摘要
目的:观察不同浓度过氧化氢(H2O2)致心肌细胞损伤的作用,探讨心肌细胞凋亡和坏死时HMGB1的表达变化。方法:用H2O2作用于新生SD大鼠心肌细胞,建立心肌细胞损伤模型。观察心肌细胞状态,测定心肌细胞存活率、乳酸脱氢酶(LDH)、超氧化物歧化酶(SOD)浓度,并对心肌细胞用Western blot检测HMGB1。结果:H2O2致心肌细胞过氧化损伤,细胞存活率明显下降(P<0.01),培养液LDH增高(P<0.05),而SOD降低(P<0.05)。Westernblot显示HMGB1在正常对照组和H2O2A组表达量相同,H2O2B组表达量明显增加。结论:心肌细胞凋亡时HMGB1表达正常、死亡时HMGB1表达增加。
Objective:To observe the action of hydrogen peroxide(H2O2) inducing cardiomyocytes over-oxidation injury and to investigate the expression of HMGB1 in apoptosis and necrosis of myocardiocyte. Methods:A model for primary culture of cardiomyocytes injuried by H2O2 was established, the morphology of cardiomyocytes was observed, and cardiomyocytes fraction surviving were measured. The activity of lactate dehydrogenase(LDH), superoxide dismutase(SOD),HMGB1 were assayed. Results: Cardiomyocytes survival rate decreased by H2O2 treatment(P 〈 0.05), and the activity of LDH increased(P 〈 0.05),whereas the activity of SOD decreased(P 〈 0.05). Expression of HMGB1 in H2O2 group A was the same as that in control group, whereas the expression of HMGB1 in H2O2 group B was higher than that in control group and H2O2 group A. Conclusion:The HMGB1 expression increased in the necrosis of cardiomyocytes, while it had no change in the apoptosis of cardiomyocytes.
出处
《南京医科大学学报(自然科学版)》
CAS
CSCD
北大核心
2007年第9期956-959,共4页
Journal of Nanjing Medical University(Natural Sciences)
基金
南京医科大学科技发展基金资助(NJ03048)