Diabetes related
cognitive impairment is a severe complication. The diabetes-induced
cognitive impairment is associated with
insulin resistance and
glucose-induced neuron apoptosis in the brain. We intended to investigate the association of long non-coding RNAs with diabetes-induced
cognitive impairment in rats. Here, Type 1diabetes (T1D) rat model was induced using
streptozotocin (STZ). The diabetic rats showed significant
cognitive dysfunction, with increased latency period to find the hidden platform during morris water maze test. The
brain injury and reduced neuronsin STZ-induced diabetic rats was determined using
hematoxylin and
eosin staining and Nissl's staining. We performed the
LncRNA microarray analysis and identified 101 differentially expressed lncRNAs in
streptozotocin (STZ)-induced
type 1 diabetes (T1D) comparing with control. Among these
lncRNA, LOC103690121 was upregulated. in vitro
glucose treatment in hippocampal neurons showed LOC103690121 and neuron apoptosis was increased by
glucose treatment. Transfection experiments showed LOC103690121 overexpression promoted neuron apoptosis, and its inhibition suppressed
glucose-induced apoptosis. Western blot analysis showed that the expression profiles of apoptosis related
proteins (cleaved-caspase-3, -8, -9, and Bax) were in line with LOC103690121 expression, while the profiles of Bcl-2 and PI3K/Akt signaling pathway was contrast to LOC103690121 expression. In conclusion, the results of our study confirmed
lncRNA LOC103690121 promoted STZ-induced
cognitive impairment in diabetic rats by promoting neuron apoptosis through PI3K/Akt signaling pathway.