Tarbiat Modares University Pathobiology Research 2538-3000 26 1 2023 11 01 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 35 42 19469 EN Ali Khorasani Department of Biology, Faculty of Sciences, Shahid Bahonar University of Kerman, Kerman, Iran Mehdi Abbasnejad Department of Biology, Faculty of Sciences, Shahid Bahonar University of Kerman, Kerman, Iran Mahnaz Zamyad Department of Biology, Faculty of Sciences, Shahid Bahonar University of Kerman, Kerman, Iran Saeed Esmaeili-Mahani 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 Journal Article 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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