1,721,200 research outputs found
Role of Scavenger Receptor B1 (SR-B1) in Improving Food Benefits for Human Health
No full textScavenger receptor class B member 1 (SR-B1) is a multiligand receptor with a broad range of functions spanning from the uptake of cholesteryl esters from high-density lipoproteins (HDLs) and transport of micronutrients such as fat-soluble vitamins and carotenoids across cell membranes
to roles in tumor progression, pathogen recognition, and inflammatory responses. As a target of exposome factors such as environmental stressors and unhealthy lifestyle choices, as well as aging, dysregulated expression and activity of SR-B1 can negatively impact human health. Intriguingly, not only is SR-B1 a major determinant of nutrient homeostasis and, hence, metabolic
health status, but these same nutrients and some phytochemicals have also
demonstrated their ability to modulate SR-B1. Therefore, an integrated
approach that, taking into account human health, nutrition, and food tech-
nology sciences, aims to produce foods with health-promoting effects should
take advantage of the multifaceted properties of SR-B1. Improved func-
tional foods and novel nanoparticle-based delivery systems, rich in nutrients
and phytochemicals, with precise targeting to SR-B1 in specific tissues or
structures could represent a strategic advance to improve human health and
promote well-being
Ultraviolet Light Protection: Is It Really Enough?
No full textOur current understanding of the pathogenesis of skin aging includes the role of ultraviolet light, visible light, infrared, pollution, cigarette smoke and other environmental exposures. The mechanism of action common to these exposures is the disruption of the cellular redox balance by the directly or indirectly increased formation of reactive oxygen species that overwhelm the intrinsic antioxidant defense system, resulting in an oxidative stress condition. Altered redox homeostasis triggers downstream pathways that contribute to tissue oxinflammation (cross-talk between inflammation and altered redox status) and accelerate skin aging. In addition, both ultraviolet light and pollution increase intracellular free iron that catalyzes reactive oxygen species generation via the Fenton reaction. This disruption of iron homeostasis within the cell further promotes oxidative stress and contributes to extrinsic skin aging. More recent studies have demonstrated that iron chelators can be used topically and can enhance the benefits of topically applied antioxidants. Thus, an updated, more comprehensive approach to environmental or atmospheric aging protection should include sun protective measures, broad spectrum sunscreens, antioxidants, chelating agents, and DNA repair enzymes
Editorial: Cell cycle control as a new therapeutic approach for SARS-CoV-2 infection
No full textSARS-CoV-2 can manipulate cellular pathways, changing how well they can resist viral infection. Because of SARS-CoV-2 capacity to destroy p53, less cell death occurs in infected cells, which promotes viral replication, and p53 antiviral action is lost. Regarding this, p53 is a pleiotropic molecule associated with antiviral innate immune responses, which are specifically carried out by triggering apoptosis of infected cells and facilitating type I interferon (IFN) production/signaling. p53 consequently plays a crucial role in the setting of antiviral immunity, which may be why it is frequently targeted by viruses. By preventing virus-targeted cells from
undergoing apoptosis, inflammation is made worse and a “cytokine storm” is produced. The major goals of the current pharmacological techniques to control SARS-CoV2 infection are to prevent viral binding and entry into human cells, to obstruct polyprotein complex translation and proteolysis, to obstruct viral RNA replication, and to limit viral release.
The severity of COVID-19 disease is linked to heightened inflammatory responses, according to newly available clinical data, indicating that patient treatment plans should go beyond antiviral drugs
Rottlerin: bases for a possible usage in psoriasis
No full textRottlerin is a natural polyphenolic compound, which was initially indicated and marketed as a PKC delta inhibitor and recently proposed and patented as an anti-hypertensive drug. In vitro results from our Laboratory and data from the literature suggest a potential use of Rottlerin in the treatment/control of psoriasis, a skin disease characterized by abnormal cellular proliferation, abnormal angiogenesis and inflammation. Rottlerin, indeed, is an antioxidant and a potent inhibitor of the transcription factor NFkappaB, a key mediator of immune responses and a crucial regulator of cell cycle and apoptosis in immune cells, endothelial cells and keratinocytes. Herein, we will review the multiple activities of Rottlerin (antioxidant, antiproliferative, antiangiogenic and anti-inflammatory) that give to the drug the potential to be used as a new therapeutic approach against psoriasis
Early elevation of BACE1 in dementia
No full textInterest in the role of Beta-secretase1 (BACE1) in Alzheimer’s disease (AD) pathogenesis and patho-physiology has been remarkably growing in the last 10 year
Proteome composition and profiling of bioactive peptides of edible Antheraea assamensis pupae by sequential enzymatic digestion and kinetic modeling of in vitro gastrointestinal digestion
No full textAmong several foods-derived peptides/protein hydrolysates tested to treat fluctuation in oxidative stress, Angiotensin-I converting enzyme (ACE) and dipeptidyl peptidase IV (DPP-IV) activities linked with physiological complications of type II diabetes and hypertension, only limited numbers sourced from insects have been implemented. Aim of this study is to profile the indigenous Muga (Antheraea assamensis) pupae proteome and evaluate the suitable parameters to procure ACE inhibitory, DPP-IV inhibitory and antioxidative peptide mix with suitable enzymatic interventions. Total 72 distinct proteins distributed in 22 insect protein families were identified through MS/MS analysis. Aldehyde dehydrogenase (6.79%), pupae cuticle protein (17.02%) and haemolymph protein (9.03%) were the most abundant enzymatic and non-enzymatic protein families. The highest ACE inhibition and DPPH scavenging activities were demonstrated by Alcalase (H1) and Papain (H3) hydrolysates at 3.0% enzyme–substrate (E/S) ratio with incubation of 3 and 5 h, respectively. The Flavourzyme (H5) and Papain (H6) hydrolysates at 2.3% E/S for 5 and 3 h incubations resulted in the best DPP-IV inhibition activity. Further, Flavourzyme (H2) and Thermolysin (H4) hydrolysates with 3.0 E/S for 5 and 2 h incubation resulted in higher ABTS scavenging activity. The respective potential activities of H1 and H3 increased while H4 and H5 were retained after simulated gastrointestinal digestion. Liquid chromatography, free amino acids and molecular mass analysis further supported variation between the profiles of non-hydrolysed and hydrolysed samples under enzymatic and simulated gastrointestional conditions. Gastrointestinal digests of protein extract, H1 and H3 displayed an uncompetitive, mixed and competitive inhibiting pattern towards ACE. While gastrointestinal digests of H5 and H6 revealed an uncompetitive and non-competitive DPP-IV inhibition. The bioactive protein hydrolysates from edible A. assamensis pupae generated using enzymatic digestion can be an effective supplement for functional or nutraceutical food formulations. Graphic abstract: [Figure not available: see fulltext.]
Skin damage by tropospheric ozone [Hautschäden durch troposphärisches Ozon]
No full textTropospheric (ground level) ozone (O 3 ) is a secondary pollutant, emerging from other pollutants in the sunshine. Exposure to O 3 correlates with higher pulmonary and cardiovascular mortality and affects reproductive health and the central nervous system acutely and chronically. Skin might be a potentially overlooked target organ of ambient O 3 . The experimental evidence suggests a positive correlation of O 3 exposure with oxidative damage, impaired antioxidant defence and proinflammatory response in the skin. In time series studies it was observed that acute rises in O 3 levels correlated with seeking medical help for skin conditions; however, whether these findings are specific to O 3 , is not yet clear. There is preliminary epidemiological evidence that long-term exposure to O 3 is associated with premature skin aging. This finding was independent of co-exposure to other environmental factors affecting skin (e.g. ultraviolet radiation and air pollution). As concentrations of O 3 are rising in many regions of the world, adverse cutaneous effects of O 3 present a relevant public health concern
Mitochondrial involvement in the development and progression of diseases
No full textMitochondria arose evolutionally through a fateful endosymbiosis more than 1.45 billion years ago. While the functions of mitochondria are fairly well characterized under normal physiological conditions, there are important aspects of mitochondrial involvement in several pathological settings that still remain poorly understood/investigated. In this context, this Special Issue was designed to better clarify the mitochondrial role in the progression and development of specific pa- thologies, including neurological and rare/orphan diseases. Mitochon- drial involvement in these disorders has been attributed to the ability of these organelles to trigger deadly machineries such as apoptosis, ne- crosis, and autophagy that will then affect tissues and organs [1,2]. More recently, it has been shown that ferroptosis and inflammasome activa- tion are also associated with atypical mitochondrial function [3–5]. Therefore, the aim of this special issue was to bring together the state of the art on the still unexplained and unexplored role of mitochondria in orphan and neurological disorders. A total of 19 manuscripts were accepted for publication and most of them related to the link between mitochondria and neurological conditions
BACE1 role in Alzheimer's disease and other dementias: From the theory to the practice
No full textNon disponibil
Oxidative-Stress-Sensitive microRNAs in UV-Promoted Development of Melanoma
No full textSIMPLE SUMMARY: Exposure to ultraviolet (UV) rays from the sun is one of the most important modifiable risk factors for skin cancer. Melanoma is the most life-threatening type of skin cancer. UV-induced DNA damage and oxidative stress represent two main mechanisms that, directly and indirectly, contribute to melanomagenesis. In addition, an interplay of abnormally expressed microRNAs (miRNAs) and redox imbalance is a hallmark in several cancers, including melanoma. UV radiation can be the central hub between these two cellular aberrations, as it is able to stimulate both. Here, to gain new mechanistic insights into melanomagenesis and identify new therapeutic targets for the prevention and treatment of melanoma, we report current evidence suggesting a complex interaction between UV-promoted deregulation of redox-sensitive miRNAs and known signal-transduction pathways underlying malignant transformation of melanocytes to melanoma. ABSTRACT: Melanoma is the most aggressive and life-threatening form of skin cancer. Key molecular events underlying the melanocytic transformation into malignant melanoma mainly involve gene mutations in which exposure to ultraviolet (UV) radiation plays a prominent role. However, several aspects of UV-induced melanomagenesis remain to be explored. Interestingly, redox-mediated signaling and perturbed microRNA (miRNA) profiles appear to be interconnected contributing factors able to act synergistically in melanoma initiation and progression. Since UV radiation can promote both redox imbalance and miRNA dysregulation, a harmful crosstalk between these two key cellular networks, with UV as central hub among them, is likely to occur in skin tissue. Therefore, decoding the complex circuits that orchestrate the interaction of UV exposure, oxidative stress, and dysregulated miRNA profiling can provide a deep understanding of the molecular basis of the melanomagenesis process. Furthermore, these mechanistic insights into the reciprocal regulation between these systems could have relevant implications for future therapeutic approaches aimed at counteracting UV-induced redox and miRNome imbalances for the prevention and treatment of malignant melanoma. In this review, we illustrate current information on the intricate connection between UV-induced dysregulation of redox-sensitive miRNAs and well-known signaling pathways involved in the malignant transformation of normal melanocytes to malignant melanoma
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