吡格列酮在晚期糖基化终产物抑制内皮细胞增殖与促凋亡中的保护作用及机制
发布时间：2018-10-13 07:36
【摘要】：[目的]研究200ug/ml晚期糖基化终产物(advanced glycation end products, AGEs)对体外培养的人脐静脉细胞(human umbilical vein endothelial cells, HUVEC)增殖与凋亡的影响,以及10nmol/ml吡格列酮的干预作用,并探讨该作用的可能机制。[方法]1)取体外培养的人脐静脉内皮细胞第2代进行试验。2)实验分组：1.空白对照组；2.晚期糖基化终产物组每毫升培养基内加入200ug晚期糖基化终产物,作用24小时；3.吡格列酮组每毫升培养基内加入10nmol比格列酮,预处理24小时；4.吡格列酮加晚期糖基化终产物组每毫升培养基内先加入10nmol吡格列酮预处理24小时,再加入200ug晚期糖基化终产物作用24小时。3)采用CCK-8检测96孔板内细胞的吸光值(0D),评价各组细胞的增殖活性,每组重复5个孔。采用凋亡试剂盒检测各组细胞凋亡情况,每组重复三个孔。[结果]1)与对照组相比,吡格列酮组细胞增殖无明显变化,AGEs组与AGEs-吡格列酮组细胞增殖明显减少,但AGEs+吡格列酮组较单纯的AGEs组细胞增殖多。2)与对照组相比,吡格列酮组细胞凋亡无明显变化,AGEs组与AGEs+吡格列酮组细胞凋亡明显增多,但单纯AGEs组细胞凋亡更多。3)正常条件下,内皮细胞A20表达水平很低,AGEs刺激后A20表达显著升高,但给予毗格列酮10nmol/L预处理后A20表达水平减低。[结论]AGEs可抑制HUVECs增殖,毗格列酮预处理后可减少AGEs诱导的增殖抑制。AGEs可诱导HUVECs凋亡,吡格列酮预处理后可抑制AGEs诱导的细胞凋亡。吡格列酮抑制AGEs诱导的HUVECs的凋亡可能是通过抑制NF-kB通路起作用的。
[Abstract]:[objective] to study the effect of advanced glycation end product (advanced glycation end products, AGEs) of 200ug/ml on the proliferation and apoptosis of cultured human umbilical vein cells (human umbilical vein endothelial cells, HUVEC) and the intervention of 10nmol/ml pioglitazone, and to explore the possible mechanism of this effect. [methods] 1) the second passage of human umbilical vein endothelial cells (HUVECs) was cultured in vitro. 2) the experimental groups were as follows: 1. Blank control group 2. The advanced glycosylation end product of 200ug was added into the culture medium of late glycosylation end product for 24 hours. Pioglitazone group was pretreated with 10nmol bioglitazone for 24 hours. Pioglitazone plus advanced glycation end product group was pretreated with 10nmol pioglitazone for 24 hours per ml medium. The late glycation end product of 200ug was added for 24 hours. (3) CCK-8 was used to detect the absorptivity (0D) of 96-well intraplate cells, and to evaluate the proliferation activity of the cells in each group. The cells were repeated for 5 holes in each group. Apoptosis test kit was used to detect apoptosis in each group, and three holes were repeated in each group. [results] 1) compared with the control group, the cell proliferation of pioglitazone group did not change significantly, but that of AGEs group and AGEs- pioglitazone group decreased significantly, but the cell proliferation of AGEs pioglitazone group was more than that of AGEs group. 2) compared with the control group, the cell proliferation of pioglitazone group was higher than that of control group. In pioglitazone group, there was no obvious change in cell apoptosis. The apoptosis of AGEs group and AGEs pioglitazone group was significantly increased, but the apoptosis was more in AGEs group.) under normal condition, the expression of A20 in endothelial cells was very low, and the expression of A20 in endothelial cells was significantly increased after AGEs stimulation. However, the expression of A 20 decreased after preconditioning with piglazone 10nmol/L. [conclusion] AGEs can inhibit the proliferation of HUVECs, and pioglitazone can reduce the proliferation inhibition induced by AGEs. AGEs can induce HUVECs apoptosis, and pioglitazone can inhibit AGEs induced apoptosis. Pioglitazone inhibits HUVECs apoptosis induced by AGEs by inhibiting NF-kB pathway.
【学位授予单位】：扬州大学
【学位级别】：硕士
【学位授予年份】：2015
【分类号】：R587.2
[Abstract]:[objective] to study the effect of advanced glycation end product (advanced glycation end products, AGEs) of 200ug/ml on the proliferation and apoptosis of cultured human umbilical vein cells (human umbilical vein endothelial cells, HUVEC) and the intervention of 10nmol/ml pioglitazone, and to explore the possible mechanism of this effect. [methods] 1) the second passage of human umbilical vein endothelial cells (HUVECs) was cultured in vitro. 2) the experimental groups were as follows: 1. Blank control group 2. The advanced glycosylation end product of 200ug was added into the culture medium of late glycosylation end product for 24 hours. Pioglitazone group was pretreated with 10nmol bioglitazone for 24 hours. Pioglitazone plus advanced glycation end product group was pretreated with 10nmol pioglitazone for 24 hours per ml medium. The late glycation end product of 200ug was added for 24 hours. (3) CCK-8 was used to detect the absorptivity (0D) of 96-well intraplate cells, and to evaluate the proliferation activity of the cells in each group. The cells were repeated for 5 holes in each group. Apoptosis test kit was used to detect apoptosis in each group, and three holes were repeated in each group. [results] 1) compared with the control group, the cell proliferation of pioglitazone group did not change significantly, but that of AGEs group and AGEs- pioglitazone group decreased significantly, but the cell proliferation of AGEs pioglitazone group was more than that of AGEs group. 2) compared with the control group, the cell proliferation of pioglitazone group was higher than that of control group. In pioglitazone group, there was no obvious change in cell apoptosis. The apoptosis of AGEs group and AGEs pioglitazone group was significantly increased, but the apoptosis was more in AGEs group.) under normal condition, the expression of A20 in endothelial cells was very low, and the expression of A20 in endothelial cells was significantly increased after AGEs stimulation. However, the expression of A 20 decreased after preconditioning with piglazone 10nmol/L. [conclusion] AGEs can inhibit the proliferation of HUVECs, and pioglitazone can reduce the proliferation inhibition induced by AGEs. AGEs can induce HUVECs apoptosis, and pioglitazone can inhibit AGEs induced apoptosis. Pioglitazone inhibits HUVECs apoptosis induced by AGEs by inhibiting NF-kB pathway.
【学位授予单位】：扬州大学
【学位级别】：硕士
【学位授予年份】：2015
【分类号】：R587.2
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