中华神经医学杂志
中華神經醫學雜誌
중화신경의학잡지
CHINESE JOURNAL OF NEUROMEDICINE
2011年
8期
779-783
,共5页
黎雪松%朱元昌%倪膺佳%刘冠杰%韦建鸽%钟鸣%刘誉
黎雪鬆%硃元昌%倪膺佳%劉冠傑%韋建鴿%鐘鳴%劉譽
려설송%주원창%예응가%류관걸%위건합%종명%류예
阿尔茨海默病%晚期糖基化终产物%SH-SY5Y细胞
阿爾茨海默病%晚期糖基化終產物%SH-SY5Y細胞
아이자해묵병%만기당기화종산물%SH-SY5Y세포
Alzheimer disease%Advanced glycation end product%SH-SYSY cell
目的 研究晚期糖基化终产物(AGEs)对人神经母细胞瘤SH-SY5Y细胞株增殖、凋亡以及AD相关mRNA的影响。 方法 利用小牛血清白蛋白(BSA)和葡萄糖体外制备BSA-AGEs;将SH-SY5Y细胞与不同浓度BSA-AGEs保温后,MTT法测定SH-SY5Y细胞的增殖率,流式细胞仪测定细胞凋亡和细胞周期的变化,RT-PCR检测细胞中AD相关mRNA的表达水平。 结果 BSA-AGEs对SH-SY5Y细胞增殖有明显抑制作用,明显促进神经元的凋亡,细胞周期被阻滞于G1/G0期,呈药物浓度依赖性。RT-PCR结果表明,经过BSA-AGEs刺激后,IL-6、高迁移率族蛋白B1(HMGB1)、淀粉先质蛋白(APLP1) mRNA表达水平均明显升高。 结论 BSA-AGEs能有效抑制SH-SY5Y细胞的增殖,促进炎症细胞因子产生,诱导细胞凋亡,提示AGEs在AD的发生与发展过程中具有促进作用。
目的 研究晚期糖基化終產物(AGEs)對人神經母細胞瘤SH-SY5Y細胞株增殖、凋亡以及AD相關mRNA的影響。 方法 利用小牛血清白蛋白(BSA)和葡萄糖體外製備BSA-AGEs;將SH-SY5Y細胞與不同濃度BSA-AGEs保溫後,MTT法測定SH-SY5Y細胞的增殖率,流式細胞儀測定細胞凋亡和細胞週期的變化,RT-PCR檢測細胞中AD相關mRNA的錶達水平。 結果 BSA-AGEs對SH-SY5Y細胞增殖有明顯抑製作用,明顯促進神經元的凋亡,細胞週期被阻滯于G1/G0期,呈藥物濃度依賴性。RT-PCR結果錶明,經過BSA-AGEs刺激後,IL-6、高遷移率族蛋白B1(HMGB1)、澱粉先質蛋白(APLP1) mRNA錶達水平均明顯升高。 結論 BSA-AGEs能有效抑製SH-SY5Y細胞的增殖,促進炎癥細胞因子產生,誘導細胞凋亡,提示AGEs在AD的髮生與髮展過程中具有促進作用。
목적 연구만기당기화종산물(AGEs)대인신경모세포류SH-SY5Y세포주증식、조망이급AD상관mRNA적영향。 방법 이용소우혈청백단백(BSA)화포도당체외제비BSA-AGEs;장SH-SY5Y세포여불동농도BSA-AGEs보온후,MTT법측정SH-SY5Y세포적증식솔,류식세포의측정세포조망화세포주기적변화,RT-PCR검측세포중AD상관mRNA적표체수평。 결과 BSA-AGEs대SH-SY5Y세포증식유명현억제작용,명현촉진신경원적조망,세포주기피조체우G1/G0기,정약물농도의뢰성。RT-PCR결과표명,경과BSA-AGEs자격후,IL-6、고천이솔족단백B1(HMGB1)、정분선질단백(APLP1) mRNA표체수평균명현승고。 결론 BSA-AGEs능유효억제SH-SY5Y세포적증식,촉진염증세포인자산생,유도세포조망,제시AGEs재AD적발생여발전과정중구유촉진작용。
Objective To study the effect of advanced glycation end products (AGEs) on the proliferation, cell cycle and apoptosis of SH-SY5Y cells, and the mRNA expression of AD related protiens. Methods Bovine serum albumin-AGEs (BSA-AGEs) were prepared by incubation of BSA with glucose in vitro. SH-SY5Y cells were incubated with different concentrations of BSA-AGEs. Cell proliferation was measured by MTT assay; cell cycle and apoptosis were determined by flow cytometry; mRNA levels of APLP1, IL-6 and HMGB-1 were determined by RT-PCR. Results After incubation with BSA-AGEs for 48 h, SH-SYSY cell proliferation was significantly inhibited and cell apoptosis was induced; the cells were found to be arrested at G1/G0; these effects were dose-dependent. RT-PCR results showed that mRNA levels of IL-6, APLP1 and HMGB-1 were significantly up-regulated. Conclusion BSA-AGEs inhibit the cell proliferation and induce the apoptosis of SH-SY5Y cells, and stimulate the expression of some pro-inflammatory cytokines, suggesting a possible important role of AGEs in pathogenesis and development of AD.