2016
DOI: 10.1016/j.brainres.2016.10.017
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Neuroprotection of Cilostazol against ischemia/reperfusion-induced cognitive deficits through inhibiting JNK3/caspase-3 by enhancing Akt1

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Cited by 35 publications
(21 citation statements)
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“…contributing to its oncogenic potential. through many signalling pathways including PI3K (Wang et al, ), ERK1/2 (Li et al, ) and JNK (Qi et al, ). However, the interaction between miR‐149‐3P and Akt1 had not been confirmed in pancreatic cancer.…”
Section: Discussionmentioning
confidence: 99%
“…contributing to its oncogenic potential. through many signalling pathways including PI3K (Wang et al, ), ERK1/2 (Li et al, ) and JNK (Qi et al, ). However, the interaction between miR‐149‐3P and Akt1 had not been confirmed in pancreatic cancer.…”
Section: Discussionmentioning
confidence: 99%
“…BNG-1 can also inhibit several phosphodiesterase (PDE) isoforms 20 with potency order of the following rank: PDE1 > PDE7A > PDE3 > PDE6 > PDE2 > PDE4 > PDE5. A potent PDE3 inhibitor, cilostazol 3739 , is used clinically as an anti-platelet drug to treat ischemic stroke 40, 41 . Intravenous administration of cilostazol nanoparticles was found to ameliorates acute ischemic stroke in cerebral ischemia/reperfusion-induced injury after middle cerebral artery occlusion in mice 42 .…”
Section: Discussionmentioning
confidence: 99%
“…As a primary cause of paralysis and death around the world, ischemic stroke and the accompanying reperfusion injury are widely known for such complications as hemiplegia, coma, and even death. Although new and advanced tools and medications are available for earlier diagnosis and treatment, such as magnetic resonance imaging (MRI) technology [ 1 , 2 ], high morbidity and mortality still constitute the most disturbing prognosis of this vascular disease. Many pathological changes happen during the obstinate illness, including cell death (necrosis and apoptosis), angiogenesis, inflammation, and cerebral edema [ 3 5 ].…”
Section: Introductionmentioning
confidence: 99%