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Oxymatrine on Hsp90a expression and apoptosis in a model of lung ischemia-reperfusion injury

  • Authors:
    • Bing Zhu
    • Jianru Yang
    • Sifeng Chen
    • Pei Zhang
    • Lin Shen
    • Xiaolong Li
    • Jing Li
  • View Affiliations / Copyright

    Affiliations: Department of Cardiothoracic Surgery, The Second Affiliated Hospital of Chongqing Medical University, Chongqing 400010, P.R. China, Central Laboratory of Handan Infectious Diseases Hospital, Handan, Hebei 056002, P.R. China
    Copyright: © Zhu et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
  • Pages: 1381-1385
    |
    Published online on: February 3, 2017
       https://doi.org/10.3892/etm.2017.4098
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Abstract

The protective effects of oxymatrine (OMT) on apoptosis and heat shock protein 90a (Hsp90a) expression in a rabbit model of lung ischemia‑reperfusion injury (LIRI) were investigated. The model of LIRI was established in rabbits and they were randomly divided into two groups: The control group (group C, n=10), and experimental group (further divided into groups E1, n=10; and group E2, n=10), to measure the levels of malondialdehyde (MDA) and superoxide dismutase (SOD) activity in lung tissue homogenates at several time points (T0, 0 min; T1, 60 min; T2, 120 min; T3, 180 min; and T4, 240 min), and to measures changes in lung tissue wet/dry weight ratio (W/D), apoptosis index (AI), and Hsp90a expression and organization at T2, T3 and T4. Comparing group C with groups E1 and E2, the levels of SOD activity and MDA were not significantly different at T0 and T1 (P>0.05); W/D ratio and AI were significantly higher than in groups E1 and E2 (P<0.05, P<0.01); 120 min after LIR, MDA, W/D ratio, and AI were lower than in groups E1 and E2 (P<0.05, P<0.01). MDA, W/D ratio and AI were lower in E2 than in E1 (P<0.05), and SOD and Hsp90a expression increased (P<0.05). The ultrastructure in group E showed less injury compared with group C. In conclusion, by scavenging oxygen free radicals, OMT can inhibit apoptosis, increase Hsp90a expression, and reduce the injury caused by lung ischemia reperfusion.
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Copy and paste a formatted citation
Spandidos Publications style
Zhu B, Yang J, Chen S, Zhang P, Shen L, Li X and Li J: Oxymatrine on Hsp90a expression and apoptosis in a model of lung ischemia-reperfusion injury. Exp Ther Med 13: 1381-1385, 2017.
APA
Zhu, B., Yang, J., Chen, S., Zhang, P., Shen, L., Li, X., & Li, J. (2017). Oxymatrine on Hsp90a expression and apoptosis in a model of lung ischemia-reperfusion injury. Experimental and Therapeutic Medicine, 13, 1381-1385. https://doi.org/10.3892/etm.2017.4098
MLA
Zhu, B., Yang, J., Chen, S., Zhang, P., Shen, L., Li, X., Li, J."Oxymatrine on Hsp90a expression and apoptosis in a model of lung ischemia-reperfusion injury". Experimental and Therapeutic Medicine 13.4 (2017): 1381-1385.
Chicago
Zhu, B., Yang, J., Chen, S., Zhang, P., Shen, L., Li, X., Li, J."Oxymatrine on Hsp90a expression and apoptosis in a model of lung ischemia-reperfusion injury". Experimental and Therapeutic Medicine 13, no. 4 (2017): 1381-1385. https://doi.org/10.3892/etm.2017.4098
Copy and paste a formatted citation
x
Spandidos Publications style
Zhu B, Yang J, Chen S, Zhang P, Shen L, Li X and Li J: Oxymatrine on Hsp90a expression and apoptosis in a model of lung ischemia-reperfusion injury. Exp Ther Med 13: 1381-1385, 2017.
APA
Zhu, B., Yang, J., Chen, S., Zhang, P., Shen, L., Li, X., & Li, J. (2017). Oxymatrine on Hsp90a expression and apoptosis in a model of lung ischemia-reperfusion injury. Experimental and Therapeutic Medicine, 13, 1381-1385. https://doi.org/10.3892/etm.2017.4098
MLA
Zhu, B., Yang, J., Chen, S., Zhang, P., Shen, L., Li, X., Li, J."Oxymatrine on Hsp90a expression and apoptosis in a model of lung ischemia-reperfusion injury". Experimental and Therapeutic Medicine 13.4 (2017): 1381-1385.
Chicago
Zhu, B., Yang, J., Chen, S., Zhang, P., Shen, L., Li, X., Li, J."Oxymatrine on Hsp90a expression and apoptosis in a model of lung ischemia-reperfusion injury". Experimental and Therapeutic Medicine 13, no. 4 (2017): 1381-1385. https://doi.org/10.3892/etm.2017.4098
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