摘要
目的:探讨三七皂甙Rg1对心肌细胞缺血/再灌注(I/R)损伤的作用。方法:分离培养SD乳鼠心肌细胞,建立I/R模型。分组:①正常对照组;②I/R组:缺氧2h,复氧1h;③Rg1治疗组:在缺氧前24h予三七皂甙Rg-1;④ST+Rg1治疗组:在缺氧前24h予Rg-1及缺氧前1h予蛋白激酶C特异性阻断剂Staurosporine(ST)。计算心肌细胞锥虫蓝摄取率、测定细胞内游离钙、细胞凋亡率(流式细胞法)。结果:锥虫蓝摄取率、细胞内游离钙、细胞凋亡率分别为:正常对照组为(2.3±0.3)%、(117.1±14.3)%、(2.6±0.4)%;I/R组为(21.5±2.0)%、(355.3±31.9)%、(20.1±2.3)%;Rg1治疗组为(9.8±0.9)%,(179.5±11.3),(10.4±0.94)%;ST+Rg1治疗组为(16.2±1.7)%、(294.7±18.5)%、(15.9±2.8)%。3项检测数据I/R组明显高于各组(P<0.05);Rg1治疗组明显低于I/R组(P<0.05)和高于正常对照组(P<0.05);ST+Rg1治疗组明显高于Rg1组(P<0.05)。结论:细胞死亡、细胞凋亡、钙超载参与了心肌I/R损伤;三七总甙Rg1可减少SD乳鼠心肌细胞I/R的损伤;三七总甙Rg1的抗I/R损伤的作用可能通过激活蛋白激酶C途径。
Objective： To investigate the effects of panax notoginsenoside Rg1 on cardiomyocytes injury induced by ischemiareperfusion in neonatal SD rat. Methods： The cultured neonatal SD rat cardiomyocytes were divided into four groups： control group, ischemia-reperfusion group （I/R）： deoxygenation for 2 h and reoxygenation for 1 h, Rg1 group： administered panax notoginsenoside Rg1 before degxygenation for 24 h, ST ＋ Rg1 group： administered Staurosporine before deoxygenation for 1 hour in Rg1 group. The trypan blue absorbance, [Ca^2＋]i and apoptosis rate were detected. Results： The trypan blue uptake, change ratio of [Ca^2＋]i and apoptosis rate were （2.3 ± 0.3）%, （117.1 ± 14.3）%, （2.6 ± 0.4）% in control group; （21.5 ± 2.0）%, （355.3 ± 31.9）%, （20.1 ± 2.3）% in I/R group; （9.8 ± 0.9）%, （179.5 ± 11.3）%, （10.4 ± 0.94）% in Rg1 group; （16.2 ± 1.7）%,（294.7 ± 18.5）%,（15.9 ±2.8）% in ST ＋ Rg1 group. There were statistical differences between I/R group and every other group （P 〈 0.05）, between Rg1 group and control group （P 〈 0.05）, between ST ＋ Rg1 and Rg1 group （P 〈 0.05）. Conclusion, Myocardial death, apoptosis and Ca^2＋ overload are involved in ischemia-reperfusion injury, and panax notoginsenoside can protect neonatal SD rat cardiomyocytes from ischemiareperfusion injury. The protective effects may be mediated by PKC pathway.
出处
《南京医科大学学报（自然科学版）》
CAS
CSCD
北大核心
2006年第4期242-245,F0003,共5页
Journal of Nanjing Medical University(Natural Sciences)
基金
江苏省科技厅基金资助项目(BS2000044)
关键词
心肌细胞
缺血
再灌注损伤
三七皂甙
游离钙
凋亡
cardiomyocytes
ischemia-reperfusion injury
panax notoginsenoside
[Ca^2＋]i
apoptosis
