Neural Regeneration Research ›› 2016, Vol. 11 ›› Issue (6): 944-950.doi: 10.4103/1673-5374.184493

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Rosiglitazone ameliorates diffuse axonal injury by reducing loss of tau and up-regulating caveolin-1 expression

Yong-lin Zhao, Jin-ning Song*, Xu-dong Ma, Bin-fei Zhang, Dan-dong Li, Hong-gang Pang   

  1. Department of Neurosurgery, the First Affiliated Hospital of Xi’an Jiaotong University, Xi’an, Shaanxi Province, China
  • Received:2015-12-22 Online:2016-06-30 Published:2016-06-30
  • Contact: Jin-ning Song, M.D., jinningsong@126.com.
  • Supported by:

    This study was funded by the New Century Supporting Programs to Excellent Talents in China, No. NCET-05-0831.

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Abstract:

Rosiglitazone up-regulates caveolin-1 levels and has neuroprotective effects in both chronic and acute brain injury. Therefore, we postulated that rosiglitazone may ameliorate diffuse axonal injury via its ability to up-regulate caveolin-1, inhibit expression of amyloid-beta precursor protein, and reduce the loss and abnormal phosphorylation of tau. In the present study, intraperitoneal injection of rosiglitazone significantly reduced the levels of amyloid-beta precursor protein and hyperphosphorylated tau (phosphorylated at Ser404 (p-tau (S404)), and it increased the expression of total tau and caveolin-1 in the rat cortex. Our results show that rosiglitazone inhibits the expression of amyloid-beta precursor protein and lowers p-tau (S404) levels, and it reduces the loss of total tau, possibly by up-regulating caveolin-1. These actions of rosiglitazone may underlie its neuroprotective effects in the treatment of diffuse axonal injury.

Key words: nerve regeneration, diffuse axonal injury, rosiglitazone, hyperphosphorylated tau, total tau, caveolin-1, rats, amyloid precursor protein, ser404, cortex, immunocytochemistry, western blot assay, neural regeneration