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Translocator Protein 18 kDa Involved in the Cognitive Impairment Induced by Isoflurane Inhalation Anesthesia

Received: 23 August 2016     Accepted: 6 September 2016     Published: 14 October 2016
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Abstract

Background. Translocator protein 18 kDa (TSPO) plays a key role both in microglial activation and neuroinflammation. Postoperative cognitive decline (POCD), a notable hazard to both patients and society, maybe contribute to deficiently controlled neuroinflammatory processes initiated by anesthesia and surgery. So far it is unclear that whether TSPO is involved in the pathogenesis of POCD or not. Materials and Methods. Twelve adult rats and twelve aged rats were divided into control and isoflurane groups respectively. POCD was induced by a 4-hour exposure of 2% isoflurane. The memory retention capability was assessed by the Morris water maze trial, the mRNA and the protein expression of both TSPO and Iba1 were assessed by real-time quantitative PCR and Western Blot analysis separately. Results. Compared to the control group, the latency time to find platform was longer in the groups exposed to isoflurane (p<0.05); the mRNA and the protein expression of both TSPO and Iba1 were correspondingly upregulated (p<0.05); especially that the severity of cognitive decline and the degree of TSPO and Iba1 over-expression were significantly different between the adult and aged rats (p<0.05); The twice times across the platform showed no significant difference among all the groups. Conclusions. Our study for the first time showed that TSPO may be involved in the pathogenesis of the cognitive decline induced by isoflurane anesthesia. Its role for being a biomarker and an interventional target of POCD deserves future investigation.

Published in International Journal of Clinical and Experimental Medical Sciences (Volume 2, Issue 6)
DOI 10.11648/j.ijcems.20160206.11
Page(s) 101-106
Creative Commons

This is an Open Access article, distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution and reproduction in any medium or format, provided the original work is properly cited.

Copyright

Copyright © The Author(s), 2016. Published by Science Publishing Group

Keywords

Postoperative Cognitive Decline (POCD), Translocator Protein 18 kDa (TSPO), Neuroinflammation

References
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  • APA Style

    Rui Zhang, Shanshan Zou, Lingzhong Meng, Ming Ding, Huirong Han. (2016). Translocator Protein 18 kDa Involved in the Cognitive Impairment Induced by Isoflurane Inhalation Anesthesia. International Journal of Clinical and Experimental Medical Sciences, 2(6), 101-106. https://doi.org/10.11648/j.ijcems.20160206.11

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    ACS Style

    Rui Zhang; Shanshan Zou; Lingzhong Meng; Ming Ding; Huirong Han. Translocator Protein 18 kDa Involved in the Cognitive Impairment Induced by Isoflurane Inhalation Anesthesia. Int. J. Clin. Exp. Med. Sci. 2016, 2(6), 101-106. doi: 10.11648/j.ijcems.20160206.11

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    AMA Style

    Rui Zhang, Shanshan Zou, Lingzhong Meng, Ming Ding, Huirong Han. Translocator Protein 18 kDa Involved in the Cognitive Impairment Induced by Isoflurane Inhalation Anesthesia. Int J Clin Exp Med Sci. 2016;2(6):101-106. doi: 10.11648/j.ijcems.20160206.11

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  • @article{10.11648/j.ijcems.20160206.11,
      author = {Rui Zhang and Shanshan Zou and Lingzhong Meng and Ming Ding and Huirong Han},
      title = {Translocator Protein 18 kDa Involved in the Cognitive Impairment Induced by Isoflurane Inhalation Anesthesia},
      journal = {International Journal of Clinical and Experimental Medical Sciences},
      volume = {2},
      number = {6},
      pages = {101-106},
      doi = {10.11648/j.ijcems.20160206.11},
      url = {https://doi.org/10.11648/j.ijcems.20160206.11},
      eprint = {https://article.sciencepublishinggroup.com/pdf/10.11648.j.ijcems.20160206.11},
      abstract = {Background. Translocator protein 18 kDa (TSPO) plays a key role both in microglial activation and neuroinflammation. Postoperative cognitive decline (POCD), a notable hazard to both patients and society, maybe contribute to deficiently controlled neuroinflammatory processes initiated by anesthesia and surgery. So far it is unclear that whether TSPO is involved in the pathogenesis of POCD or not. Materials and Methods. Twelve adult rats and twelve aged rats were divided into control and isoflurane groups respectively. POCD was induced by a 4-hour exposure of 2% isoflurane. The memory retention capability was assessed by the Morris water maze trial, the mRNA and the protein expression of both TSPO and Iba1 were assessed by real-time quantitative PCR and Western Blot analysis separately. Results. Compared to the control group, the latency time to find platform was longer in the groups exposed to isoflurane (p<0.05); the mRNA and the protein expression of both TSPO and Iba1 were correspondingly upregulated (p<0.05); especially that the severity of cognitive decline and the degree of TSPO and Iba1 over-expression were significantly different between the adult and aged rats (p<0.05); The twice times across the platform showed no significant difference among all the groups. Conclusions. Our study for the first time showed that TSPO may be involved in the pathogenesis of the cognitive decline induced by isoflurane anesthesia. Its role for being a biomarker and an interventional target of POCD deserves future investigation.},
     year = {2016}
    }
    

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  • TY  - JOUR
    T1  - Translocator Protein 18 kDa Involved in the Cognitive Impairment Induced by Isoflurane Inhalation Anesthesia
    AU  - Rui Zhang
    AU  - Shanshan Zou
    AU  - Lingzhong Meng
    AU  - Ming Ding
    AU  - Huirong Han
    Y1  - 2016/10/14
    PY  - 2016
    N1  - https://doi.org/10.11648/j.ijcems.20160206.11
    DO  - 10.11648/j.ijcems.20160206.11
    T2  - International Journal of Clinical and Experimental Medical Sciences
    JF  - International Journal of Clinical and Experimental Medical Sciences
    JO  - International Journal of Clinical and Experimental Medical Sciences
    SP  - 101
    EP  - 106
    PB  - Science Publishing Group
    SN  - 2469-8032
    UR  - https://doi.org/10.11648/j.ijcems.20160206.11
    AB  - Background. Translocator protein 18 kDa (TSPO) plays a key role both in microglial activation and neuroinflammation. Postoperative cognitive decline (POCD), a notable hazard to both patients and society, maybe contribute to deficiently controlled neuroinflammatory processes initiated by anesthesia and surgery. So far it is unclear that whether TSPO is involved in the pathogenesis of POCD or not. Materials and Methods. Twelve adult rats and twelve aged rats were divided into control and isoflurane groups respectively. POCD was induced by a 4-hour exposure of 2% isoflurane. The memory retention capability was assessed by the Morris water maze trial, the mRNA and the protein expression of both TSPO and Iba1 were assessed by real-time quantitative PCR and Western Blot analysis separately. Results. Compared to the control group, the latency time to find platform was longer in the groups exposed to isoflurane (p<0.05); the mRNA and the protein expression of both TSPO and Iba1 were correspondingly upregulated (p<0.05); especially that the severity of cognitive decline and the degree of TSPO and Iba1 over-expression were significantly different between the adult and aged rats (p<0.05); The twice times across the platform showed no significant difference among all the groups. Conclusions. Our study for the first time showed that TSPO may be involved in the pathogenesis of the cognitive decline induced by isoflurane anesthesia. Its role for being a biomarker and an interventional target of POCD deserves future investigation.
    VL  - 2
    IS  - 6
    ER  - 

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Author Information
  • Department of Anesthesiology, Weifang Medical University, Weifang, China

  • Department of Anesthesiology, Weifang Medical University, Weifang, China

  • Department of Anesthesiology, Yale University Medical School, USA

  • Department of Anesthesiology, No.89 Hospital of People’s Liberation Army, Weifang, China

  • Department of Anesthesiology, Weifang Medical University, Weifang, China

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