Abstract
Zanthoxylum bungeanum Maxim (Rutaceae), a popular condiment and dietetic herbal medicine, has been used traditionally in the treatment of forgetfulness, as recorded in Shen Nong's Herbal Medicine, an old Chinese medicine book. To explore effects and potential mechanisms of it, extracts of Z. bungeanum through water (WEZ), volatile oil (VOZ), petroleum ether (PEZ), and methylene chloride (MCZ) were used to treat the memory loss induced in D-galactose-induced aging mice. The impaired memory was significantly alleviated after WEZ and VOZ extract treatment. WEZ and VOZ extracts also prevented D-galactose-induced hippocampal neuron damage. In addition, WEZ and VOZ extracts upregulated nuclear factor erythroid 2-related factor 2 (Nrf2) and heme oxygenase 1 (HO-1), which suggests that the effects of WEZ and VOZ extracts on oxidative stress and apoptosis might be involved in the cognitive dysfunctions. Furthermore, WEZ and VOZ extracts enhanced the activation of phosphoinositide 3-kinase (PI3K)/protein kinase B (Akt), which suggests that Z. bungeanum has an appreciable therapeutic effect on learning and memory disabilities, and its mechanism may be related to activate PI3K/Akt signaling pathway. Collectively, our study suggested that Z. bungeanum extracts are promising agents for prevention of aging-related cognitive dysfunction and neurological deficits.
Highlights
Aging is a major cause for inducing cognitive impairment in humans, and it is a major risk factor for neurodegenerative diseases that are associated with neurological deficits (Liang et al, 2019)
Compared with the model group, the escape latencies of WEZ group and VOZ group were prolonged; the numbers of errors of the WEZ group and VOZ group were significantly decreased. While those of PEZ group and MCZ group did not show a significant difference from the model group (P > 0.05). These results showed that WEZ and VOZ extracts ameliorated the Dgalactose-induced fear memory impairment
The mice treated with WEZ and VOZ extracts lengthened the residence time in the target quadrant and enhanced the number of passing the platform zone compared with the model group (P < 0.05)
Summary
Aging is a major cause for inducing cognitive impairment in humans, and it is a major risk factor for neurodegenerative diseases that are associated with neurological deficits (Liang et al, 2019). The mitochondrial free-radical theory suggests that aging is caused by oxidative damage to macromolecules caused by mitochondrial reactive oxygen species (ROS) (Barja, 2019). Preventing oxidative stress-induced neuronal degeneration might be crucial to prevent the aging process and its associated neurodegenerative diseases such as Alzheimer's disease (AD). D-galactose is a physiological nutrient that is involved in glucose metabolism, but its excessive accumulation produces redundant ROS formation and decreases endogenous antioxidant enzyme activity, cognitive dysfunction, and neurological deficits in rodents (Hao et al, 2014; Sadigheteghad et al, 2017). D-galactose-induced aging mice were used to mimic aging brain pathology in this present study
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