A Brief Review on the Neuroprotective Mechanisms of Vitexin

Lima, Layana Karine Farias; Pereira, Suyanne Kássia S.; Sousa, Ronaldo dos Santos; Santos, Felipe Pereira da Silva; Nascimento, Alyandra de Sousa; Feitosa, Chistiane Mendes; Figuerêdo, Juliana de Sousa; Cavalcante, Antônio do Nascimento; Araújo, Edigênia Cavalcante da Cruz; Rai, Mahendra

doi:10.1155/2018/4785089

Cited by 33 publications

(13 citation statements)

References 62 publications

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“…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.…”

Section: Discussionmentioning

confidence: 99%

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

Liu

Huang

et al. 2019

Front. Immunol.

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Microglia are the brain's immune cells and play an important role in regulating the microenvironment in the central nervous system. Activated microglia are capable of acquiring the pro-inflammatory (M1) phenotype and anti-inflammatory (M2) phenotype. Overactivation of microglia is neurotoxic and may lead to neuroinflammatory brain disorders. Neuroinflammation in the brain plays a crucial role part in the pathophysiology of many psychiatric and neurological diseases. The inhibition of M1 microglia and promotion of M2 microglia was demonstrated to treat and prevent these diseases through reduced neuroinflammation. Isovitexin (IVX) has anti-inflammatory properties and passes through the blood-brain barrier; however, the molecular mechanism that modulates IVX-mediated microglial polarization remains unclear. In BV-2 cells and mouse primary microglia, IVX suppressed the expression of M1 microglial markers, enhanced the expression of M2 microglial markers, and enhanced the release of interleukin 10 (IL-10). IVX promoted the expression of peroxisome proliferator-activated receptor-γ (PPARγ) and PPARγ coactivator-1α (PGC-1α) in LPS-induced microglial activation. The inhibition of PPARγ and PGC-1α attenuated the regulatory effect of IVX in LPS-induced microglial polarization. IVX increased the expression of p-CaMKKβ, p-AMPK, and PGC-1α in BV-2 cells. Inhibition of CaMKKβ with STO-609 or knockdown of CaMKKβ with CaMKKβ siRNA attenuated IVX-mediated M2 microglial polarization in LPS-treated cells. In LPS-treated mice, the inhibition of CaMKKβ and PGC-1α attenuated the IVX-mediated prevention of sickness behavior and enhanction of IVX-mediated M2 microglial polarization. IVX promoted M2 microglial polarization which exerted anti-inflammatory effects on LPS-induced neuroinflammation via the activation of the CaMKKβ/AMPK-PGC-1α signaling axis.

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Section: Discussionmentioning

confidence: 99%

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

Liu

Huang

et al. 2019

Front. Immunol.

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“…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).…”

Section: Discussionmentioning

confidence: 74%

“…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].…”

Section: Introductionmentioning

confidence: 99%

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

Amedu

Omotoso

2020

Environ Anal Health Toxicol

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This study was aimed at investigating the neuroprotective effect of Vitexin against lead (Pb) induced neurodegenerative changes in the dorsolateral prefrontal cortex (DLPFC) and working memory in mice. Thirty-two adolescent male albino mice were divided into four groups (n=8). Control group received 0.2 mL of normal saline; Pb group received 100 mg/kg of Pb acetate for 14 days, Vitexin group received 1mg/kg of Vitexin for 14 days, and Pb+Vitexin group received 100 mg/kg of Pb acetate and 1 mgkg of Vitexin for 14 days. Barnes maze test and novel object recognition test were done to ascertain working memory. Histoarchitectural assessment of DLPFC was done with haematoxylin and eosin (H&E), cresyl fast violet and congo red stains. Furthermore, cell count and other morphometric measurements were done. There was significant decline in working memory in the Pb group, but a combination of Pb+Vitexin improved the working memory. Vitexin significantly reduced neuronal death and chromatolysis caused by Pb. Amyloid aggregation was not observed in any of the groups. This study has shown that concurrent administration of Vitexin and Pb will significantly reduce neurodegeneration and improve working memory. However, Pb treatment or Pb+Vitexin treatment does not have any effect on intercellular distance, neuronal length and the cross-sectional area of neurons in layer III of DLPFC.

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“…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…”

Section: Discussionmentioning

confidence: 99%

“…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…”

Section: Discussionmentioning

confidence: 99%

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

Wang¹,

Cheng²,

Gu³

et al. 2019

OTT

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Background and objectives: Vitexin is a natural flavonoid glycoside mainly extracted from the leaves of vitex, which has a variety of physiological activities. For example, vitexin has antitumor and anti-inflammation activities, and it can also promote blood circulation in the body. However, the function and mechanism of vitexin in nasopharyngeal carcinoma (NPC) are still unclear. Materials and methods: Cell Counting Kit-8 assay and cell cycle analysis were performed to examine cell survival in response to vitexin. Immunoblotting was used to analyze relative proteins’ expression. NPC xenograft models were established to assess the effect of vitexin in vivo. The luciferase activity of pNFκB-Luc was analyzed by using Dual-Luciferase Reporter Assay System. Quantitative real-time polymerase chain reaction was performed to detect relative genes’ expression. Kinase activity of IKKβ was analyzed in a cell-free system. Results: In this study, vitexin was found to display significant antitumor activity in NPC in vitro and in vivo. In NPC cells, vitexin inhibited cell cycle progression in NPC cells and induced the cleavages of PARP and inhibited antiapoptotic proteins’ expression, including Bcl-2 and Mcl1. Further studies indicated that vitexin significantly suppressed the luciferase activity of pNF-κB-Luc and inhibited the activation of NF-κB key regulators, including p65, IκBα and IKKs in NPC cells. Moreover, the kinase activity of IKKβ could be suppressed by vitexin in a cell-free system, and overexpression of CA-IKKβ could attenuate the inhibitory effect of vitexin on p65 phosphorylation. Conclusion: These results indicated that vitexin displayed antitumor activity by suppressing NF-κB signaling in NPC, which suggested that vitexin could be as a potential drug for the treatment of NPC in the future.

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A Brief Review on the Neuroprotective Mechanisms of Vitexin

Cited by 33 publications

References 62 publications

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

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

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

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

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