A review on the pharmacological effects of vitexin and isovitexin.

Quinoa (Chenopodium quinoa Willd.) was known as the “golden grain” by the native Andean people in South America, and has been a source of valuable food over thousands of years. It can produce a variety of secondary metabolites with broad spectra of bioactivities. At least 193 secondary metabolites from quinoa have been identified in the past 40 years. They mainly include phenolic acids, flavonoids, terpenoids, steroids, and nitrogen-containing compounds. These metabolites exhibit many physiological functions, such as insecticidal, molluscicidal and antimicrobial activities, as well as various kinds of biological activities such as antioxidant, cytotoxic, anti-diabetic and anti-inflammatory properties. This review focuses on our knowledge of the structures, biological activities and functions of quinoa secondary metabolites. Biosynthesis, development and utilization of the secondary metabolites especially from quinoa bran were prospected.

Quinoa Secondary Metabolites and Their Biological Activities or Functions.

Vitexin is an apigenin flavone glycoside found in food and medicinal plants. It has a variety of pharmacological effects, including antioxidant, anti-inflammatory, anticancer, antinociceptive, and neuroprotective effects. This review study summarizes all the protective effects of vitexin as an antioxidant against reactive oxygen species, lipid peroxidation, and other oxidative damages in a variety of oxidative stress-related diseases, including seizure, memory impairment, cerebral ischemia, neurotoxicity, myocardial and respiratory injury, and metabolic dysfunction, with possible molecular and cellular mechanisms. This review describes any activation or inhibition of the signaling pathways that depend on the antioxidant activity of vitexin. More basic research is needed on the antioxidative effects of vitexin in vivo, and carrying out clinical trials for the treatment of oxidative stress-related diseases is also recommended.

https://onlinelibrary.wiley.com/doi/pdf/10.1002/fsn3.1567

Review of the effects of vitexin in oxidative stress-related diseases.

Nose to brain drug delivery - A promising strategy for active components from herbal medicine for treating cerebral ischemia reperfusion.

Vitexin reverses the autophagy dysfunction to attenuate MCAO-induced cerebral ischemic stroke via mTOR/Ulk1 pathway.

Vitexin protects brain against ischemia/reperfusion injury via modulating mitogen-activated protein kinase and apoptosis signaling in mice

Use of cellular metabolomics and lipidomics to decipher the mechanism of Huachansu injection-based intervention against human hepatocellular carcinoma cells.

The role of RhoA/ROCK pathway in the ischemic stroke-induced neuroinflammation.

Ischemic stroke is one of the most cases worldwide, with high rate of morbidity and mortality. In the pathological process of ischemic stroke, neuroinflammation is an essential process that defines the functional prognosis. After stroke onset, microglia, astrocytes and the infiltrating immune cells contribute to a complicated neuroinflammation cascade and play the complicated roles in the pathophysiological variations of ischemic stroke. Both microglia and astrocytes undergo both morphological and functional changes, thereby deeply participate in the neuronal inflammation via releasing pro-inflammatory or anti-inflammatory factors. Flavonoids are plant-specific secondary metabolites and can protect against cerebral ischemia injury via modulating the inflammatory responses. For instances, quercetin can inhibit the expression and release of pro-inflammatory cytokines, such as tumor necrosis factor (TNF)-α, IL-6 and IL-1β, in the cerebral nervous system (CNS). Apigenin and rutin can promote the polarization of microglia to anti-inflammatory genotype and then inhibit neuroinflammation. In this review, we focused on the dual roles of activated microglia and reactive astrocyte in the neuroinflammation following ischemic stroke and discussed the anti-neuroinflammation of some flavonoids. Importantly, we aimed to reveal the new strategies for alleviating the cerebral ischemic stroke. 

Flavonoids and ischemic stroke-induced neuroinflammation: Focus on the glial cells.

The effect of lipopolysaccharide (LPS)-based neuroinflammation following cerebral ischemia/reperfusion (I/R) on the genotypic transformation of reactive astrocytes and its relationship with endogenous hydrogen sulfide (H2S) were investigated in present study. We found that LPS promoted the cerebral I/R-induced A1 astrocytes proliferation in mouse hippocampal tissues and deteriorated the reduction of hydrogen sulfide (H2S) content in mouse sera, H2S donor NaHS could inhibit A1 astrocytes proliferation. Similarly, knockout of cystathionine γ-lyase (CSE), one of endogenous H2S synthases, likewise up-regulated the cerebral I/R-induced A1 astrocytes proliferation, which could also be blocked by NaHS. Besides, supplement with H2S promoted the A2 astrocytes proliferation in hippocampal tissues of CSE knockout (CSE KO) mice or LPS-treated mice following cerebral I/R. In the oxygen glucose deprivation/reoxygenation (OGD/R) model of astrocytes, H2S also promoted the transformation of astrocytes into A2 subtype. Moreover, we found that H2S could up-regulate the expression of α-subunit of large-conductance Ca2+-activated K+ (BKCa) channels in astrocytes, and the channel opener BMS-191011 likewise promoted the transformation of astrocyte into A2 subtype. In conclusion, H2S inhibits the proliferation of A1 astrocytes induced by LPS-based neuroinflammation following cerebral I/R and promotes the transformation of astrocytes into A2 subtype, which may be related to up-regulation of BKCa channels. 

Hydrogen sulfide inhibits lipopolysaccharide-based neuroinflammation-induced astrocyte polarization after cerebral ischemia/reperfusion injury.

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