Effects of abscisic acid on Streptozotocin-induced changes in hippocampal expression of cyclooxygenase-2 (COX-2) and phosphorylated ERK signaling (p-ERK) in male rats

نویسندگان

1 Department of Biology, Faculty of Sciences, Shahid Bahonar University of Kerman, Kerman, Iran Kerman Neuroscience Research Center, Institute of Neuropharmacology, Kerman University of Medical Sciences, Kerman, Iran

2 Department of Biology, Faculty of Sciences, Shahid Bahonar University of Kerman, Kerman, Iran

3 Department of Biology, Faculty of Sciences, Shahid Bahonar University of Kerman, Kerman, Iran

4 Department of Biology, Faculty of Sciences, Shahid Bahonar University of Kerman, Kerman, Iran

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چکیده

Abstract Introduction: Central administration of STZ (Streptozotocin) induces oxidative damage, neuroinflammation, cholinergic deficits, β-amyloid and tau protein accumulation in the brain. Abscisic acid (ABA) as a phytohormone is produced in a variety of animal tissues, including brain. Recently data show it has been involved in a wide spectrum of activities in CNS including, learning and memory and pain regulation. Here, the alternative effects of abscisic acid and the possibility of involving PKA and PPARβ/δ receptors, on Streptozotocin-induced changes in hippocampal expression of cyclooxygenase-2 (COX-2) and ERK signaling (p-ERK) in male Wister rats was investigated. Methods: STZ was injected intracerebroventricularly (i.c.v.) (3 mg/kg), ABA was administrated alone (10 μg/rat, i.c.v.) or accompanied with PPARβ/δ receptor antagonist (GSK0660, 80 nM/rat) or selective inhibitor of PKA (H89, 80nM/rat) for 14 days. Western blot analysis was used to indicate changes in hippocampal COX-2 and p-ERK expression. Results: The results showed that STZ produced a significant increase in hippocampal expression of COX-2 and a decrease in expression of p-ERK. ABA significantly prevented the effects of STZ. However, ABA effects were blocked by PPARβ/δ receptor antagonist (GSK0660) and selective inhibitor of PKA (H89). Conclusions: It seems that the ABA moderates STZ-induced neuronal inflammation and ERK signaling deficiency by PPARβ/δ receptor and PKA signaling. Keywords: Abscisic acid; Streptozotocin; COX-2; p-ERK; Rats

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