Protective Effects of Puerarin against Aβ 1–42-Induced Learning and Memory Impairments in Mice

Abstract

Puerarin is a major isoflavone glycoside from the root of It has been reported that puerarin can protect neurons from oxidative stress-induced apoptosis. Emerging evidence suggests that oxidative damage is associated with A-induced neuronal death. In the current study, we evaluated the effect of puerarin on Alzheimer's disease induced by A and explored the potential mechanisms underlying this effect. We found that the escape latency of the Morris water maze was decreased in groups treated with puerarin compared to the model group (p < 0.01). In addition, there were significant differences between treated groups and the model group mice in a Y-maze test (p < 0.01). Furthermore, puerarin recovered the levels of brain-derived neurotrophic factor, phosphorylated tau, malondialdehyde, acetylcholine esterase, glycogen synthase kinase-3beta, and the activity of superoxide dismutase to some extent in the hippocampus and cerebral cortex. Shrinkage of nuclei and swollen and eccentrically dispersed neuronal bodies were observed in the hippocampus of A-treated mice. These data demonstrate that puerarin might protect against cognitive deficits, oxidative stress, and neurodegeneration induced by A.

Neuroprotective Effects of Spinosin on Recovery of Learning and Memory in a Mouse Model of Alzheimer’s Disease

“…Pathological conditions of AD are evidenced to link with oxidative stress, and the level of lipid peroxidation is considered as an important factor in AD (Gao et al ., 2012). The level of MDA, a marker of lipid peroxidation index, was evaluated in hippocampus rather than cortex since a high level of MDA is induced in hippocampus after ICV injection of Aβ 1–42 (Ziech et al ., 2010; Wu et al ., 2017). Our results showed that spinosin significantly attenuated the up-regulation of MDA in hippocampus induced by ICV injection of Aβ 1–42 .…”

Active compounds of herbs ameliorate impaired cognition in APP/PS1 mouse model of Alzheimer’s disease

“…More specifically, the treatments were administered with Epimedium, Astragaoside and Puerarin, which are composed of active compounds, icariin, astragalosideIV and puerarin, respectively. Many studies have confirmed the uses of these active compounds in the treatment of neurological disorders [13, 18, 25]. Several studies have reported that these compounds may antagonize Aβ formation, scavenge free radicals, reduce inflammation, regulate mitochondrial functions and promote axonal maturation in the central nervous system [13, 18, 26, 27].…”

“…Many studies have confirmed the uses of these active compounds in the treatment of neurological disorders [13, 18, 25]. Several studies have reported that these compounds may antagonize Aβ formation, scavenge free radicals, reduce inflammation, regulate mitochondrial functions and promote axonal maturation in the central nervous system [13, 18, 26, 27]. Icariin, a component extracted from Epimedium, has a beneficiary action on experimental spinal cord injury through its anti-oxidant, anti-neuroinflammatory, and anti-apoptotic role [28].…”

“…Astragalus membranaceus inhibits oxidative stress induced by metal [16] and antagonizes Aβ1-42 neurotoxicity in Human SK-N-SH neuroblastoma cells [17]. Puerarin, an isoflavone purified from the root of Pueraria lobata , has been reported to attenuate learning and memory impairments in the transgenic mouse model of AD [18] and could protect neurons from oxidative stress-induced apoptosis [19]. Collectively, these compounds have the potential to impact the development and progression of AD.…”

Plants‐Derived Neuroprotective Agents: Cutting the Cycle of Cell Death through Multiple Mechanisms

“…Other studies have also shown the neuroprotective effects of 23 in AD [ 214 , 215 ]. Puerarin also suppresses the A β (1–42) -induced primary cortical neuron death [ 216 ] thus protecting against A β (1–42) -induced learning and memory impairments in mice [ 217 ]. It also attenuates myocardial hypoxia/reoxygenation injury by inhibiting autophagy via the Akt signaling pathway and inhibits oxidative stress in STZ-induced SAD mice [ 218 , 219 ].…”