Retracted: Rutin protects against cognitive deficits and brain damage in rats with chronic cerebral hypoperfusion

Abstract

Background and Purpose Chronic cerebral hypoperfusion is a critical causative factor for the development of cognitive decline and dementia in the elderly, which involves many pathophysiological processes. Consequently, inhibition of several pathophysiological pathways is an attractive therapeutic strategy for this disorder. Rutin, a biologically active flavonoid, protects the brain against several insults through its antioxidant and anti‐inflammatory properties, but its effect on cognitive deficits and brain damage caused by chronic cerebral hypoperfusion remains unknown. Here, we investigated the neuroprotective effect of rutin on cognitive impairments and the potential mechanisms underlying its action in rats with chronic cerebral hypoperfusion. Experimental Approach We used Sprague‐Dawley rats with permanent bilateral common carotid artery occlusion (BCCAO), a well‐established model of chronic cerebral hypoperfusion. After rutin treatment for 12 weeks, the neuroprotective effect of rutin in rats was evaluated by behavioural tests, biochemical and histopathological analyses. Key Results BCCAO rats showed marked cognitive deficits, which were improved by rutin treatment. Moreover, BCCAO rats exhibited central cholinergic dysfunction, oxidative damage, inflammatory responses and neuronal damage in the cerebral cortex and hippocampus, compared with sham‐operated rats. All these effects were significantly alleviated by treatment with rutin. Conclusion and Implications Our results provide new insights into the pharmacological actions of rutin and suggest that rutin has multi‐targeted therapeutical potential on cognitive deficits associated with conditions with chronic cerebral hypoperfusion such as vascular dementia and Alzheimer's disease.

Inhibition of c‐Jun N‐terminal kinase activation reverses Alzheimer disease phenotypes in APPswe/PS1dE9 mice

“…33,34 As shown in Figure 2C, acquisition latency in the acquisition trail did not differ among the 4 groups of mice (p > 0.05). 33,34 As shown in Figure 2C, acquisition latency in the acquisition trail did not differ among the 4 groups of mice (p > 0.05).…”

“…To further confirm the improvement of memory impairment by SP600125 treatment in APPswe/PS1dE9 mice, the contextual memory performance of all mice was assessed using the step-through passive avoidance task, which is widely used to evaluate drug effects on contextual memory in rodents. 33,34 As shown in Figure 2C, acquisition latency in the acquisition trail did not differ among the 4 groups of mice (p > 0.05). However, we demonstrated that the vehicle-treated APPswe/ PS1dE9 mice exhibited impaired contextual memory in the passive avoidance task, as indicated by decreased retention latency compared with vehicle-and SP600125treated wild-type mice (p < 0.001).…”

“…33,34 Briefly, the apparatus consisted of a 2-compartment dark/light shuttle box with a guillotine door separating each compartment. The contextual memory of all mice was assessed by using the passive avoidance task in the 2way shuttle box as described previously.…”

“…The contextual memory of all mice was assessed by using the passive avoidance task in the 2way shuttle box as described previously. 33,34 Briefly, the apparatus consisted of a 2-compartment dark/light shuttle box with a guillotine door separating each compartment. The dark compartment had a stainless steel shock grid floor.…”

Rutin Acid Ameliorates Neural Apoptosis Induced by Traumatic Brain Injury via Mitochondrial Pathways in Mice

“…It has a broad spectrum of pharmacological properties, including antioxidative, anti-inflammatory, antiallergenic, anticarcinogenic, antimicrobial, antiviral and cytoprotective activities [3,4]. Rutin is a naturally occurring substance that acts as an essential cofactor for various enzymes required in oxidative metabolism that also has therapeutic potential for treating mitochondria-related disorders.…”