Abstract
Chronic cerebral hypoperfusion (CCH) causes cognitive impairment and neurogenic inflammation by reducing blood flow. We previously showed that Fructus mume (F. mume) improves cognitive impairment and inhibits neuroinflammation in a CCH rat model. One of the components of F. mume, Mumefural (MF), is known to improve blood flow and inhibit platelet aggregation. Whether MF affects cerebral and cognitive function remains unclear. We investigated the effects of MF on cognitive impairment and neurological function-related protein expression in the rat CCH model, established by bilateral common carotid arterial occlusion (BCCAo). Three weeks after BCCAo, MF (20, 40, or 80 mg/kg) was orally administrated once a day for 42 days. Using Morris water maze assessment, MF treatment significantly improved cognitive impairment. MF treatment also inhibited cholinergic system dysfunction, attenuated choline acetyltransferase-positive cholinergic neuron loss, and regulated cholinergic system-related protein expressions in the basal forebrain and hippocampus. MF also inhibited myelin basic protein degradation and increased the hippocampal expression of synaptic markers and cognition-related proteins. Moreover, MF reduced neuroinflammation, inhibited gliosis, and attenuated the activation of P2X7 receptor, TLR4/MyD88, NLRP3, and NF-κB. This study indicates that MF ameliorates cognitive impairment in BCCAo rats by enhancing neurological function and inhibiting neuroinflammation.
Highlights
Chronic cerebral hypoperfusion (CCH) is a major cause of vascular dementia (VaD) and can result from disorders that affect the cerebral vascular system [1,2]
We evaluated the effect of MF on cognitive impairment using Morris water maze (MWM)
Escape latency was significantly higher in the bilateral common carotid artery occlusion (BCCAo) + Vehicle group than in the Sham + Vehicle group (P < 0.01), indicating that BCCAo leads to spatial learning deficits
Summary
Chronic cerebral hypoperfusion (CCH) is a major cause of vascular dementia (VaD) and can result from disorders that affect the cerebral vascular system [1,2]. The important role of CCH in dementia has emerged at the front edge of neurological studies. Accumulating evidence indicates that CCH might promote neurodegeneration through the production of reactive oxygen species and proinflammatory cytokines by activating glial, leading to neuronal damage [3,4,5,6]. The main clinical feature of CCH is chronic neurodegeneration, which leads to cognitive impairment, mood disorder, impaired problem-solving ability, and loss of executive function because of impaired blood supply [7,8,9,10]. We have investigated the therapeutic candidates, such as Fructus mume (F. mume), Ginkgo biloba L., Salvia miltiorrhiza, and cardiotonic pill, for CCH in the Nutrients 2019, 11, 2755; doi:10.3390/nu11112755 www.mdpi.com/journal/nutrients
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