人参皂甙Rb1对肺缺血-再灌注损伤细胞凋亡及其调控基因表达的影响

目的:探讨人参皂甙Rb1对肺缺血再灌注(I/R)损伤细胞凋亡及其调控基因Bcl2、Bax表达的影响。方法:应用兔单肺原位热I/R模型,将24只健康家兔随机分为假手术组(S组)、I/R组及人参皂甙Rb1治疗组(Rb1组);I/R组行左肺缺血60min、再灌注120min,Rb1组在行左肺I/R前静脉给予人参皂甙Rb120mg/kg。应用末端脱氧核苷酸转移酶介导的dUTP缺口末端标记法(TUNEL)检测肺凋亡细胞,免疫组化法检测Bcl2、Bax基因表达,并利用图像分析系统进行定量分析。结果:I/R组及Rb1组细胞凋亡指数(AI)均明显高于S组(P均<0.01),Rb1组AI较I/R组明显降低(P<0.01)。I/R组及Rb1组Bcl2、Bax表达均较S组显著增加(P均<0.01),Rb1组Bcl2表达虽高于I/R组,但差异无显著性(P>0.05);Rb1组Bax表达明显低于I/R组(P<0.05)。Rb1组Bcl2/Bax比值显著高于I/R组(P<0.05),与S组较接近。结论:人参皂甙Rb1能抑制肺I/R的促凋亡基因Bax表达,但不影响抑制凋亡基因Bcl2表达的上调,可使Bcl2/Bax比值增加,从而减少细胞凋亡,减轻肺I/R损伤。

Effects of ginsenoside Rb1 on apoptosis and Bcl-2, Bax gene expression in rabbits with lung ischemia/reperfusion injury

Objective: To investigate the effect of ginsenoside Rb1 on apoptosis and Bcl2, Bax gene expression in rabbits with lung ischemia/reperfusion(I/R) injury. Methods: The rabbit model of single lung in situ warm I/R was established. Twentyfour healthy rabbits were randomly divided into three groups (n=8 in each group). The shamoperation group (S group) did not receive I/R injury. The I/R group received ischemia (60 minutes) and reperfusion (120 minutes ) in the left lung. The ginsenoside Rb1 group(Rb1 group) received ginsenoside Rb1 20 mg/kg intravenous injection before I/R. The lung apoptotic cells were detected by the terminal deoxynucleotidyl transferasemediated dUTP nick end labeling (TUNEL) technique. The gene expressions of Bcl2 and Bax were studied by immunohistochemical staining, and the mean optical density values of the positive fields of protein expression were quantitatively examined by image analysis system. Results: The apoptosis indexes (AI) of lung cells in I/R group and Rb1 group were significantly higher than that in S group (both P<0.01). The AI in Rb1 group was much more reduced than that in I/R group (P<0.01). The gene expressions of Bcl2 and Bax were increased significantly in I/R group and Rb1 group compared with that in S group (both P<0.01). There was no significant difference in Bcl2 gene expression between I/R and Rb1 group (P>0.05), but the expression of Bax was decreased more significantly in Rb1 group than that in I/R group (P<0.05). The expression ratio of Bcl2/Bax in Rb1 group was more significantly increased than that in I/R group(P<0.05), and meanwhile it was close to that of the S group. Conclusion: Ginsenoside Rb1 can significantly inhibit the gene expression of Bax that is the apoptosisimproving gene, but it does not influence the gene expression of Bcl2, that is the apoptosis inhibiting gene. Therefore, it can increase the ratio of Bcl2/Bax and inhibit the apoptosis in lung I/R injury.