采用乙二胺、乙烯磺酸钠和癸酸等为主要原料,在低温常压下,经过加成、酰化等反应,合成了一种新的Gem in i(双子)表面活性剂——N,N’-双癸酰基乙二胺二乙磺酸钠,以1H NMR和IR进行结构表征,考察了原料的物料比、反应温度、反应时间等工...采用乙二胺、乙烯磺酸钠和癸酸等为主要原料,在低温常压下,经过加成、酰化等反应,合成了一种新的Gem in i(双子)表面活性剂——N,N’-双癸酰基乙二胺二乙磺酸钠,以1H NMR和IR进行结构表征,考察了原料的物料比、反应温度、反应时间等工艺条件对产物收率的影响。结果表明,最佳合成条件:以水和丙酮混合溶液作溶剂,中间体与癸酰氯的摩尔比为1∶2.1,反应温度10℃,反应时间5 h。展开更多
[Objectives] To study the effect of PPARγ agonist DA on the cognitive function of AD mice as well as the mechanism.[Methods]50 Kunming male mice were randomly divided into normal control group,model group and decanoi...[Objectives] To study the effect of PPARγ agonist DA on the cognitive function of AD mice as well as the mechanism.[Methods]50 Kunming male mice were randomly divided into normal control group,model group and decanoic acid administration group,the AD mice model was established by subcutaneous injection of D-galactose for 8 weeks,and the treatment group was administered orally with different doses of decanoic acid( low dose of 50 mg/kg,middle dose of 100 mg/kg,high dose of 200 mg/kg). After 8 weeks,the Morris water maze was used to detect the learning and memory capability of mice; HE staining was used to observe the morphological change of hippocampal cells in brain tissue; Western-blot and immunohistochemistry technique were used to detect the expression of PPARγ and Aβ42 protein in brain tissue; the ELISA method was used for the determination of TNF-α and i NOS level in serum. [Results]Morris water maze results showed that DA could significantly improve the learning and memory function in AD mice( P < 0. 05); HE staining showed that DA could significantly reduce degeneration in hippocampal cells; Western-blot and immunohistochemistry results showed that DA could promote the expression of PPARγ and reduce the expression of Aβ42 in brain tissue( P < 0. 05); ELISA results showed that the TNF-α,i NOS levels decreased in AD mice serum after DA treatment( P < 0. 05). [Conclusions] DA could significantly improve the cognitive function of AD mice,improve the degeneration of hippocampal cells in brain tissue,and decrease the expression of Aβ42 in brain tissue. The mechanism might be related to activation of PPARγ protein and down-regulation of expression of relevant inflammatory factors.展开更多
文摘采用乙二胺、乙烯磺酸钠和癸酸等为主要原料,在低温常压下,经过加成、酰化等反应,合成了一种新的Gem in i(双子)表面活性剂——N,N’-双癸酰基乙二胺二乙磺酸钠,以1H NMR和IR进行结构表征,考察了原料的物料比、反应温度、反应时间等工艺条件对产物收率的影响。结果表明,最佳合成条件:以水和丙酮混合溶液作溶剂,中间体与癸酰氯的摩尔比为1∶2.1,反应温度10℃,反应时间5 h。
基金Supported by Guangxi Experimental Animal Resource Sharing Platform Construction Project(2060499)
文摘[Objectives] To study the effect of PPARγ agonist DA on the cognitive function of AD mice as well as the mechanism.[Methods]50 Kunming male mice were randomly divided into normal control group,model group and decanoic acid administration group,the AD mice model was established by subcutaneous injection of D-galactose for 8 weeks,and the treatment group was administered orally with different doses of decanoic acid( low dose of 50 mg/kg,middle dose of 100 mg/kg,high dose of 200 mg/kg). After 8 weeks,the Morris water maze was used to detect the learning and memory capability of mice; HE staining was used to observe the morphological change of hippocampal cells in brain tissue; Western-blot and immunohistochemistry technique were used to detect the expression of PPARγ and Aβ42 protein in brain tissue; the ELISA method was used for the determination of TNF-α and i NOS level in serum. [Results]Morris water maze results showed that DA could significantly improve the learning and memory function in AD mice( P < 0. 05); HE staining showed that DA could significantly reduce degeneration in hippocampal cells; Western-blot and immunohistochemistry results showed that DA could promote the expression of PPARγ and reduce the expression of Aβ42 in brain tissue( P < 0. 05); ELISA results showed that the TNF-α,i NOS levels decreased in AD mice serum after DA treatment( P < 0. 05). [Conclusions] DA could significantly improve the cognitive function of AD mice,improve the degeneration of hippocampal cells in brain tissue,and decrease the expression of Aβ42 in brain tissue. The mechanism might be related to activation of PPARγ protein and down-regulation of expression of relevant inflammatory factors.
