摘要
目的研究对乙酰氨基酚(acetaminophen,APAP)对H2O2引起的心肌细胞损伤的保护作用。方法原代SD大鼠乳鼠心肌细胞培养,48h后加入H2O2造成心肌细胞损伤,损伤前1h加入不同浓度的APAP作为保护剂。损伤6h后,甲基四唑蓝比色(MTT)法测定线粒体脱氢酶活性,试剂盒测定培养液中乳酸脱氢酶(LDH)活性、心肌细胞中脂质过氧化产物丙二醛(MDA)含量、超氧化物歧化酶(SOD)活性、Caspase-3活性。结果H2O2能明显造成心肌细胞损伤,表现为:细胞活力降低、LDH活性增加、MDA含量增加、SOD活性下降、caspase-3活性增高;20μmol·L-1、60μmol.L-1、180μmol·L-1的APAP对H2O2引起的心肌细胞损伤有保护作用,并随浓度增加保护作用加强。结论APAP能减轻H2O2对心肌细胞的损伤作用,抑制H2O2引起的培养心肌细胞凋亡。
Objective The purpose of this investigation was to determine the role of aeetaminophen on cultured neonatal rat eardiae myocytes injured by H2O2. Methods Cultured neonatal rat cardiac myoeytes were pretreated with aeetaminophen (20μmol · L^-1 , 60 μmol · L^-1 and 180 μmol · L^-1 ) for I h before treated with H2O2 (0.2 mmol · L^-1 ) for 6 h. The activity of dehydrogenase in mitochondria was detected by MTT assay. The activity of LDH, content of MDA, activity of SOD and easpase - 3 were determined by LDH, MDA, SOD and easpase - 3 kit. Results The descent of the activity of dehydrogenase in mitoehondria detected by (MTT), the increase of LDH in culture medium, the elevation of MDA and the increase activity of easpase -3 induced by treatment of H2O2 were significantly reversed by aeetaminophen. The effect of aeetaminophen was increased with the rising of its concentration. Conclusions Aeetaminophen could decrease the injury of eardiomyoeytes induced by H2 O2, inhibit the apoptosis of eardiomyoeytes induced by H2O2, and this eardioproteetive effect may be related to the antioxidant nature of the drug.
出处
《辽宁医学院学报》
CAS
2008年第3期206-209,共4页
Journal of Liaoning Medical University (LNMU) Bimonthly