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作 者:杨征[1] 邱敏[2] 郭晓华[1] 李俊萍[1] 陈丽珠[1] 孙淑艳[1]
机构地区:[1]包头医学院第一附属医院心内二科,内蒙古包头市014010 [2]包头医学院药学院,内蒙古包头市014060
出 处:《中国动脉硬化杂志》2012年第10期899-902,共4页Chinese Journal of Arteriosclerosis
摘 要:目的研究瓜蒌皮提取物对血小板源生长因子BB所致血管平滑肌细胞增殖周期的影响并探讨其可能机制。方法组织块贴块法培养SD大鼠胸主动脉平滑肌细胞,3H-TdR掺入观察瓜蒌皮提取物(10、20和30mg/L)对血小板源生长因子BB(20μg/L)所致血管平滑肌细胞DNA合成的影响;流式细胞仪分析细胞增殖周期;real time RT-PCR检测血管平滑肌细胞中c-fos、c-myc mRNA表达。结果血小板源生长因子BB可明显升高细胞每分钟脉冲数(P<0.01),并增加S期细胞比例而降低G0/G1期细胞比例(P<0.01),并上调c-fos、c-myc mRNA表达(P<0.01)。瓜蒌皮提取物各浓度组均明显抑制血小板源生长因子BB诱导的每分钟脉冲数升高(P<0.01),降低S期细胞比例而升高G0/G1期细胞比例,明显下调血小板源生长因子BB所致的c-fos、c-myc mRNA高表达(P<0.01)。结论瓜蒌皮提取物通过阻止血管平滑肌细胞由G0/G1期进入S期而抑制血小板源生长因子BB所致的增殖,其作用机制可能与降低细胞内c-fos、c-myc mRNA高表达有关。Aim To investigate the effect of extractive of pericarpium trichosanthis (EPT) on cell cycle of rat vascular smooth muscle (VSMC) proliferation induced by platelet-derived growth factor-BB (PDGF-BB) and to probe es- pecially into its mechanism. Methods VSMC from the thoracic aorta of SD rats were cultured by tissue explant meth- od. Effect of EPT ( 10, 20 and 30 mg/L) on PDGF-BB-induced VSMC proliferation was assessed by 3H-TdR method, the cell cycle was analyzed by flow cytometry, expression of c-fos and c-myc mRNA in VSMC were detected by real-time quantitative reverse transcription-polymerase chain reaction (real-time RT-PCR). Results PDGF-BB could signifi- cantly increase the rate of ^3 H-TdR incorporation (P 〈 0. 01 ) and the percentage of S phase cells, and degrade the G0/G1 phase cell percentage in the cell cycle ( P 〈 0. 01 ). At the same time, PDGF-BB could up-regulate c-fos and c-myc mR- NA expression (P 〈 0. 01 ). Addition of EPT ( 10, 20 and 30 mg/L) markedly inhibited the PDGF-BB-induced prolifera- tion of the VSMC (P 〈 0. 01 ), decreased the S phase cell percentage and upgraded the G0/G1 phase cell percentage in the cell cycle, EPT could also depress the elevated expression of c-fos and c-myc mRNA indcued by PDGF-BB. Conclu- sions EPT could inhibit the VSMC proliferation induced by PDGF-BB through preventing the transformation of the G0/G1 phase cell to S phase cell in the cell cycle. The mechanism may be related to its down-regulatory effect on c-fos and c- myc mRNA expressions.
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