A gold catalyst of Au/pyrenyl‑graphdiyne(Pyr‑GDY)was prepared by anchoring small size of gold nanoparticles(Au NPs)on the surface of Pyr‑GDY for electrocatalytic nitrogen reduction reaction(eNRR),in which Au NPs with ...A gold catalyst of Au/pyrenyl‑graphdiyne(Pyr‑GDY)was prepared by anchoring small size of gold nanoparticles(Au NPs)on the surface of Pyr‑GDY for electrocatalytic nitrogen reduction reaction(eNRR),in which Au NPs with a size of approximately 3.69 nm was evenly distributed on spongy‑like porous Pyr‑GDY.The catalyst exhibited a good electrocatalytic activity for N_(2)reduction in a nitrogen‑saturated electrolyte,with an ammonia yield of 32.1μg·h^(-1)·mg_(cat)^(-1)at-0.3 V(vs RHE),3.5 times higher than that of Au/C(Au NPs anchored on carbon black).In addition,Au/Pyr‑GDY showed a Faraday efficiency(FE)of 26.9%for eNRR,and a good catalysis durability for over 22 h.展开更多
目的探究加味补阳还五汤联合镜像疗法对气虚血瘀型脑梗死后中重度上肢偏瘫患者脑侧支循环建立及肢体康复的影响分析。方法选取气虚血瘀型脑梗死后中重度上肢偏瘫患者100例,随机分为两组,每组50例。对照组使用常规治疗,观察组在对照组基...目的探究加味补阳还五汤联合镜像疗法对气虚血瘀型脑梗死后中重度上肢偏瘫患者脑侧支循环建立及肢体康复的影响分析。方法选取气虚血瘀型脑梗死后中重度上肢偏瘫患者100例,随机分为两组,每组50例。对照组使用常规治疗,观察组在对照组基础上联合加味补阳还五汤及镜像疗法治疗,疗程为4周,对比两组患者临床治疗效果、美国国会卫生研究院卒中量表(National Institute of Health stroke scale,NIHSS)评分、蒙特利尔认知评估量表(Montreal Cogni-tive Assessmen,MoCA)、基质细胞源性因子1(Stromal cell-derived factor 1,SDF1)、S100钙结合蛋白B(S100 calcium bind-ing proteinB,S100B)、血小板源性生长因子(Platelet-derived growth factor,PDGF)、福格-米勒运动功能评分量表(Fugl-Meyer motor function assessment,FMA)评分及巴塞尔指数(Barthel index,BI)评分。结果治疗后对照组总有效率为68.00%(34/50),显著低于观察组的90.00%(45/50)(P<0.05);治疗后两组NIHSS评分较治疗前显著降低(P<0.05),观察组评分显著低于对照组(P<0.05);治疗后两组MoCA评分均较治疗前提高(P<0.05),观察组评分显著高于对照组(P<0.05);治疗后两组PDG水平均显著升高,观察组显著高于对照组(P<0.05);SDF-1、S100B水平均显著降低,且观察组显著低于对照组(P<0.05);治疗后两组FMA评分及BI评分均较治疗前显著提升(P<0.05),观察组显著高于对照组(P<0.05)。结论加味补阳还五汤联合镜像疗法治疗气虚血瘀型脑梗死后中重度上肢偏瘫患者具有良好的临床治疗效果,显著改善患者神经功能及认知水平,促进脑血管新生和侧支循环形成,并改善患者肢体运动功能,全面提升患者生存质量。展开更多
目的通过观察补阳还五汤对高血压病大鼠硫氧还蛋白互作蛋白-消皮素D(TXNIP/GSDMD)信号转导通路的影响,从焦亡角度探讨补阳还五汤对高血压病大鼠主动脉血管内皮损伤的保护机制。方法将大鼠随机分为空白对照组,模型组,补阳还五汤低、中、...目的通过观察补阳还五汤对高血压病大鼠硫氧还蛋白互作蛋白-消皮素D(TXNIP/GSDMD)信号转导通路的影响,从焦亡角度探讨补阳还五汤对高血压病大鼠主动脉血管内皮损伤的保护机制。方法将大鼠随机分为空白对照组,模型组,补阳还五汤低、中、高剂量组,氢氯噻嗪组,每组10只,所有大鼠于SPF级动物实验中心普通饲料适应性饲养7 d。空白对照组每日给予低盐饲料喂养,其余各组采用高盐饲料喂养,同时,补阳还五汤低、中、高剂量组分别以0.275、0.55、1.1 g/mL浓度中药干预,氢氯噻嗪组以10 mg/(kg·d)浓度药物干预。3周后,观察到大鼠血压比造模前升高大于或等于30 mm Hg(1 mm Hg≈0.133 kPa),且收缩压(SBP)≥160 mm Hg即高血压病大鼠造模成功。取大鼠主动脉进行检测,HE染色观察大鼠主动脉病理形态改变;采用ELISA检测大鼠主动脉中血管紧张素Ⅱ(AngⅡ)、白细胞介素18(IL-18)、白细胞介素1β(IL-1β)、超氧化物歧化酶(superoxide dismutase,SOD)以及丙二醛(malondialdehyde,MDA)蛋白表达;荧光定量PCR检测大鼠主动脉中TXNIP、GSDMD、还原性辅酶Ⅱ氧化酶4(NOX4)、IL-1β的mRNA表达,免疫印迹实验(Western blot)检测大鼠主动脉中GSDMD的蛋白表达,免疫组化(IHC)检测大鼠主动脉中TXNIP、NOD样受体蛋白3(NLRP3)、GSDMD的蛋白表达。结果与空白对照组相比,模型组大鼠血压明显升高,主动脉内外膜都有一定脱落,界线模糊,血管中膜弹性纤维结构比较疏松,排列有一定紊乱;TXNIP、GSDMD、IL-1β、NOX4的mRNA表达上升(P<0.05);TXNIP、NLRP3、GSDMD、IL-1β、IL-18、AngⅡ、MDA的蛋白表达升高(P<0.05),SOD蛋白表达降低(P<0.05)。与模型组相比,补阳还五汤中剂量组和氢氯噻嗪组大鼠血压明显降低,血管内外膜更加完整、光滑,结构更加致密,界线较为清晰明显,补阳还五汤低、高剂量组内外膜仍有一定脱落,弹性纤维排列比较杂乱,变化不明显;药物干预后各组TXNIP、GSDMD、IL-1β、NOX4的mRNA表达均下降(P<0.05);补阳还五汤中剂量组和氢氯噻嗪组TXNIP、NLRP3、GSDMD、IL-1β、IL-18、AngⅡ、MDA的蛋白表达降低(P<0.05),SOD蛋白表达升高(P<0.05)。结论补阳还五汤可通过抑制氧化应激,调节TXNIP/GSDMD信号通路的分子表达,调控血管内皮焦亡,从而发挥保护血管、治疗高血压病的作用。展开更多
目的观察补阳还五汤(BYHW)对过氧化氢(H_(2)O_(2))诱导的衰老内皮细胞沉默信息调节因子1(silent information regulator 1,SIRT1)-自噬通路的作用。方法以人脐静脉内皮细胞(HUVEC)作为研究对象,H_(2)O_(2)诱导的内皮细胞作为模型,体外培...目的观察补阳还五汤(BYHW)对过氧化氢(H_(2)O_(2))诱导的衰老内皮细胞沉默信息调节因子1(silent information regulator 1,SIRT1)-自噬通路的作用。方法以人脐静脉内皮细胞(HUVEC)作为研究对象,H_(2)O_(2)诱导的内皮细胞作为模型,体外培养HUVECs,并将细胞分为正常组、模型组(H_(2)O_(2)400μmol/L)、BYHW组(H_(2)O_(2)400μmol/L+BYHW 2500μg/mL)。衰老相关β半乳糖苷酶(SA-β-Gal)染色检测细胞衰老,蛋白质免疫印迹法检测SIRT1、纤溶酶原激活物抑制因子1(PAI-1)、泛素结合蛋白p62及微管相关蛋白1轻链3β(LC3)蛋白的表达,ELISA法检测细胞上清液中超氧化物歧化酶(superoxide dismutase,SOD)、丙二醛(malondialdehyde,MDA)含量,免疫荧光观察SIRT1、LC3的表达。结果400μmol/L的H_(2)O_(2)处理可成功诱导HUVECs衰老。与正常组相比,衰老模型组中SA-β-Gal阳染率增加,SIRT1、LC3蛋白表达降低,SOD含量降低,PAI-1、p62蛋白表达升高,MDA含量升高,细胞免疫荧光显示SIRT1、LC3表达降低。与模型组比较,BYHW组细胞蓝染比率降低,PAI-1、p62蛋白表达降低,SOD水平升高,SIRT1、LC3蛋白表达升高,细胞免疫荧光BYHW组SIRT1、LC3表达明显升高。结论在过氧化氢诱导的HUVECs衰老模型中,补阳还五汤能够上调SIRT1,激活自噬,从而对衰老的内皮细胞起到保护作用。展开更多
OBJECTIVE To investigate whether aldo-keto reductases(AKRs)can act as a nitrore⁃ductase(NR)and bioactivate aristolochic acidⅠ(AA-Ⅰ)to produce AA-Ⅰ-DNA adducts.METHODS①Human-induced hepatocytes(hiHeps)and human bla...OBJECTIVE To investigate whether aldo-keto reductases(AKRs)can act as a nitrore⁃ductase(NR)and bioactivate aristolochic acidⅠ(AA-Ⅰ)to produce AA-Ⅰ-DNA adducts.METHODS①Human-induced hepatocytes(hiHeps)and human bladder RT4 cells were used as tool cells and treated with AA-Ⅰ0,0.5,1.0 and 2μmol·L^(-1)for 24 h.Cell viability was detected using the CCK-8 method,and the half maximal inhibition concentration(IC_(50))was calculated using the CCK-8 method and the level of DNA adduct production was calculated.②hiHeps and RT4 cells were treated with AKR inhibitor luteotin(0,5,10 and 25μmol·L^(-1))+AA-Ⅰ0.2 and 1.0μmol·L^(-1)for 24 h,respectively,and the levels of DNA adducts were detected by a liquid chromatography-tandem mass spectrometer(LC-MS/MS).③hiHeps cells were incubated with 80 nmol·L^(-1)small interfering RNAs(si-AKRs)for 48 h and treated with AA-Ⅰ1.0μmol·L^(-1)for 24 h.Real-time qualitative PCR(RT-qPCR)method was used to detect the mRNA expression of AKRs gene and LC-MS/MS technology was used to investigate the effect of specific AKR gene knockdown on DNA adduct levels.④500 nmol·L^(-1)human AKR recombinant proteins AKR1A1 and AA-Ⅰwere incubated in vitro under anaerobic conditions and the formation of AA-Ⅰ-DNA adducts was detected.RESULTS①The IC_(50)of AA-Ⅰto hiHeps and RT4 cells was 1.9 and 0.42μmol·L^(-1),respec⁃tively.The level of DNA adduct production of the two cell lines was significantly different(P<0.01).②Luteolin≥5μmol·L^(-1)significantly inhibited the production of AA-Ⅰ-DNA adducts in both cells(P<0.05),and there was a concentration-dependent effect in hiHeps cells(P<0.01,R=0.84).③In the AKR family,the knockdown of AKR1A1 gene up to 80%inhibited the generation of AA-Ⅰ-DNA adducts by 30%-40%.④The AA-Ⅰ-DNA adducts were detected in the incubation of recombinant protein AKR1A1 and AA-Ⅰunder anaerobic conditions in vitro,approximately 1 adduct per 107 nucleotides.CONCLU⁃SION AKR1A1 is involved in AA-Ⅰbioactivation,providing a reference for elucidation of the carcino⁃genic mechanism of AA-Ⅰ.展开更多
To reduce the production cost of titanium,a new method for direct preparation of low-oxygen titanium powder by the magnesiothermic reduction of TiO_(2) with the assistance of a MgCl_(2)−HoCl_(3) molten salt was propos...To reduce the production cost of titanium,a new method for direct preparation of low-oxygen titanium powder by the magnesiothermic reduction of TiO_(2) with the assistance of a MgCl_(2)−HoCl_(3) molten salt was proposed.Thermodynamic calculations showed that the magnesiothermic reduction of TiO_(2) was feasible.However,hindrance of the reduction reaction by the reduction by-product of MgO resulted in a considerably high O concentration in the titanium powder.The addition of HoCl_(3) to the system significantly reduces the activity of MgO to produce low-oxygen titanium powder.Thermochemical deoxidation and reduction experiments were conducted with MgCl_(2)−HoCl_(3) molten salt in the temperature range of 1023−1273 K.The results showed that titanium powder with oxygen concentration(mass fraction)below 5.00×10^(-4) can be prepared at the Mg−MgCl_(2)−HoOCl−HoCl_(3) equilibrium.展开更多
文摘A gold catalyst of Au/pyrenyl‑graphdiyne(Pyr‑GDY)was prepared by anchoring small size of gold nanoparticles(Au NPs)on the surface of Pyr‑GDY for electrocatalytic nitrogen reduction reaction(eNRR),in which Au NPs with a size of approximately 3.69 nm was evenly distributed on spongy‑like porous Pyr‑GDY.The catalyst exhibited a good electrocatalytic activity for N_(2)reduction in a nitrogen‑saturated electrolyte,with an ammonia yield of 32.1μg·h^(-1)·mg_(cat)^(-1)at-0.3 V(vs RHE),3.5 times higher than that of Au/C(Au NPs anchored on carbon black).In addition,Au/Pyr‑GDY showed a Faraday efficiency(FE)of 26.9%for eNRR,and a good catalysis durability for over 22 h.
文摘目的探究加味补阳还五汤联合镜像疗法对气虚血瘀型脑梗死后中重度上肢偏瘫患者脑侧支循环建立及肢体康复的影响分析。方法选取气虚血瘀型脑梗死后中重度上肢偏瘫患者100例,随机分为两组,每组50例。对照组使用常规治疗,观察组在对照组基础上联合加味补阳还五汤及镜像疗法治疗,疗程为4周,对比两组患者临床治疗效果、美国国会卫生研究院卒中量表(National Institute of Health stroke scale,NIHSS)评分、蒙特利尔认知评估量表(Montreal Cogni-tive Assessmen,MoCA)、基质细胞源性因子1(Stromal cell-derived factor 1,SDF1)、S100钙结合蛋白B(S100 calcium bind-ing proteinB,S100B)、血小板源性生长因子(Platelet-derived growth factor,PDGF)、福格-米勒运动功能评分量表(Fugl-Meyer motor function assessment,FMA)评分及巴塞尔指数(Barthel index,BI)评分。结果治疗后对照组总有效率为68.00%(34/50),显著低于观察组的90.00%(45/50)(P<0.05);治疗后两组NIHSS评分较治疗前显著降低(P<0.05),观察组评分显著低于对照组(P<0.05);治疗后两组MoCA评分均较治疗前提高(P<0.05),观察组评分显著高于对照组(P<0.05);治疗后两组PDG水平均显著升高,观察组显著高于对照组(P<0.05);SDF-1、S100B水平均显著降低,且观察组显著低于对照组(P<0.05);治疗后两组FMA评分及BI评分均较治疗前显著提升(P<0.05),观察组显著高于对照组(P<0.05)。结论加味补阳还五汤联合镜像疗法治疗气虚血瘀型脑梗死后中重度上肢偏瘫患者具有良好的临床治疗效果,显著改善患者神经功能及认知水平,促进脑血管新生和侧支循环形成,并改善患者肢体运动功能,全面提升患者生存质量。
文摘目的通过观察补阳还五汤对高血压病大鼠硫氧还蛋白互作蛋白-消皮素D(TXNIP/GSDMD)信号转导通路的影响,从焦亡角度探讨补阳还五汤对高血压病大鼠主动脉血管内皮损伤的保护机制。方法将大鼠随机分为空白对照组,模型组,补阳还五汤低、中、高剂量组,氢氯噻嗪组,每组10只,所有大鼠于SPF级动物实验中心普通饲料适应性饲养7 d。空白对照组每日给予低盐饲料喂养,其余各组采用高盐饲料喂养,同时,补阳还五汤低、中、高剂量组分别以0.275、0.55、1.1 g/mL浓度中药干预,氢氯噻嗪组以10 mg/(kg·d)浓度药物干预。3周后,观察到大鼠血压比造模前升高大于或等于30 mm Hg(1 mm Hg≈0.133 kPa),且收缩压(SBP)≥160 mm Hg即高血压病大鼠造模成功。取大鼠主动脉进行检测,HE染色观察大鼠主动脉病理形态改变;采用ELISA检测大鼠主动脉中血管紧张素Ⅱ(AngⅡ)、白细胞介素18(IL-18)、白细胞介素1β(IL-1β)、超氧化物歧化酶(superoxide dismutase,SOD)以及丙二醛(malondialdehyde,MDA)蛋白表达;荧光定量PCR检测大鼠主动脉中TXNIP、GSDMD、还原性辅酶Ⅱ氧化酶4(NOX4)、IL-1β的mRNA表达,免疫印迹实验(Western blot)检测大鼠主动脉中GSDMD的蛋白表达,免疫组化(IHC)检测大鼠主动脉中TXNIP、NOD样受体蛋白3(NLRP3)、GSDMD的蛋白表达。结果与空白对照组相比,模型组大鼠血压明显升高,主动脉内外膜都有一定脱落,界线模糊,血管中膜弹性纤维结构比较疏松,排列有一定紊乱;TXNIP、GSDMD、IL-1β、NOX4的mRNA表达上升(P<0.05);TXNIP、NLRP3、GSDMD、IL-1β、IL-18、AngⅡ、MDA的蛋白表达升高(P<0.05),SOD蛋白表达降低(P<0.05)。与模型组相比,补阳还五汤中剂量组和氢氯噻嗪组大鼠血压明显降低,血管内外膜更加完整、光滑,结构更加致密,界线较为清晰明显,补阳还五汤低、高剂量组内外膜仍有一定脱落,弹性纤维排列比较杂乱,变化不明显;药物干预后各组TXNIP、GSDMD、IL-1β、NOX4的mRNA表达均下降(P<0.05);补阳还五汤中剂量组和氢氯噻嗪组TXNIP、NLRP3、GSDMD、IL-1β、IL-18、AngⅡ、MDA的蛋白表达降低(P<0.05),SOD蛋白表达升高(P<0.05)。结论补阳还五汤可通过抑制氧化应激,调节TXNIP/GSDMD信号通路的分子表达,调控血管内皮焦亡,从而发挥保护血管、治疗高血压病的作用。
文摘OBJECTIVE To investigate whether aldo-keto reductases(AKRs)can act as a nitrore⁃ductase(NR)and bioactivate aristolochic acidⅠ(AA-Ⅰ)to produce AA-Ⅰ-DNA adducts.METHODS①Human-induced hepatocytes(hiHeps)and human bladder RT4 cells were used as tool cells and treated with AA-Ⅰ0,0.5,1.0 and 2μmol·L^(-1)for 24 h.Cell viability was detected using the CCK-8 method,and the half maximal inhibition concentration(IC_(50))was calculated using the CCK-8 method and the level of DNA adduct production was calculated.②hiHeps and RT4 cells were treated with AKR inhibitor luteotin(0,5,10 and 25μmol·L^(-1))+AA-Ⅰ0.2 and 1.0μmol·L^(-1)for 24 h,respectively,and the levels of DNA adducts were detected by a liquid chromatography-tandem mass spectrometer(LC-MS/MS).③hiHeps cells were incubated with 80 nmol·L^(-1)small interfering RNAs(si-AKRs)for 48 h and treated with AA-Ⅰ1.0μmol·L^(-1)for 24 h.Real-time qualitative PCR(RT-qPCR)method was used to detect the mRNA expression of AKRs gene and LC-MS/MS technology was used to investigate the effect of specific AKR gene knockdown on DNA adduct levels.④500 nmol·L^(-1)human AKR recombinant proteins AKR1A1 and AA-Ⅰwere incubated in vitro under anaerobic conditions and the formation of AA-Ⅰ-DNA adducts was detected.RESULTS①The IC_(50)of AA-Ⅰto hiHeps and RT4 cells was 1.9 and 0.42μmol·L^(-1),respec⁃tively.The level of DNA adduct production of the two cell lines was significantly different(P<0.01).②Luteolin≥5μmol·L^(-1)significantly inhibited the production of AA-Ⅰ-DNA adducts in both cells(P<0.05),and there was a concentration-dependent effect in hiHeps cells(P<0.01,R=0.84).③In the AKR family,the knockdown of AKR1A1 gene up to 80%inhibited the generation of AA-Ⅰ-DNA adducts by 30%-40%.④The AA-Ⅰ-DNA adducts were detected in the incubation of recombinant protein AKR1A1 and AA-Ⅰunder anaerobic conditions in vitro,approximately 1 adduct per 107 nucleotides.CONCLU⁃SION AKR1A1 is involved in AA-Ⅰbioactivation,providing a reference for elucidation of the carcino⁃genic mechanism of AA-Ⅰ.
基金financially supported by the National Natural Science Foundation of China (No.21968013)。
文摘To reduce the production cost of titanium,a new method for direct preparation of low-oxygen titanium powder by the magnesiothermic reduction of TiO_(2) with the assistance of a MgCl_(2)−HoCl_(3) molten salt was proposed.Thermodynamic calculations showed that the magnesiothermic reduction of TiO_(2) was feasible.However,hindrance of the reduction reaction by the reduction by-product of MgO resulted in a considerably high O concentration in the titanium powder.The addition of HoCl_(3) to the system significantly reduces the activity of MgO to produce low-oxygen titanium powder.Thermochemical deoxidation and reduction experiments were conducted with MgCl_(2)−HoCl_(3) molten salt in the temperature range of 1023−1273 K.The results showed that titanium powder with oxygen concentration(mass fraction)below 5.00×10^(-4) can be prepared at the Mg−MgCl_(2)−HoOCl−HoCl_(3) equilibrium.
