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  3. Treatment effects of Cardiotrophin-1 (CT-1) on streptozotocin-induced memory deficits in mice

Treatment effects of Cardiotrophin-1 (CT-1) on streptozotocin-induced memory deficits in mice

  • Exp Gerontol. 2017 Jun:92:42-45. doi: 10.1016/j.exger.2017.03.007.
Dongmei Wang 1,  Xiaozhuan Liu 2,  Yumei Liu 3,  Guomin Shen 4,  Xiaoying Zhu 5,  Sanqiang Li 4
Affiliations

Affiliations

  • 1 Department of Pathogen Biology, Medical College, Henan University of Science and Technology, Luoyang, China. Electronic address: [email protected].
  • 2 Department of Immunology, Medical College, Henan University of Science and Technology, Luoyang, China.
  • 3 College of Animal Science and Technology, Henan University of Science and Technology, Luoyang, China.
  • 4 Department of Biochemistry and Molecular Biology, Medical College, Henan University of Science and Technology, Luoyang, China.
  • 5 Department of Pathogen Biology, Medical College, Henan University of Science and Technology, Luoyang, China.
PMID: 28285145 DOI: 10.1016/j.exger.2017.03.007
Abstract

Increasing evidence has shown that diabetes-associated cognitive impairment is correlated with mitochondrial dysfunction and resultant synaptic injury as well as brain Insulin resistance. Cardiotrophin-1 (CT-1), a regulator of energy metabolism, has been shown to exhibit impressive neuroprotective effects. In this study, we evaluated the effects of CT-1 on brain pathological features in intracerebroventrical-streptozotocin (ICV-STZ)-treated mouse model, and explored its potential mechanisms. STZ was injected twice (3mg/kg, ICV) on alternate days (day 1 and day 3) in mice. Daily treatment with CT-1 (1μg/day, ICV) starting from the first dose of STZ for 14days showed that CT-1 significantly improved learning and memory deficits, alleviated mitochondrial dysfunction, and increased synaptic density in the CA1 region of the hippocampus in ICV-STZ-treated mice. Moreover, CT-1 significantly enhanced Insulin signaling pathway in the hippocampus of ICV-STZ-treated mice when compared with the control. However, all the protective effects including biochemistry, pathological changes and cognitive function could be blocked by an ICV injection of Compound C, a specific AMPK Inhibitor. Taken together, these results suggested that CT-1 improves pathological changes and cognitive impairments via AMPK activation in ICV-STZ mice.

Keywords

AMPK; CT-1; Insulin signal; Mitochondrial dysfunction; Streptozotocin.

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