摘要
目的观察二氢石蒜碱(dihydrolycorine,DL)对Wistar大鼠的乳鼠培养心肌细胞缺氧/复氧损伤(H/R)的保护作用。方法采用培养的Wistar乳鼠的心肌细胞,建立H/R损伤模型,检测指标包括:①心肌细胞存活率;②超氧化物歧化酶(SOD)活性;③丙二醛(MDA)含量;④乳酸脱氢酶(LDH)活性。结果模型组缺氧后心肌细胞存活率降低,复氧后进一步下降,各个时间点细胞内SOD活性下降,MDA含量升高,乳酸脱氢酶(LDH)活性升高,与正常组比较差异具有显著性(P<0.01);在DL1、10、100μmol·L-1组,随着给药浓度的增加,细胞存活率升高,LDH活性变低,MDA含量逐渐趋于恢复正常,SOD活性逐渐回升,表明经DL干预之后,心肌细胞抗损伤能力加强,发生损伤的程度减轻。结论DL对培养的乳鼠心肌细胞H/R损伤具有保护作用,其作用在一定范围内呈剂量依赖关系,机制可能与其阻断α、β受体、抑制心肌细胞脂质过氧化反应有关。
Aim To investigate the protective effects of dihydrolycorine on hypoxia/reoxygenation (H/R) injury in cultured neonatal rat cardiomyocytes. Methods The hypoxia/ reoxygenation injury model of cultured neonatal rat cardiomyocytes was developed. The cell livability, the activity of lactate dehdrogenase (LDH) and superoxide dismutase (SOD) , and the content of malondialdehyde (MDA) were determined in the cultured neonatal rat cardiomyocytes injured by H/R. Resuits Compared with normal group, the cell livability and the SOD activity of model group were decreased respectively, whereas the activity of LDH and the contentof MDA of model group were increased significantly ( P 〈0. 01 ). In cardiomyocytes injured by H/R that were treated with 1 ~100μmol· L^-1 dihydrolycorine, LDH release and MDA content were decreased, while cell livability and SOD activity were enhanced in dose-dependent manner (P〈0. 01). Conclusion dihydrolycorine has protective effects on the cultured neonatal rat cardiomyocytes injured by H/R. the mechanisms are related to its antioxidation effects.
出处
《中国药理学通报》
CAS
CSCD
北大核心
2005年第8期999-1002,共4页
Chinese Pharmacological Bulletin