Protective effects of salicylate on PKA inhibitor (H-89)-induced spatial memory deficit via lessening autophagy and apoptosis in rats

Azimi, Leila; Kachooeian, Maryam; Khodagholi, Fariba; Yans, Asal; Heysieattalab, Soomaayeh; Vakilzadeh, Gelareh; Vosoughi, Nasim; Sanati, Mehdi; Taghizadeh, Ghorban; Sharifzadeh, Mohammad

doi:10.1016/j.pbb.2016.10.008

Cited by 3 publications

(1 citation statement)

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“…However, the effect of DP1 (PKA pathway) on autophagy remains unknown. Some studies indicated that the PKA inhibitor significantly increased the LC3BII expression in the rats hippocampus (Azimi et al, 2016), and another study indicated that neuropeptide Y via PKA stimulates autophagy in hypothalamic neurons to delay aging and produce protective effects against hypothalamic impairments associated with age (Aveleira et al, 2015). The decreased expression of p-AKT(S473) will increase the expression of p-AMPK(T172), and then, the increase expression of Beclin1 and LC3BII may promote autophagy.…”

Section: Discussionmentioning

confidence: 99%

Inhibition of COX2/PGD2-Related Autophagy Is Involved in the Mechanism of Brain Injury in T2DM Rat

Yang

Chen

Zhao

et al. 2019

Front. Cell. Neurosci.

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The present study was designed to observe the effect of COX2/PGD2-related autophagy on brain injury in type 2 diabetes rats. The histopathology was detected by haematoxylin–eosin staining. The learning and memory functions were evaluated by Morris water maze. The levels of insulin and PGD2 were measured by enzyme-linked immunosorbent assay. The expressions of COX2, p-AKT(S473), p-AMPK(T172), Aβ, Beclin1, LC3BII, and p62 were measured by immunohistochemistry and Western blotting. In model rats, we found that the body weight was significantly decreased, the blood glucose levels were significantly increased, the plasma insulin content was significantly decreased, the learning and memory functions were impaired and the cortex and hippocampus neurons showed significant nuclear pyknosis. The levels of COX2, p-AKT(S473), PGD2, Aβ, Beclin1 and p62 were significantly increased, whereas the expression of p-AMPK(T172) and LC3BII was significantly decreased in the cortex and hippocampus of model rats. In meloxicam-treated rats, the body weight, blood glucose and the content of plasma insulin did not significantly change, the learning and memory functions were improved and nuclear pyknosis was improved in the cortex and hippocampus neurons. The expression of p-AMPK(T172), Beclin1 and LC3BII was significantly increased, and the levels of COX2, p-AKT(S473), PGD2, Aβ, and p62 were significantly decreased in the cortex and hippocampus of meloxicam-treated rats. Our results suggested that the inhibition of COX2/PGD2-related autophagy was involved in the mechanism of brain injury caused by type 2 diabetes in rats.

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Section: Discussionmentioning

confidence: 99%