A Brief Review on the Neuroprotective Mechanisms of Vitexin

Abstract

The neural dysfunction is triggered by cellular and molecular events that provoke neurotoxicity and neural death. Currently, neurodegenerative diseases are increasingly common, and available treatments are focused on relieving symptoms. Based on the above, in this review we describe the participation of vitexin in the main events involved in the neurotoxicity and cell death process, as well as the use of vitexin as a therapeutic approach to suppress or attenuate neurodegenerative progress. Vitexin contributes to increasing neuroprotective factors and pathways and counteract the targets that induce neurodegeneration, such as redox imbalance, neuroinflammation, abnormal protein aggregation, and reduction of cognitive and/or motor impairment. The results obtained provide substantial evidence to support the scientific exploration of vitexin in these pathologies, since their effects are still little explored for this direction.

Isovitexin-Mediated Regulation of Microglial Polarization in Lipopolysaccharide-Induced Neuroinflammation via Activation of the CaMKKβ/AMPK-PGC-1α Signaling Axis

“…Fifteen unreported compounds isolated from the rhizomes of Anemarrhena asphodeloides have anti-inflammatory activities (47). It has been reported and summarized that vitexin and isovitexin could be potential substitute medicines for diversity diseases, and may be adjuvants for stubborn diseases or health products (48, 49). However, the effect of isovitexin on brain disorder associated with neuroinflammation hasn't been reported yet.…”

Lead acetate-induced neurodegenerative changes in the dorsolateral prefrontal cortex of mice: the role of Vitexin

“…In the group, where both Pb and Vitexin was concurrently administered, there was a significant improvement in a possible degenerative change and chromatolysis was significantly reduced (Figure 4). As part of previous studies, Vitexin has demonstrated its ability to decrease neuronal cell death [43,44] through a different mechanism and to significantly improve neuronal cell structure and function [24,45]. This result in the Pb+Vitexin group, indicates that the number of healthy neurons in DLPFC will be more than the degenerated ones when compared to Pb group (as Figure 4, 6).…”

“…Vitexin is a flavonoid that is extracted from various plants including pearl millet, hawthorn, pigeon pea, mung bean, mosses, Passiflora, bamboo, mimosa, wheat leaves, and chaste berry [21]. Its effects are reported in pharmacological roles range from anti-oxidative anti tumour, anti-viral, anti-inflammatory, anti-bacterial, antihypertensive, antinociceptive, antispasmodic, anti-diabetic, antidepressant, neuroprotective and cognitive improving functions [22][23][24][25][26][27][28]. The contribution of Vitexin to neuroprotection is through counteracting the targets that induce neurodegeneration, such as redox imbalance, neuroinflammation and abnormal protein aggregation, which then lead to a reduction of cognitive or motor impairment [24].…”

<p>The natural flavonoid glycoside vitexin displays preclinical antitumor activity by suppressing NF-κB signaling in nasopharyngeal carcinoma</p>

“…Interestingly, vitexin has been used as a traditional Chinese medicine for the treatment of a variety of diseases for a long year,13 and previous studies have also shown that vitexin has effective antitumor roles in some other tumors, including colorectal cancer,14 leukemia,15 glioblastoma,16 bladder cancer17 and breast cancer,18 which further supported our research that vitexin had significant antitumor activity. Additionally, vitexin was reported to participate in the main events involved in the process of neurotoxicity 19. Vitexin enhanced the production of neuroprotective factors and reduced neurodegeneration, such as abnormal protein aggregation, neuroinflammation, redox imbalance, etc 19…”

“…Additionally, vitexin was reported to participate in the main events involved in the process of neurotoxicity 19. Vitexin enhanced the production of neuroprotective factors and reduced neurodegeneration, such as abnormal protein aggregation, neuroinflammation, redox imbalance, etc 19…”