| Literature DB >> 35482135 |
Amarjot Kaur1, Thakur Gurjeet Singh2, Heena Khan1, Manish Kumar1, Nirmal Singh1,3, Mohamed M Abdel-Daim4.
Abstract
Various studies have evidenced the neuroprotective role of PDE4 inhibitors. However, whether PDE4 inhibitor, Piclamilast pharmacological post-treatment is protective during cerebral ischemia reperfusion-induced injury remains unknown. Therefore, this study design included testing the hypothesis that Piclamilast administered at the beginning of a reperfusion phase (Piclamilast pPost-trt) shows protective effects and explores & probes underlying downstream mechanisms. Swiss albino male mice were subjected to global ischemic and reperfusion injury for 17 min. The animals examined cerebral infarct size, biochemical parameters, inflammatory mediators, and motor coordination. For memory, assessment mice were subjected to morris water maze (MWM) and elevated plus maze (EPM) test. Histological changes were assessed using HE staining. Piclamilast pPost-trt significantly reduced I/R injury-induced deleterious effects on biochemical parameters of oxidative stress, inflammatory parameters, infarct size, and histopathological changes, according to the findings. These neuroprotective effects of pPost-trt are significantly abolished by pre-treatment with selective CREB inhibitor, 666-15. Current study concluded that induced neuroprotective benefits of Piclamilast Post-trt, in all probability, maybe mediated through CREB activation. Hence, its neuroprotective effects can be further explored in clinical settings.Entities:
Keywords: Cerebral Ischemic reperfusion injury; Neuroprotective effect; Phosphodiesterase 4; Piclamilast; Post-treatment; cAMP response element-binding protein
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Year: 2022 PMID: 35482135 DOI: 10.1007/s11064-022-03609-w
Source DB: PubMed Journal: Neurochem Res ISSN: 0364-3190 Impact factor: 4.414