Effects of ginsenoside Rb1 on apoptosis and Bcl-2, Bax gene expression in rabbits with lung ischemia/reperfusion injury
Yin Weihu
Abstract
Yin Weihu
Abstract
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 P0.01). The AI in Rb1 group was much more reduced than that in I/R group (P0.01). The gene expressions of Bcl2 and Bax were increased significantly in I/R group and Rb1 group compared with that in S group (both P0.01). There was no significant difference in Bcl2 gene expression between I/R and Rb1 group (P0.05), but the expression of Bax was decreased more significantly in Rb1 group than that in I/R group (P0.05). The expression ratio of Bcl2/Bax in Rb1 group was more significantly increased than that in I/R group(P0.05), 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.
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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 P0.01). The AI in Rb1 group was much more reduced than that in I/R group (P0.01). The gene expressions of Bcl2 and Bax were increased significantly in I/R group and Rb1 group compared with that in S group (both P0.01). There was no significant difference in Bcl2 gene expression between I/R and Rb1 group (P0.05), but the expression of Bax was decreased more significantly in Rb1 group than that in I/R group (P0.05). The expression ratio of Bcl2/Bax in Rb1 group was more significantly increased than that in I/R group(P0.05), 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.
Key concepts: TUNEL assay, Apoptosis, Lung, Ginsenoside, Andrology, Ischemia, Immunohistochemistry, Gene expression