中国神经再生研究(英文版) ›› 2014, Vol. 9 ›› Issue (5): 534-539.doi: 10.4103/1673-5374.130084

• 原著:脑损伤修复保护与再生 • 上一篇    下一篇

术后认知功能障碍老年大鼠的适应性调节机制

  

  • 收稿日期:2014-01-28 出版日期:2014-03-12 发布日期:2014-03-12

Adaptive and regulatory mechanisms in aged rats with postoperative cognitive dysfunction

Yanlin Bi 1, 2, Shuyun Liu 2, Xinjuan Yu 3, Mingshan Wang 3, Yuelan Wang 1   

  1. 1 Department of Anesthesiology, Affiliated Qianfoshan Hospital, Shandong University, Jinan, Shandong Province, China
    2 Department of Anesthesiology, Shaoxing People’s Hospital, Shaoxing, Zhejiang Province, China
    3 Department of Anesthesiology, Qingdao Municipal Hospital, Qingdao, Shandong Province, China
  • Received:2014-01-28 Online:2014-03-12 Published:2014-03-12
  • Contact: Yuelan Wang, M.D., Department of Anesthesiology, Affiliated Qianfoshan Hospital, Shandong University, Jinan 250014, Shandong Province, China, wyldgf@163.com.

摘要:

由于炎症可能是术后认知功能障碍的诱因之一,而AMP活化蛋白激酶、核因子κB,白细胞介素1β和肿瘤坏死因子α参与炎症反应,因而推测他们可能也参与术后认知功能障碍的发生。实验以Western blot结果表明术后1-7d认知功能障碍大鼠海马中AMP活化蛋白激酶和核因子κB的表达增加,而白细胞介素1β和肿瘤坏死因子α表达上调后逐渐下降。提示海马AMP活化蛋白激酶和这些炎症因子可能参与术后认知功能障碍,是机体对术后认知功能障碍做出的适应性调节。

关键词: 神经再生, 海马, 术后认知功能障碍, 脾切除, 大脑, 衰老, AMP活化蛋白激酶, 核因子κB, 肿瘤坏死因子α, 白细胞介素1β, 炎症

Abstract:

Inflammation may play a role in postoperative cognitive dysfunction. 5′ Adenosine monophosphate-activated protein kinase, nuclear factor-kappa B, interleukin-1β, and tumor necrosis factor-α are involved in inflammation. Therefore, these inflammatory mediators may be involved in postoperative cognitive dysfunction. Western immunoblot analysis revealed 5′ adenosine monophosphate-activated protein kinase and nuclear factor-kappa B in the hippocampus of aged rats were increased 1–7 days after splenectomy. Moreover, interleukin-1β and tumor necrosis factor-α were upregulated and gradually decreased. Therefore, these inflammatory mediators may participate in the splenectomy model of postoperative cognitive dysfunction in aged rats.

Key words: nerve regeneration, postoperative cognitive dysfunction, splenectomy, brain, aging, 5′adenosine monophosphate-activated protein kinase, nuclear factor-kappa B, tumor necrosis factor-α, interleukin-1β, neural regeneration