degradation of SD in the TiO2/Fe^3＋ suspended solution.
文摘Pathological cardiac hypertrophy is an early and significant cardiac structural characteristic that contributes to the onset and progression of heart failure(HF).Its mainly structural feature is the abnormally enlarged cardiomyocyte.Effective intervention targets for abnormally enlarged cardiomyocyte remain to be identified.Previous studies have shown that the cellular shape and size can be regulated by the actin related protein 2/3(Arp2/3)complex,which is an actin-binding protein complex involved in the actin nucleation and assembly.However,the roles of the Arp2/3 complex in cardiomyocyte hypertrophy remain unknown.Here our study identifies its novel roles in the occurrence and development of cardiomyocyte hypertrophy.We found that mRNA levels of all subunits from the Arp2/3 complex are significantly upregulated(P<0.05)in the angiotensin Ⅱ(Ang Ⅱ)-induced neonatal rat primary and H9c2 cardiomyocyte hypertrophy.Further studies showed that siRNA-directed ARPC 2 silencing inhibits the reactivation of fetal genes and enlargement of cardiomyocyte area induced by Ang Ⅱ in neonatal rat primary cardiomyocytes(NRCMs)and H9c2 cells(P<0.05).In addition,the upstream activators of the Arp2/3 complex including SH3 protein interacting with Nck,90 kD(SPIN90)and Ras-related C3 botulinum toxin substrate 1(Rac1)/WASp family Verprolin-homologous protein-2(WAVE-2)are upregulated(P<0.05)in Ang Ⅱ-induced neonatal rat primary and H9c2 cardiomyocyte hypertrophy,indicating the excessive activation of the Arp2/3 complex.We further show that CK666,a specific Arp2/3 complex inhibitor,prevents the reactivation of fetal genes and the enlargement of cardiomyocyte area induced by Ang Ⅱ in NRCMs and H9c2 cells(P<0.05).Our results reveal that the Arp2/3 complex plays a crucial role in Ang Ⅱ-induced cardiomyocyte hypertrophy,which is beneficial to further studies about the molecular mechanisms by which the Arp2/3 complex regulates pathological cardiac hypertrophy.
