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The comprehensive quantitative analysis of the flavonoid chemistry of Artemisia vulgaris L., a plant used as an emmenagogue in traditional medicine, is presented in conjunction with an evaluation of its estrogenic activity. Twenty known flavonoids were isolated and identified as tricine, jaceosidine, eupafolin, chrysoeriol, diosmetin, homoeriodictyol, isorhamnetin, apigenin, eriodictyol, luteolin, luteolin 7-glucoside, kaempferol 3-glucoside, kaempferol 7-glucoside, kaempferol 3-rhamnoside, kaempferol 3-rutinoside, quercetin 3-glucoside, quercetin 3-galactoside, quercetrin, rutin, and vitexin. The most abundant compounds were eriodictyol and luteolin. The estrogenic activity of all flavonoids was assayed by employing a reconstituted estrogen transcription unit in Saccharomyces cerevisiae transformed with both a human estrogen receptor expression plasmid and a reporter plasmid. Two flavonoids, eriodictyol and apigenin, were able to induce the transcription of the reporter gene in transgenic yeast. The transcriptional activity increased proportionally with increased amounts of purified eriodictyol or apigenin added to the yeast cells. Keywords: Artemisia vulgaris; estrogenic activity; estrogen transcriptional system in yeast; flavonoids; apigenin; eriodictyol; luteolin

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Lesion or disease of the somatosensory system leads to the development of neuropathic pain. Peripheral neuropathic pain encompasses damage or injury of the peripheral nervous system. On the other hand, 10–15% of individuals suffer from acute postoperative pain followed by persistent pain after undergoing surgeries. Antidepressants, anticonvulsants, baclofen, and clonidine are used to treat peripheral neuropathy, whereas opioids are used to treat postoperative pain. The negative effects associated with these drugs emphasize the search for alternative therapeutics with better efficacy and fewer side effects. Curcumin, a polyphenol isolated from the roots of Curcuma longa, possesses antibacterial, antioxidant, and anti-inflammatory properties. Furthermore, the low bioavailability and fast metabolism of curcumin have led to the advent of various curcumin formulations. The present review provides a comprehensive analysis on the effects of curcumin and its formulations in preclinical and clinical studies of neuropathic and postoperative pain. Based on the positive outcomes from both preclinical and clinical studies, curcumin holds the promise of mitigating or preventing neuropathic and postoperative pain conditions. However, more clinical studies with improved curcumin formulations are required to involve its use as adjuvant to neuropathic and postoperative drugs.

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Oxidative stress, resulting from an imbalance between the formation of damaging free radicals and availability of protective antioxidants, can contribute to peripheral neuropathic pain conditions. Reactive oxygen and nitrogen species, as well as products of the mitochondrial metabolism such as superoxide anions, hydrogen peroxide, and hydroxyl radicals, are common free radicals. Nuclear factor erythroid 2 (NFE2)-related factor 2 (Nrf2) is a transcription factor encoded by the NFE2L2 gene and is a member of the cap ‘n’ collar subfamily of basic region leucine zipper transcription factors. Under normal physiological conditions, Nrf2 remains bound to Kelch-like ECH-associated protein 1 in the cytoplasm that ultimately leads to proteasomal degradation. During peripheral neuropathy, Nrf2 can translocate to the nucleus, where it heterodimerizes with muscle aponeurosis fibromatosis proteins and binds to antioxidant response elements (AREs). It is becoming increasingly clear that the Nrf2 interaction with ARE leads to the transcription of several antioxidative enzymes that can ameliorate neuropathy and neuropathic pain in rodent models. Current evidence indicates that the antinociceptive effects of Nrf2 occur via reducing oxidative stress, neuroinflammation, and mitochondrial dysfunction. Here, we will summarize the preclinical evidence supporting the role of Nrf2 signaling pathways and Nrf2 inducers in alleviating peripheral neuropathic pain.

Mammalian sex hormones are spread in the environment from natural and anthropogenic sources. In the present study, the effect of estradiol on Arabidopsis thaliana growth primary metabolism, phenylpropanoid and flavonoid pathways and pathogen resistance were investigated. Treatments of Arabidopsis plants with 10 and 100 nM 17β-estradiol resulted in enhanced root growth and shoot biomass. In addition, treated plants had an increased rate of photosynthesis with a concomitant increase in carbohydrate and protein accumulation. Plants exposed to higher concentrations of 17β-estradiol (10 μM) had significantly lower root growth, biomass, photosynthesis rate, primary metabolite and phenylpropanoid and flavonoid contents indicating a toxic effect of estradiol. Treatments with increasing estradiol concentrations (10 nM, 100 nM and 10 μM) resulted in the downregulation of phenylpropanoid-flavonoid pathway genes (PAL1, PAL4, CHI and ANS) and subsequent decreased accumulation of phenolics, flavonoids and anthocyanins. Estradiol-treated plants were inoculated with Pseudomonas syringae pv. Tomato DC3000 and basal resistance was determined. Estradiol treatments rendered plants susceptible to the pathogen, thus compromising the plant defense mechanisms. These results indicate that at low concentrations, estradiol functions as a biostimulant of growth, yield and primary metabolism of Arabidopsis. However, estradiol functions as a potential transcriptional regulator of the phenylpropanoid pathway genes in Arabidopsis, having a negative effect on the phenylpropanoid and flavonoid biosynthetic pathways.