Abstract
Poststroke dementia commonly occurs following stroke, with its pathogenesis related to β-amyloid production and apoptosis. The present study evaluate the effects of paeonol, one of the phenolic phytochemicals isolated from the Chinese herb Paeonia suffruticosa Andrews (MC), on protection from memory loss after ischemic stroke in the subacute stage. Rats were subjected to transient middle cerebral artery occlusion (tMCAo) with 10 min of ischemia. The data revealed that paeonol recovered the step-through latency in the retrieval test seven days after tMCAo, but did not improve the neurological deficit induced by tMCAo. Levels of Amyloid precursor protein (APP)- and beta-site APP cleaving enzyme (BACE; β-secretase)-immunoreactive cells, and terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling (TUNEL)-positive cells decreased in the paeonol-administered group. Western blotting revealed decreased levels of Bax protein in mitochondria and apoptosis-inducing factor (AIF) in cytosol following paeonol treatment. In conclusion, we speculate that paeonol protected memory after ischemic stroke via reducing APP, BACE, and apoptosis. Supression the level of Bax and blocking the release of AIF into cytosol might participate in the anti-apoptosis provided by paeonol.
Highlights
Cognitive impairment is a commonly occurring sequela following stroke and is the second leading cause of dementia in the elderly, after Alzheimer’s disease [1, 2]
The present study evaluate the effects of paeonol, one of the phenolic phytochemicals isolated from the Chinese herb Paeonia suffruticosa Andrews (MC), on protection from memory loss after ischemic stroke in the subacute stage
Levels of Amyloid precursor protein (APP)- and beta-site APP cleaving enzyme (BACE; β-secretase)-immunoreactive cells, and terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling (TUNEL)-positive cells decreased in the paeonoladministered group
Summary
Cognitive impairment is a commonly occurring sequela following stroke and is the second leading cause of dementia in the elderly, after Alzheimer’s disease [1, 2]. With recent improvements in the medical treatment of stroke, survival rates have increased, and the prevention and treatment of vascular cognitive impairment and vascular dementia after stroke have become increasingly important [3]. The interactions between β-amyloid and several factors, including apolipoproteins, presenilins, tau protein, α-synuclein, inflammation factors, and neuronal survival/death decisions in the brain, contribute to ischemic brain degeneration, leading to white matter damage and neuronal cell death [5, 7]. Therapies which can salvage neuronal cells from apoptosis in ischemic penumbra might improve patient outcomes after ischemic stroke [11]
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