Abstract
The seeds of Cuscuta chinensis Lam. and C. campestris Yuncker have been commonly used as Chinese medical material for preventing aging. Our previous studies have found that C. chinensis and C. campestris possess anti-inflammatory activities in rodents. However, their other biological activities, such as memory-improving properties, have not yet been explored. In the present study, we examined the memory-improving effects of the extracts of C. chinensis and C. campestris on scopolamine (SCOP)-induced memory deficit and explored their underlying mechanism in mice. Both Cuscuta species improved SCOP-induced memory deficits in the passive avoidance test, elevated plus-maze, and spatial performance test of the Morris water maze in mice. In addition, compared with mice injected with SCOP, mice pretreated with both Cuscuta species stayed for a longer time on the platform for the probe test of the Morris water maze. Moreover, both Cuscuta species reduced brain acetylcholinesterase activity and malondialdehyde levels that were increased by SCOP, and the species restored the activities of antioxidant enzymes (superoxide dismutase and catalase) and the levels of glutathione that were decreased by SCOP in the brains of mice. Both Cuscuta species further decreased brain interleukin-1β and tumor necrosis factor-α levels that were elevated by SCOP. We demonstrated that both Cuscuta species exhibited a protective activity against SCOP-induced memory deficit, cholinergic dysfunction, oxidative damage, and neuroinflammation in mice, and C. campestris has better potential than C. chinensis. In addition, we provided evidence that the seeds of C. campestris can be used as Cuscutae Semen in Traditional Chinese Medicine.
Highlights
Alzheimer’s disease (AD), a progressive neurodegenerative disorder, endures major clinical symptoms such as behavioral and cognitive decline
SCOP slightly increased the number of entries and the time spent in the hole, but no significant difference was observed between the SCOP
This behavioral alteration caused by SCOP in mice was consistent with that described the previous reports in rodents [10,25,26], indicating that SCOP-induced memory deficit in the passive avoidance test, elevated plus-maze, and MWM is related to hyperactivity, poor attention, and subsequent learning acquisition impairment
Summary
Alzheimer’s disease (AD), a progressive neurodegenerative disorder, endures major clinical symptoms such as behavioral and cognitive decline. These symptoms are caused by three major and neuropathological mechanism including the degeneration of cholinergic neuronal circuits in the basal forebrain (BF), extracellular amyloid β peptide (Aβ) deposition, and intracellular neurofibrillary tangles formation from hyperphosphorylated tau protein [1]. Scopolamine (SCOP), a muscarinic receptor antagonist, impairs learning and memory in rodents and humans mainly by decreasing cholinergic activity [8,9]. Some recent reports have indicated that SCOP causes cerebral oxidative damage and neuroinflammation, which are the same as the neuropathological mechanism of AD [10,11]. SCOP has been used to induce amnesia and/or dementia in experimental rodent models
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