Abstract
Salicin is a major natural compound of willow bark and displays diverse beneficial biological properties, such as antioxidant activity. However, little information available for the neuroprotective potential of salicin against ischemic brain injury has been reported. Thus, this study was performed to investigate the neuroprotective potential of salicin against ischemia and reperfusion (IR) injury and its mechanisms in the hippocampus using a gerbil model of 5-min transient ischemia (TI) in the forebrain, in which a massive loss (death) of pyramidal neurons cells occurred in the subfield Cornu Ammonis 1 (CA1) among the hippocampal subregions (CA1-3) at 5 days after TI. To examine neuroprotection by salicin, gerbils were pretreated with salicin alone or together with LY294002, which is a phosphatidylinositol 3-kinase (PI3K) inhibitor, once daily for 3 days before TI. Treatment with 20 mg/kg of salicin significantly protected CA1 pyramidal neurons against the ischemic injury. Treatment with 20 mg/kg of salicin significantly reduced the TI-induced increase in superoxide anion generation and lipid peroxidation in the CA1 pyramidal neurons after TI. The treatment also reinstated the TI-induced decrease in superoxide dismutases (SOD1 and SOD2), catalase, and glutathione peroxidase in the CA1 pyramidal cells after TI. Moreover, salicin treatment significantly elevated the levels of phosphorylation of Akt and glycogen synthase kinase-3β (GSK3β), which is a major downstream target of PI3K, in the ischemic CA1. Notably, the neuroprotective effect of salicin was abolished by LY294002. Taken together, these findings clearly indicate that salicin protects against ischemic brain injury by attenuating oxidative stress and activating the PI3K/Akt/GSK3β pathway.
Highlights
Transient ischemia (TI) in whole brain happens by transient interruption or reduction in cerebral blood flow and induces selective and “delayed neuronal death (DND)” in vulnerable regions, including the hippocampus, a few days later [1,2]
Group, strong Cresyl Violet (CV) stainability is observed in the SP (n = 5/group; the vehicle-sham group was regarded as control group)
The bars indicate the means ± standard error of the mean (SEM) (n = 5/group, * p < 0.05 vs. each sham group, # p < 0.05 vs. vehicle-transient ischemia (TI) group, † p < 0.05 vs. salicin-TI group; the vehicle-sham group was regarded as control group)
Summary
Transient ischemia (TI) in whole brain happens by transient interruption or reduction in cerebral blood flow and induces selective and “delayed neuronal death (DND)” in vulnerable regions, including the hippocampus, a few days later [1,2]. The natural compounds derived from medicinal plants have been recognized for a vital source of therapeutic agents to treat neurological disorders for recent several decades of years due to their diverse biological properties [9,10]. A precursor to acetylsalicylic acid (aspirin), is a major active compound in willow bark that has been utilized as a traditional medicine for the treatment of diverse ailments, such as fever, mild rheumatic complaints, and pain [11,12]. Recent studies have reported that salicin possesses a broad range of pharmacological activities, including antioxidant [13], anti-inflammatory [14], anti-cancer [15], and neurite outgrowth effects [16]
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