Two new coordination compounds of rare earth chloride with N-acetyl-DL-alanine and imidazole have been prepared from absolute alcohol. The general formula RE(C5H8NO3)2(C3H5N2)2Cl3·4H2O (RE=Ce, Pr) of these compou...Two new coordination compounds of rare earth chloride with N-acetyl-DL-alanine and imidazole have been prepared from absolute alcohol. The general formula RE(C5H8NO3)2(C3H5N2)2Cl3·4H2O (RE=Ce, Pr) of these compounds were identified, by chemical and elemental analysis, FTIR spectra, UV spectra, 1H NMR and 13C NMR spectra, and molar conductance. The processes of thermal decomposition were identified by TG-DSC curves. The possible reaction mechanisms and the kinetics equation were investigated by comparing the kinetics parameters. The activation entropy of dehydration, as well as enthalpy values of dehydration and decomposition were obtained by DSC curve. The three-dimensional fluorescence spectra of liquid compounds were measured. The phenomenon of the up-conversion fluorescence is discussed.展开更多
目的探讨胰高血糖素样肽(GLP-1)类似物利拉鲁肽对糖尿病肾病(diabetic nephropathy,DN)炎症性损伤及高糖刺激下肾小管上皮细胞的作用及其可能机制。方法将实验小鼠随机分为对照组(db/m组)、糖尿病肾病模型组(db/db组)和利拉鲁肽治疗组(d...目的探讨胰高血糖素样肽(GLP-1)类似物利拉鲁肽对糖尿病肾病(diabetic nephropathy,DN)炎症性损伤及高糖刺激下肾小管上皮细胞的作用及其可能机制。方法将实验小鼠随机分为对照组(db/m组)、糖尿病肾病模型组(db/db组)和利拉鲁肽治疗组(db/db+Li组),分别给予生理盐水或利拉鲁肽(1 mg·kg^(-1)·d^(-1))腹腔注射,持续给药8周。实验结束时,检测各组小鼠体质量、血糖、24 h尿白蛋白以及血肌酐水平。体外培养TCMK-1细胞,无血清DMEM培养基同步培养24 h,分为对照组(control)、高糖组(high glucose,HG)、HG+Li组、HG+VER、HG+HSP70组、HG+HSP70+NC si RNA(negative control si RNA,NC si RNA)组及HG+HSP70+TLR4 si RNA组,TLR4的小干扰RNA(si RNA)转染TCMK-1细胞后采用Western blot法检测TLR4蛋白表达。Real-time PCR检测肾组织及细胞中TNF-α、IL-6、IL-1β和CCL2 m RNA表达,Western blot分析TLR4及HSP70蛋白表达。结果实验结束时,各组小鼠均存活。与db/m组相比,db/db组小鼠体质量、空腹血糖、24 h尿白蛋白及血肌酐水平均显著升高(P<0.05),利拉鲁肽治疗能显著逆转db/db小鼠上述指标的升高(P<0.05)。db/db小鼠及高糖刺激下TCMK-1细胞炎症相关因子TNF-α、IL-6、IL-1β及CCL2 m RNA相对表达显著增加(P<0.05),TLR4及HSP70蛋白表达显著升高(P<0.05),利拉鲁肽治疗能显著降低db/db小鼠及高糖刺激下TCMK-1细胞炎症因子TNF-α、IL-1β及CCL2表达,TLR4 si RNA干扰TLR4蛋白表达能显著降低高糖刺激下TCMK-1细胞炎症相关因子TNF-α、IL-1β及CCL2 m RNA相对表达量(P<0.05)。结论利拉鲁肽通过调控HSP70-TLR4轴活性抑制DN肾小管炎症性损伤,继而抑制DN病程进展。展开更多
文摘Two new coordination compounds of rare earth chloride with N-acetyl-DL-alanine and imidazole have been prepared from absolute alcohol. The general formula RE(C5H8NO3)2(C3H5N2)2Cl3·4H2O (RE=Ce, Pr) of these compounds were identified, by chemical and elemental analysis, FTIR spectra, UV spectra, 1H NMR and 13C NMR spectra, and molar conductance. The processes of thermal decomposition were identified by TG-DSC curves. The possible reaction mechanisms and the kinetics equation were investigated by comparing the kinetics parameters. The activation entropy of dehydration, as well as enthalpy values of dehydration and decomposition were obtained by DSC curve. The three-dimensional fluorescence spectra of liquid compounds were measured. The phenomenon of the up-conversion fluorescence is discussed.
文摘目的探讨胰高血糖素样肽(GLP-1)类似物利拉鲁肽对糖尿病肾病(diabetic nephropathy,DN)炎症性损伤及高糖刺激下肾小管上皮细胞的作用及其可能机制。方法将实验小鼠随机分为对照组(db/m组)、糖尿病肾病模型组(db/db组)和利拉鲁肽治疗组(db/db+Li组),分别给予生理盐水或利拉鲁肽(1 mg·kg^(-1)·d^(-1))腹腔注射,持续给药8周。实验结束时,检测各组小鼠体质量、血糖、24 h尿白蛋白以及血肌酐水平。体外培养TCMK-1细胞,无血清DMEM培养基同步培养24 h,分为对照组(control)、高糖组(high glucose,HG)、HG+Li组、HG+VER、HG+HSP70组、HG+HSP70+NC si RNA(negative control si RNA,NC si RNA)组及HG+HSP70+TLR4 si RNA组,TLR4的小干扰RNA(si RNA)转染TCMK-1细胞后采用Western blot法检测TLR4蛋白表达。Real-time PCR检测肾组织及细胞中TNF-α、IL-6、IL-1β和CCL2 m RNA表达,Western blot分析TLR4及HSP70蛋白表达。结果实验结束时,各组小鼠均存活。与db/m组相比,db/db组小鼠体质量、空腹血糖、24 h尿白蛋白及血肌酐水平均显著升高(P<0.05),利拉鲁肽治疗能显著逆转db/db小鼠上述指标的升高(P<0.05)。db/db小鼠及高糖刺激下TCMK-1细胞炎症相关因子TNF-α、IL-6、IL-1β及CCL2 m RNA相对表达显著增加(P<0.05),TLR4及HSP70蛋白表达显著升高(P<0.05),利拉鲁肽治疗能显著降低db/db小鼠及高糖刺激下TCMK-1细胞炎症因子TNF-α、IL-1β及CCL2表达,TLR4 si RNA干扰TLR4蛋白表达能显著降低高糖刺激下TCMK-1细胞炎症相关因子TNF-α、IL-1β及CCL2 m RNA相对表达量(P<0.05)。结论利拉鲁肽通过调控HSP70-TLR4轴活性抑制DN肾小管炎症性损伤,继而抑制DN病程进展。
