Редактирование: SFN

14-3-3 protein sigma (Epithelial cell marker protein 1) (Stratifin) [HME1]

==Publications==

{{medline-entry
|title=The phytoprotective agent sulforaphane prevents inflammatory degenerative diseases and age-related pathologies via Nrf2-mediated hormesis.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33160067
|abstract=In numerous experimental models, sulforaphane ([[SFN]]) is shown herein to induce hormetic dose responses that are not only common but display endpoints of biomedical and clinical relevance. These hormetic responses are mediated via the activation of nuclear factor erythroid- derived 2 (Nrf2) antioxidant response elements (AREs) and, as such, are characteristically biphasic, well integrated, concentration/dose dependent, and specific with regard to the targeted cell type and the temporal profile of response. In experimental disease models, the [[SFN]]-induced hormetic activation of Nrf2 was shown to effectively reduce the occurrence and severity of a wide range of human-related pathologies, including Parkinson's disease, Alzheimer's disease, stroke, age-related ocular damage, chemically induced brain damage, and renal nephropathy, amongst others, while also enhancing stem cell proliferation. Although [[SFN]] was broadly chemoprotective within an hormetic dose-response context, it also enhanced cell proliferation/cell viability at low concentrations in multiple tumor cell lines. Although the implications of the findings in tumor cells are largely uncertain at this time and warrant further consideration, the potential utility of [[SFN]] in cancer treatment has not been precluded. This assessment of [[SFN]] complements recent reports of similar hormesis-based chemoprotections by other widely used dietary supplements, such as curcumin, ginkgo biloba, ginseng, green tea, and resveratrol. Interestingly, the mechanistic profile of [[SFN]] is similar to that of numerous other hormetic agents, indicating that activation of the Nrf2/ARE pathway is probably a central, integrative, and underlying mechanism of hormesis itself. The Nrf2/ARE pathway provides an explanation for how large numbers of agents that both display hormetic dose responses and activate Nrf2 can function to limit age-related damage, the progression of numerous disease processes, and chemical- and radiation- induced toxicities. These findings extend the generality of the hormetic dose response to include [[SFN]] and many other chemical activators of Nrf2 that are cited in the biomedical literature and therefore have potentially important public health and clinical implications.

|keywords=* Aging
* Hormesis
* Inflammation
* Neuroprotection
* Nrf2
* Sulforaphane
|full-text-url=https://sci-hub.do/10.1016/j.phrs.2020.105283
}}
{{medline-entry
|title=Multi-Omic Analysis Reveals Different Effects of Sulforaphane on the Microbiome and Metabolome in Old Compared to Young Mice.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33003447
|abstract=Dietary factors modulate interactions between the microbiome, metabolome, and immune system. Sulforaphane ([[SFN]]) exerts effects on aging, cancer prevention and reducing insulin resistance. This study investigated effects of [[SFN]] on the gut microbiome and metabolome in old mouse model compared with young mice. Young (6-8 weeks) and old (21-22 months) male C57BL/6J mice were provided regular rodent chow ± [[SFN]] for 2 months. We collected fecal samples before and after [[SFN]] administration and profiled the microbiome and metabolome. Multi-omics datasets were analyzed individually and integrated to investigate the relationship between [[SFN]] diet, the gut microbiome, and metabolome. The [[SFN]] diet restored the gut microbiome in old mice to mimic that in young mice, enriching bacteria known to be associated with an improved intestinal barrier function and the production of anti-inflammatory compounds. The tricarboxylic acid cycle decreased and amino acid metabolism-related pathways increased. Integration of multi-omic datasets revealed [[SFN]] diet-induced metabolite biomarkers in old mice associated principally with the genera, [i]Oscillospira[/i], [i]Ruminococcus[/i], and [i]Allobaculum[/i]. Collectively, our results support a hypothesis that [[SFN]] diet exerts anti-aging effects in part by influencing the gut microbiome and metabolome. Modulating the gut microbiome by [[SFN]] may have the potential to promote healthier aging.

|keywords=* aging
* biomarkers
* gut microbiome
* metabolome
* sulforaphane
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7599699
}}
{{medline-entry
|title=Sulforaphane controls the release of paracrine factors by keratinocytes and thus mitigates particulate matter-induced premature skin aging by suppressing melanogenesis and maintaining collagen homeostasis.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32659677
|abstract=Skin aging, potentially caused by exposure to particulate matter (PM) , is characterized by wrinkling, abnormal pigmentation, and skin dryness triggered by several keratinocyte-derived paracrine factors. Sulforaphane (4-methylsulfinylbutyl isothiocyanate, [[SFN]]), commonly found in cruciferous vegetables, has diverse biological effects on skin tissue. In the present study, we have investigated whether [[SFN]] may alleviate PM -induced premature skin aging. We used keratinocyte/melanocyte or keratinocyte/fibroblast coculture models of skin cells and measured the parameters of melanogenesis, collagen homeostasis and inflammation. [[SFN]] inhibited the development of reactive oxygen species in keratinocytes exposed to PM . In keratinocyte/melanocyte cocultures, it significantly inhibited the upregulation of melanogenic paracrine mediators (including endothelin-1 and prostaglandin E2) in keratinocytes exposed to PM ; the synthesis of melanogenic proteins including microphthalmia-associated transcription factor, tyrosinase-related protein 1, and tyrosinase; and the levels of melanin in melanocytes. [[SFN]] treatment of keratinocyte/fibroblast cocultures significantly reduced the PM -induced expression of NF-κB-mediated cytokines including interleukin-1β, interleukin-6, tumor necrosis factor α, and cyclooxygenase-2. In fibroblasts of the keratinocyte/fibroblast coculture system, the expression levels of phospho-NF-κB, cysteine-rich protein 61, and matrix metalloproteinase-1 were significantly decreased whereas procollagen type I synthesis was significantly increased. Collectively, our results suggest that [[SFN]] mitigates PM -induced premature skin aging by suppressing melanogenesis and maintaining collagen homeostasis. It acts by regulating the release of paracrine factors from keratinocytes.

|keywords=* Coculture system
* Collagen homeostasis
* Melanogenesis
* Particulate matter 2.5
* Premature skin aging
* Sulforaphane
|full-text-url=https://sci-hub.do/10.1016/j.phymed.2020.153276
}}
{{medline-entry
|title=Sulforaphane Inhibits Autophagy and Induces Exosome-Mediated Paracrine Senescence via Regulating mTOR/TFE3.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32476238
|abstract=The development of novel compounds that trigger non-apoptotic cell death may represent alternative therapeutic strategies for esophageal squamous cell carcinoma (ESCC) treatment. Cellular senescence suppresses tumorigenesis by halting the proliferation of tumor cells, implying the induction of senescence as a promising anticancer strategy, especially when combined with senolytic agents that specially kill senescent cells. This study is designed to screen novel anti-ESCC compounds from a natural product resource and identify its mechanism-of-action. Identified are the significant anti-cancer effect and underlying mechanism of [[SFN]], an isothiocyanate derived from cruciferous vegetables, through RNA sequencing, western blot, and immunofluorescent assays. It is found that [[SFN]] inhibits proliferation of ESCC cells through inducing senescence. Mechanistically, [[SFN]] induces reactive oxygen species (ROS) via disrupting the balance between glutathione and oxidized glutathione, leading to DNA damage. In addition, ROS deregulates autophagy and promotes lysosome abnormal biogenesis through regulating mTOR/TFE3 axis. Finally, the inhibited autophagic flux facilitates exosome production, resulting in exosome-mediated paracrine senescence. This study suggests the important roles of autophagy and exosome-mediated paracrine senescence in cancer therapy and highlights [[SFN]] as a potent anti-ESCC drug candidate.

|keywords=* ROS
* autophagy
* exosome
* senescence
* sulforaphane
|full-text-url=https://sci-hub.do/10.1002/mnfr.201901231
}}
{{medline-entry
|title=Effects of sulforaphane on D-galactose-induced liver aging in rats: Role of keap-1/nrf-2 pathway.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31039346
|abstract=Aging; a biological phenomenon characterized by progressive decline in cellular functions, is considered as a major risk factor of various liver diseases that plays as an adverse prognostic role, thus increasing mortality rate. However, diet is the main environmental factor that has a major impact on the aging process whereas; sulforaphane ([[SFN]]), an isothiocyanate organosulfur compound in cruciferous vegetables, has been reported with myriad biological effects. In the present study, [[SFN]] antiaging properties were evaluated on D-galactose (D-Gal)-induced liver aging in rats. For this purpose, forty adult male Wistar rats were divided into five groups. All animals, except the normal control, were intraperitoneally injected with D-Gal (300 mg/kg/day for 5 days a week) for six consecutive weeks. In the hepatoprotective groups, animals received oral [[SFN]] (0.5, 1.0 and 2.0 mg/kg) for 6 weeks concurrently with D-[[GAL]]. [[SFN]] administration improved liver biomarkers through decreasing serum levels of AST, ALT, total and direct bilirubin when compared to D-Gal-aging group. [[SFN]] significantly increased hepatic GSH level as well as catalase and glutathione-S-transferase activities while counteracted the elevation in hepatic oxidative stress markers; MDA, NO and protein carbonyl in aged rats. [[SFN]] abrogated the dysregulation in hepatic Keap-1, Nrf-2 and HO-1and limited the elevation of [[TNF]]-α and TGF-β concentrations in aging liver. Histopathologically, [[SFN]] decreased the intensity of hepatic fibrous proliferation in D-Gal-induced aging. In conclusion, [[SFN]] has shown hepatic anti-aging potential through promoting the antioxidant machinery via regulating Keap-1, Nrf-2 and HO-1 and antioxidant enzyme activities as well as ameliorating oxidative stress, hampering the inflammatory cytokines; [[TNF]]-ɑ and TGF-β, and limiting hepatic fibrosis in a dose dependent manner.
|mesh-terms=* Aging
* Animals
* Antioxidants
* Biomarkers
* Galactose
* Heme Oxygenase (Decyclizing)
* Isothiocyanates
* Kelch-Like ECH-Associated Protein 1
* Liver
* Male
* NF-E2-Related Factor 2
* Oxidative Stress
* Rats
* Rats, Wistar
* Transforming Growth Factor beta
* Tumor Necrosis Factor-alpha
|keywords=* Aging
* D-galactose
* Fibrosis
* Nrf-2
* Rats
* Sulforaphane
|full-text-url=https://sci-hub.do/10.1016/j.ejphar.2019.04.043
}}
{{medline-entry
|title=Sulforaphane - role in aging and neurodegeneration.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/30941620
|abstract=In the last several years, numerous molecules derived from plants and vegetables have been tested for their antioxidant, anti-inflammatory, and anti-aging properties. One of them is sulforaphane ([[SFN]]), an isothiocyanate present in cruciferous vegetables. [[SFN]] activates the antioxidant and anti-inflammatory responses by inducing Nrf2 pathway and inhibiting NF-κB. It also has an epigenetic effect by inhibiting HDAC and DNA methyltransferases and modifies mitochondrial dynamics. Moreover, [[SFN]] preserves proteome homeostasis (proteostasis) by activating the proteasome, which has been shown to lead to increased cellular lifespan and prevent neurodegeneration. In this review, we describe some of the molecular and physical characteristics of [[SFN]], its mechanisms of action, and the effects that [[SFN]] treatment induces in order to discuss its relevance as a "miraculous" drug to prevent aging and neurodegeneration.
|mesh-terms=* Aging
* Animals
* Antioxidants
* Epigenesis, Genetic
* Humans
* Inflammation
* Isothiocyanates
* Kelch-Like ECH-Associated Protein 1
* NF-E2-Related Factor 2
* NF-kappa B
* Oxidative Stress
* Proteostasis
|keywords=* HDAC
* NF-κB
* Nrf2
* Oxidative stress
* Proteasome
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6885086
}}
{{medline-entry
|title=The secretory phenotype of senescent astrocytes isolated from Wistar newborn rats changes with anti-inflammatory drugs, but does not have a short-term effect on neuronal mitochondrial potential.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/30097900
|abstract=In the central nervous system (CNS), senescent astrocytes have been associated with neurodegeneration. Senescent cells secrete a complex mixture of pro-inflammatory factors, which are collectively called Senescence Associated Secretory Phenotype (SASP). The SASP components can vary depending on the cell type, senescence inducer and time. The SASP has been mainly studied in fibroblasts and epithelial cells, but little is known in the context of the CNS. Here, the SASP profile in senescent astrocytes isolated from Wistar newborn rats induced to senescence by oxidative stress or by proteasome inhibition was analyzed. Senescent astrocytes secreted predominantly chemokines and IL-1α, but no IL-6. The effect of the anti-inflammatory drugs, sulforaphane ([[SFN]]) and dehydroepiandrosterone (DHEA), on the SASP profile was evaluated. Our results showed that [[SFN]] and DHEA decreased IL-1α secretion while increasing IL-10, thus modifying the SASP to a less anti-inflammatory profile. Primary neurons were subjected to the conditioned media obtained from drug-treated senescent astrocytes, and their mitochondrial membrane potential was evaluated.
|mesh-terms=* Animals
* Animals, Newborn
* Anti-Inflammatory Agents
* Astrocytes
* Cellular Senescence
* Central Nervous System
* Dehydroepiandrosterone
* Inflammation
* Interleukin-1alpha
* Isothiocyanates
* Membrane Potential, Mitochondrial
* Models, Animal
* Neurons
* Oxidative Stress
* Rats
* Rats, Wistar
|keywords=* Astrocytes
* Neurons
* Senescence
* central nervous system
* inflammation
|full-text-url=https://sci-hub.do/10.1007/s10522-018-9767-3
}}
{{medline-entry
|title=Sulforaphane reactivates cellular antioxidant defense by inducing Nrf2/ARE/Prdx6 activity during aging and oxidative stress.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/29074861
|abstract=Upon oxidative stress and aging, Nrf2 (NFE2-related factor2) triggers antioxidant defense genes to defends against homeostatic failure. Using human(h) or rat(r) lens epithelial cells (LECs) and aging human lenses, we showed that a progressive increase in oxidative load during aging was linked to a decline in Prdx6 expression. DNA binding experiments using gel-shift and ChIP assays demonstrated a progressive reduction in Nrf2/ARE binding (-357/-349) of Prdx6 promoter. The promoter (-918) with ARE showed a marked reduction in young vs aged hLECs, which was directly correlated to decreased Nrf2/ARE binding. A Nrf2 activator, Sulforaphane ([[SFN]]), augmented Prdx6, catalase and GSTπ expression in dose-dependent fashion, and halted Nrf2 dysregulation of these antioxidants. [[SFN]] reinforced Nrf2/DNA binding and increased promoter activities by enhancing expression and facilitating Nrf2 translocalization in nucleus. Conversely, promoter mutated at ARE site did not respond to [[SFN]], validating the [[SFN]]-mediated restoration of Nrf2/ARE signaling. Furthermore, [[SFN]] rescued cells from UVB-induced toxicity in dose-dependent fashion, which was consistent with [[SFN]]'s dose-dependent activation of Nrf2/ARE interaction. Importantly, knockdown of Prdx6 revealed that Prdx6 expression was prerequisite for [[SFN]]-mediated cytoprotection. Collectively, our results suggest that loss of Prdx6 caused by dysregulation of ARE/Nrf2 can be attenuated through a [[SFN]], to combat diseases associated with aging.
|mesh-terms=* Active Transport, Cell Nucleus
* Adolescent
* Adult
* Aged
* Aging
* Animals
* Antioxidants
* Cell Nucleus
* Dose-Response Relationship, Drug
* Gene Expression Regulation
* Humans
* Isothiocyanates
* Middle Aged
* NF-E2-Related Factor 2
* Oxidative Stress
* Peroxiredoxin VI
* Promoter Regions, Genetic
* Rats
* Rats, Sprague-Dawley
* Response Elements
* Time Factors
* Transcription, Genetic
* Up-Regulation
* Young Adult

|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5658327
}}
{{medline-entry
|title=What do we know about sulforaphane protection against photoaging?
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/26799467
|abstract=Sulforaphane ([[SFN]]), a natural compound occurring in cruciferous vegetables, has been known for years as a chemopreventive agent against many types of cancer. Recently, it has been investigated as an antioxidant and anti-aging agent, and interesting conclusions have been made over the last decade. [[SFN]] demonstrated protective effects against ultraviolet (UV)-induced skin damage through several mechanisms of action, for example, decrease of reactive oxygen species production, inhibition of matrix metalloproteinase expression, and induction of phase 2 enzymes. [[SFN]] used as a protective agent against UV damage is a whole new matter, and it seems to be a very promising ingredient in upcoming anti-aging drugs and cosmetics. 
|mesh-terms=* Anticarcinogenic Agents
* Humans
* Isothiocyanates
* Kelch-Like ECH-Associated Protein 1
* Matrix Metalloproteinase 1
* Matrix Metalloproteinase 3
* NF-E2-Related Factor 2
* NF-kappa B
* Radiation-Protective Agents
* Signal Transduction
* Skin
* Skin Aging
* Transcription Factor AP-1
* Ultraviolet Rays
|keywords=* aging
* skin
* sulforaphane
* ultraviolet
|full-text-url=https://sci-hub.do/10.1111/jocd.12176
}}
{{medline-entry
|title=Hormetic Potential of Sulforaphane ([[SFN]]) in Switching Cells' Fate Towards Survival or Death.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/26586127
|abstract=Epidemiological evidences establish sulforaphane ([[SFN]]), a hormetic dietary isothiocyanate to be a promising chemopreventive, anti-inflammatory and anti-cancer agent. Beyond a concentration threshold [[SFN]] exerts pro-death activities (cell cycle arrest, epigenetic modifications and apoptosis) and below the threshold it either promotes prosurvival autophagy or remains latent. There is a significant lacuna in understanding the underpinning dynamic molecular networks that alternate the pharmacological responses with respect to the intracellular concentration and exposure time that renders [[SFN]] to be a characteristic hormetic molecule (display characteristic biphasic dose response curve). Unraveling this multi-targeted [[SFN]] triggered molecular interplay between apoptosis and pro-survival autophagy may have great therapeutic implications. From the available literature, here we present a review that illustrates the existence of a hormetic window and briefly discussed its role in the spectrum of activity of [[SFN]] in different pathological conditions (cancer and immune-mediated diseases). Further, we hypothesize a hormetic signaling event on how [[SFN]] triggers mutually exclusive molecular pathways such as cell survival or death signals depending on its pathophysiological environment, exposure time and in vitro working concentrations. By better understanding these altered events and underpinning mechanisms in different combinations such as concentrations and time a proper therapeutic can be designed. 
|mesh-terms=* Aging
* Animals
* Anti-Inflammatory Agents
* Anticarcinogenic Agents
* Antineoplastic Agents, Phytogenic
* Apoptosis
* Autophagy
* Cell Cycle Checkpoints
* Cell Survival
* Humans
* Isothiocyanates
* Neoplasms

|full-text-url=https://sci-hub.do/10.2174/1389557516666151120115027
}}
{{medline-entry
|title=Sulforaphane induces Nrf2 target genes and attenuates inflammatory gene expression in microglia from brain of young adult and aged mice.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/26571201
|abstract=Increased neuroinflammation and oxidative stress resulting from heightened microglial activation are associated with age-related cognitive impairment. The objectives of this study were to examine the effects of the bioactive sulforaphane ([[SFN]]) on the nuclear factor E2-related factor 2 (Nrf2) pathway in BV2 microglia and primary microglia, and to evaluate proinflammatory cytokine expression in lipopolysaccharide (LPS)-stimulated primary microglia from adult and aged mice. BV2 microglia and primary microglia isolated from young adult and aged mice were treated with [[SFN]] and LPS. Changes in Nrf2 activity, expression of Nrf2 target genes, and levels of proinflammatory markers were assessed by quantitative PCR and immunoassay. [[SFN]] increased Nrf2 DNA-binding activity and upregulated Nrf2 target genes in BV2 microglia, while reducing LPS-induced interleukin (IL-)1β, IL-6, and inducible nitric oxide synthase (iNOS). In primary microglia from adult and aged mice, [[SFN]] increased expression of Nrf2 target genes and attenuated IL-1β, IL-6, and iNOS induced by LPS. These data indicate that [[SFN]] is a potential beneficial supplement that may be useful for reducing microglial mediated neuroinflammation and oxidative stress associated with aging. 
|mesh-terms=* Aging
* Animals
* Anti-Inflammatory Agents, Non-Steroidal
* Cells, Cultured
* Cytokines
* DNA-Binding Proteins
* Drug Evaluation, Preclinical
* Gene Expression Regulation
* Inflammation Mediators
* Isothiocyanates
* Lipopolysaccharides
* Male
* Mice, Inbred BALB C
* Microglia
* NF-E2-Related Factor 2
* Up-Regulation
|keywords=* Aging
* BV2 microglia
* Neuroinflammation
* Nrf2
* Primary microglia
* Sulforaphane
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4713291
}}
{{medline-entry
|title=Epigenetic linkage of aging, cancer and nutrition.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/25568452
|abstract=Epigenetic mechanisms play a pivotal role in the expression of genes and can be influenced by both the quality and quantity of diet. Dietary compounds such as sulforaphane ([[SFN]]) found in cruciferous vegetables and epigallocatechin-3-gallate (EGCG) in green tea exhibit the ability to affect various epigenetic mechanisms such as DNA methyltransferase (DNMT) inhibition, histone modifications via histone deacetylase (HDAC), histone acetyltransferase (HAT) inhibition, or noncoding RNA expression. Regulation of these epigenetic mechanisms has been shown to have notable influences on the formation and progression of various neoplasms. We have shown that an epigenetic diet can influence both cellular longevity and carcinogenesis through the modulation of certain key genes that encode telomerase and p16. Caloric restriction (CR) can also play a crucial role in aging and cancer. Reductions in caloric intake have been shown to increase both the life- and health-span in a variety of animal models. Moreover, restriction of glucose has been demonstrated to decrease the incidence of age-related diseases such as cancer and diabetes. A diet rich in compounds such as genistein, [[SFN]] and EGCG can positively modulate the epigenome and lead to many health benefits. Also, reducing the quantity of calories and glucose in the diet can confer an increased health-span, including reduced cancer incidence. 
|mesh-terms=* Aging
* Animals
* Caloric Restriction
* Diet
* Epigenesis, Genetic
* Humans
* Neoplasms
* Nutritional Status
|keywords=* Aging
* Cancer
* Diet
* Epigenetics
* Nutrition
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4286704
}}
{{medline-entry
|title=Dietary broccoli mildly improves neuroinflammation in aged mice but does not reduce lipopolysaccharide-induced sickness behavior.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/25439028
|abstract=Aging is associated with oxidative stress and heightened inflammatory response to infection. Dietary interventions to reduce these changes are therefore desirable. Broccoli contains glucoraphanin, which is converted to sulforaphane ([[SFN]]) by plant myrosinase during cooking preparation or digestion. Sulforaphane increases antioxidant enzymes including NAD(P)H quinone oxidoreductase and heme oxygenase I and inhibits inflammatory cytokines. We hypothesized that dietary broccoli would support an antioxidant response in brain and periphery of aged mice and inhibit lipopolysaccharide (LPS)-induced inflammation and sickness. Young adult and aged mice were fed control or 10% broccoli diet for 28 days before an intraperitoneal LPS injection. Social interactions were assessed 2, 4, 8, and 24 hours after LPS, and mRNA was quantified in liver and brain at 24 hours. Dietary broccoli did not ameliorate LPS-induced decrease in social interactions in young or aged mice. Interleukin-1β (IL-1β) expression was unaffected by broccoli consumption but was induced by LPS in brain and liver of adult and aged mice. In addition, IL-1β was elevated in brain of aged mice without LPS. Broccoli consumption decreased age-elevated cytochrome b-245 β, an oxidative stress marker, and reduced glial activation markers in aged mice. Collectively, these data suggest that 10% broccoli diet provides a modest reduction in age-related oxidative stress and glial reactivity, but is insufficient to inhibit LPS-induced inflammation. Thus, it is likely that [[SFN]] would need to be provided in supplement form to control the inflammatory response to LPS. 
|mesh-terms=* Aging
* Animals
* Behavior, Animal
* Brain
* Brassica
* CX3C Chemokine Receptor 1
* Glial Fibrillary Acidic Protein
* Illness Behavior
* Interleukin-1beta
* Lipopolysaccharides
* Liver
* Mice
* Mice, Inbred BALB C
* Microglia
* NF-E2-Related Factor 2
* RNA, Messenger
* Receptors, Chemokine
* Up-Regulation
|keywords=* Aging
* BALB/c mice
* Broccoli
* Inflammation
* LPS
* Sulforaphane
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4428599
}}
{{medline-entry
|title=Contact heat evoked potentials: normal values and use in small-fiber neuropathy.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/25256002
|abstract=Contact heat evoked potentials (CHEPs) may be an objective, non-invasive diagnostic tool in small-fiber neuropathy ([[SFN]]). This study establishes normal CHEP values and examines their applicability in [[SFN]] patients. Standardized CHEPs were administered at the wrist and ankle. The N2 and P2 latencies and N2 -P2 peak-peak amplitude were recorded by electroencephalography. We examined healthy subjects (n = 97), stratified by age and gender, and [[SFN]] patients with abnormal intraepidermal nerve fiber density (n = 42). CHEP reproducibility and interobserver values were also investigated. CHEP normative values were determined. There was a 9-16% increase in latency per centimeter of height with increasing age. Amplitudes were higher in women than men, and decreased (17-71%) with aging. Test-retest reproducibility and interobserver values were >0.61 and >0.96, respectively. CHEPs were abnormal in 73.8% of the patients. In this study we have established normal values, reliability, and clinical applicability of CHEPs in [[SFN]].
|mesh-terms=* Adult
* Aged
* Aging
* Ankle
* Erythromelalgia
* Evoked Potentials, Somatosensory
* Female
* Hot Temperature
* Humans
* Male
* Middle Aged
* Observer Variation
* Reaction Time
* Reference Values
* Reproducibility of Results
* Retrospective Studies
* Sex Factors
* Skin
* Wrist
|keywords=* contact heat evoked potentials
* polyneuropathy
* quantitative sensory testing
* reference values
* small-fiber neuropathy
|full-text-url=https://sci-hub.do/10.1002/mus.24465
}}
{{medline-entry
|title=Quantitative proteomic profiling of tumor cell response to telomere dysfunction using isotope-coded protein labeling (ICPL) reveals interaction network of candidate senescence markers.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/23969227
|abstract=Telomerase inhibition causes progressive telomere shortening and cellular senescence, which constitutes a universal barrier to tumor growth and therefore an attractive target for tumor therapy. To expand our previous studies, we investigated the global effects of telomere dysfunction on the proteome of tumor cells in order to find novel senescence biomarkers. Telomerase-deficient HCT-116 cell clones were analyzed by a quantitative proteomic approach using isotope-coded protein labeling (ICPL) and nanoflow-HPLC-MS/MS. Stringent reduction of the extensive proteomic data from this tumor cell model revealed a list of 59 markers including proteins identified in our former studies and a number of novel proteins involved in tumorigenesis and metastasis such as [[SFN]], [[S100A4]], [[ANXA2]], and [[LGALS1]]. A loss of the chromatin protein [[HMGB2]] was demonstrated not only in various telomerase-inhibited clones of different tumor cell lines, but also in normal human fibroblasts undergoing replicative senescence and in aging telomerase knockout mice. Impressively, a coherent and dense network of protein-protein interactions for the bulk of the markers and their implementation in signaling pathways involving key regulators for tumorigenesis were revealed. These results have an impact on the understanding of telomere- and senescence-related signal transduction in tumor cells in consideration of the general lack of senescence markers. Induction of cellular senescence constitutes a potent concept for tumor therapy which interferes with immortalization and additional hallmarks of cancer. The application of a powerful quantitative proteomic approach using isotope-coded protein labeling to an approved model for senescence represented by telomerase inhibited tumor cells led to the identification of novel candidate biomarkers for telomere dysfunction and replicative senescence. Thereby, the identified markers not only fit in the context of the investigated processes with a relevance for additional hallmarks of cancer but are also involved in a strong interaction network and integrated in canonical pathways centered around key cancer-relevant proteins. These potential markers alone or in combination will significantly extend the view on telomere-associated signal transduction in tumor cells and contribute to the field of cellular senescence and aging in consideration of the general lack of biomarkers in this regard.
|mesh-terms=* Animals
* Biomarkers, Tumor
* Cell Line, Tumor
* Cellular Senescence
* Colonic Neoplasms
* Cytoskeleton
* Fibroblasts
* Genes, Dominant
* Humans
* Mice
* Mice, Knockout
* Mitochondria
* Mutation
* Proteomics
* Ribosomes
* Signal Transduction
* Telomerase
* Telomere
|keywords=* ICPL
* Quantitative proteomics
* Senescence
* Telomerase
* Telomere dysfunction
|full-text-url=https://sci-hub.do/10.1016/j.jprot.2013.08.007
}}