中南大学学报(医学版)
中南大學學報(醫學版)
중남대학학보(의학판)
JOURNAL OF CENTRAL SOUTH UNIVERSITY (MEDICAL SCIENCES)
2011年
10期
964-971
,共8页
李健哲%彭军%王晨静%邓汉武%李元建
李健哲%彭軍%王晨靜%鄧漢武%李元建
리건철%팽군%왕신정%산한무%리원건
降钙素基因相关肽%异丙肾上腺素%心肌细胞%凋亡%活性氧%microRNA-1%microRNA-133a
降鈣素基因相關肽%異丙腎上腺素%心肌細胞%凋亡%活性氧%microRNA-1%microRNA-133a
강개소기인상관태%이병신상선소%심기세포%조망%활성양%microRNA-1%microRNA-133a
calcitonin gene-related peptide%isoprenaline%cardiomyocyte%apoptosis%reactive oxygen species%microRNA-1%microRNA-133a
目的:探讨降钙素基因相关肽(CGRP)对心肌细胞凋亡的抑制作用及其潜在的机制.方法:异丙肾上腺素(10-5 mol/L)孵育48 h以诱导体外培养的大鼠心肌细胞凋亡,不同浓度的CGRP(10ˉ8或10-7mol/L)在异丙肾上腺素孵育前1h给药.药物处理结束后,检测心肌细胞凋亡率和细胞内活性氧的水平以及microRNA-1和microRNA-133a表达的变化.结果:异丙肾上腺素能显著增加心肌细胞的凋亡和细胞内活性氧的产生,同时伴随着microRNA-1表达的上调和microRNA-133a表达的下调,预先给予CGRP可显著抑制异丙肾上腺素的上述效应,但CGRP的有益效应可被CGRP受体拮抗剂所取消.结论:CGRP可抑制异丙肾上腺素诱导的心肌细胞凋亡,其机制可能与抑制活性氧的产生进而调节microRNA-1和microRNA-133a的表达有关.
目的:探討降鈣素基因相關肽(CGRP)對心肌細胞凋亡的抑製作用及其潛在的機製.方法:異丙腎上腺素(10-5 mol/L)孵育48 h以誘導體外培養的大鼠心肌細胞凋亡,不同濃度的CGRP(10ˉ8或10-7mol/L)在異丙腎上腺素孵育前1h給藥.藥物處理結束後,檢測心肌細胞凋亡率和細胞內活性氧的水平以及microRNA-1和microRNA-133a錶達的變化.結果:異丙腎上腺素能顯著增加心肌細胞的凋亡和細胞內活性氧的產生,同時伴隨著microRNA-1錶達的上調和microRNA-133a錶達的下調,預先給予CGRP可顯著抑製異丙腎上腺素的上述效應,但CGRP的有益效應可被CGRP受體拮抗劑所取消.結論:CGRP可抑製異丙腎上腺素誘導的心肌細胞凋亡,其機製可能與抑製活性氧的產生進而調節microRNA-1和microRNA-133a的錶達有關.
목적:탐토강개소기인상관태(CGRP)대심기세포조망적억제작용급기잠재적궤제.방법:이병신상선소(10-5 mol/L)부육48 h이유도체외배양적대서심기세포조망,불동농도적CGRP(10ˉ8혹10-7mol/L)재이병신상선소부육전1h급약.약물처리결속후,검측심기세포조망솔화세포내활성양적수평이급microRNA-1화microRNA-133a표체적변화.결과:이병신상선소능현저증가심기세포적조망화세포내활성양적산생,동시반수착microRNA-1표체적상조화microRNA-133a표체적하조,예선급여CGRP가현저억제이병신상선소적상술효응,단CGRP적유익효응가피CGRP수체길항제소취소.결론:CGRP가억제이병신상선소유도적심기세포조망,기궤제가능여억제활성양적산생진이조절microRNA-1화microRNA-133a적표체유관.
Objective To explore the inhibitory effect of calcitonin gene-related peptide (CGRP) on cardiomyocyte apoptosis and the underlying mechanism.Methods In cultured rat cardiomyocytes,apoptosis was induced by the incubation of isoprenaline ( 10ˉ5 mol/L) for 48 h.CGRP ( 10ˉ8 or 10ˉ7 mol/L) was administrated for 1 h before incubating isoprenaline to evaluate its effect on cardiomyocyte apoptosis.At the end of the drug treatment,the rate of apoptotic cells and intracellular reactive oxygen species (ROS) were determined,and RNA was extracted to examine the expression of microRNA-1 and microRNA-133a.Results Isoprenaline significantly increased the rate of apoptotic cells and intracellular ROS production concomitantly with the increased microRNA-1 expression and the decreased microRNA-133a expression,which were inhibited by pretreatment with CGRP.The effects of CGRP were reversed by CGRP receptor antagonist.Conclusion CGRP can inhibit the isoprenaline-induced cardiomyocyte apoptosis.The beneficial effect of CGRP is related to regulating microRNA-1 and microRNA-133a expression through the prevention of isoprenaline-induced ROS production.