【摘要】：[目的]研究200ug/ml晚期糖基化終產(chǎn)物(advanced glycation end products, AGEs)對體外培養(yǎng)的人臍靜脈細胞(human umbilical vein endothelial cells, HUVEC)增殖與凋亡的影響,以及10nmol/ml吡格列酮的干預作用,并探討該作用的可能機制。[方法]1)取體外培養(yǎng)的人臍靜脈內(nèi)皮細胞第2代進行試驗。2)實驗分組：1.空白對照組；2.晚期糖基化終產(chǎn)物組每毫升培養(yǎng)基內(nèi)加入200ug晚期糖基化終產(chǎn)物,作用24小時；3.吡格列酮組每毫升培養(yǎng)基內(nèi)加入10nmol比格列酮,預處理24小時；4.吡格列酮加晚期糖基化終產(chǎn)物組每毫升培養(yǎng)基內(nèi)先加入10nmol吡格列酮預處理24小時,再加入200ug晚期糖基化終產(chǎn)物作用24小時。3)采用CCK-8檢測96孔板內(nèi)細胞的吸光值(0D),評價各組細胞的增殖活性,每組重復5個孔。采用凋亡試劑盒檢測各組細胞凋亡情況,每組重復三個孔。[結(jié)果]1)與對照組相比,吡格列酮組細胞增殖無明顯變化,AGEs組與AGEs-吡格列酮組細胞增殖明顯減少,但AGEs+吡格列酮組較單純的AGEs組細胞增殖多。2)與對照組相比,吡格列酮組細胞凋亡無明顯變化,AGEs組與AGEs+吡格列酮組細胞凋亡明顯增多,但單純AGEs組細胞凋亡更多。3)正常條件下,內(nèi)皮細胞A20表達水平很低,AGEs刺激后A20表達顯著升高,但給予毗格列酮10nmol/L預處理后A20表達水平減低。[結(jié)論]AGEs可抑制HUVECs增殖,毗格列酮預處理后可減少AGEs誘導的增殖抑制。AGEs可誘導HUVECs凋亡,吡格列酮預處理后可抑制AGEs誘導的細胞凋亡。吡格列酮抑制AGEs誘導的HUVECs的凋亡可能是通過抑制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.
【學位授予單位】：揚州大學
【學位級別】：碩士
【學位授予年份】：2015
【分類號】：R587.2

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