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06 May 2019 : Animal Research

[Retracted: 21 Aug 2019] Phosphorylated Glycogen Synthase Kinase-3β (GSK-3β) Improves Cognition in Rats with Diabetes-Associated Cognitive Decline

Boxi Ke12CDE, Rong Lu3ABC*, Xu Zhang1AFG

DOI: 10.12659/MSM.914653

Med Sci Monit 2019; 25:3336-3343

The two pictures of B and C in Figure 3 are the same, but apparently, the author presented them as two groups. Reference: Phosphorylated Glycogen Synthase Kinase-3ß (GSK-3ß) Improves Cognition in Rats with Diabetes-Associated Cognitive Decline Boxi Ke, Rong Lu, Xu Zhang Med Sci Monit 2019;25: 3336-3343 10.12659/MSM.914653

Abstract

BACKGROUND: The serine/threonine kinase glycogen synthase kinase-3β (GSK-3β) is involved in a broad range of cellular processes, including cell proliferation, apoptosis, and inflammation. GSK-3β has been considered to play an important role in the pathogenesis of T2DM and AD, which is activated in both the periphery and central nervous system. However, the upstream and downstream factors and the underlying regulatory mechanisms of GSK-3β in T2DM and AD are unclear.

MATERIAL AND METHODS: Here, we investigated the production of cytochrome C, Caspase-3, and Caspase-9 in in the hippocampus of DM rats and clarify the role of GSK-3β in these processes. Streptozotocin (STZ)-induced DM rats presented increased GSK-3β activity.

RESULTS: We found that cytochrome C, Caspase-3, and Caspase-9 were overproduced in the hippocampus. Furthermore, the cytochrome C, Caspase-3, and Caspase-9 levels were restored after GSK-3β inhibitors Licl treatment.

CONCLUSIONS: Our results show that GSK-3β regulates the production of cytochrome C, Caspase-3, and Caspase-9 in STZ-induced rat brain and may therefore contribute to DM-caused cognitive dysfunction via inhibition of neural cell apoptosis.

Keywords: Retracted Publication

Retraction note

Med Sci Monit 2019; 25:6291-6291     https://medscimonit.com/abstract/index/idArt/919343
 
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Medical Science Monitor eISSN: 1643-3750
Medical Science Monitor eISSN: 1643-3750