Abstract
Bacopa monnieri extract has been implicated in the recovery of memory impairments due to various neurological disorders in animal models and humans. However, the precise molecular mechanism of the role of CDRI-08, a well characterized fraction of Bacopa monnieri extract, in recovery of the diabetes mellitus-induced memory impairments is not known. Here, we demonstrate that DM2 mice treated orally with lower dose of CDRI-08 (50- or 100 mg/kg BW) is able to significantly enhance spatial memory in STZ-DM2 mice and this is correlated with a significant decline in oxidative stress and up regulation of the AMPA receptor GluR2 subunit gene expression in the hippocampus. Treatment of DM2 mice with its higher dose (150 mg/kg BW or above) shows anti-diabetic effect in addition to its ability to recover the spatial memory impairment by reversing the DM2-induced elevated oxidative stress and decreased GluR2 subunit expression near to their values in normal and CDRI-08 treated control mice. Our results provide evidences towards molecular basis of the memory enhancing and anti diabetic role of the Bacopa monnieri extract in STZ-induced DM2 mice, which may have therapeutic implications.
Highlights
Diabetes mellitus (DM) is a metabolic disorder characterized by abnormally increased blood glucose level and is synonymously called as hyperglycemia
STZ-induced diabetes mellitus type 2 (DM2) leads to increase in blood glucose content, water intake and urine output and CDRI-08 reverses them towards their normal values
We have studied effects of diabetes mellitus type 2 (DM2) on the spatial memory in mice and its association with the oxidative stress and expression of AMPA receptor GluR2 subunit gene in the hippocampus as this is the major site in the brain for consolidation and storage of the long term memory
Summary
Diabetes mellitus (DM) is a metabolic disorder characterized by abnormally increased blood glucose level and is synonymously called as hyperglycemia. Recent evidences from human DM patients suggest that the insulin resistance leading to type-2 DM, in particular, causes impairments in the visual retention, verbal memory, working memory, immediate recall, executive function, information processing speed, verbal fluency, attention, and depression, which lead to cognitive dysfunction [8,9,10]. Number of studies from human DM2 patients and rodent DM2 model reveal that excessive oxidative stress leads to neurodegeneration as a consequence of impaired glucose metabolism and excessive operation of polyol-sorbitol pathway in neurons [13,14], altered excitatory glutamatergic synaptic transmission, early long term potentiation (eLTP) and synaptic plasticity, which altogether result into cognitive impairments [14,15]
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