Sarcopenia is generally an age-related condition that directly impacts the quality of life. It is also related to chronic diseases such as metabolic dysfunction associated with diabetes and obesity. ...This means that everyone will be vulnerable to sarcopenia at some point in their life. Research to find the precise molecular mechanisms implicated in this condition can increase knowledge for the better prevention, diagnosis, and treatment of sarcopenia. Our work gathered the most recent research regarding inflammation in sarcopenia and new therapeutic agents proposed to target its consequences in pyroptosis and cellular senescence. Finally, we compared dual X-ray absorptiometry (DXA), magnetic resonance imaging (MRI), and ultrasound (US) as imaging techniques to diagnose and follow up on sarcopenia, indicating their respective advantages and disadvantages. Our goal is for the scientific evidence presented here to help guide future research to understand the molecular mechanisms involved in sarcopenia, new treatment strategies, and their translation into clinical practice.
Prostate cancer (PC) is a polygenic disease with broad differences across ethnicities. BRCA1/2 and VDR have exhibited a featured genetic contribution to PC development in European populations. ...Nonetheless, its contribution in Latino populations specifically among Mexican men, where 70% of PC cases are detected in advanced stages, is still unknown. The contribution of seven polymorphisms in BRCA1/2 and VDR genes to PC susceptibility was evaluated in 370 incident PC cases and 759 age‐matched (±5 years) controls belonging to the Mexican population. Based on Gleason score at diagnosis, PC cases were classified as well‐differentiated PC (Gleason <7) and moderate or poorly differentiated PC (Gleason ≥7). Age at diagnosis was used to divided PC cases in earlier (<60 years) and late‐onset PC (≥60 years). Prostate and breast cancer family histories were obtained through interview. Our results provided evidences about the contribution of BRCA1‐rs1799966 (ORCC genotype = 2.30; 95% confidence interval CI = 1.36‐3.91) to the moderate or poorly differentiated PC risk, independently of the family history of prostate, breast or ovary cancer. Further, VDR‐rs2238135‐G allele was associated with early‐onset PC (ORG allele = 2.05; 95% CI = 1.06‐3.95), and marginally with moderate or poorly differentiated PC risk. The present study revealed the crucial role of BRCA1 in PC aggressiveness risk, outstanding the gender imbalance regarding the breast cancer risk in women.
The microwaves‐assisted extraction (MAE) for concentration of cherry phytochemicals has seen explored. Polyphenols from cherries, Prunus avium (L.) L., were extracted using a microwave oven at ...2,450 MHz, 453 W for a period of 60 s (T60), and was compared versus an unprocessed MAE extract (T0). The extracts were analyzed for total polyphenols, total anthocyanins, and antioxidant capacity. THP‐1 cells were stimulated with monosodium urate (MSU) crystals at 150 µg/ml for 24 hr. Cherry extracts were added to cultures concurrently with MSU or 3 hr before MSU addition as pretreatments. Reactive oxygen species (ROS), IL‐1β levels, and MSU crystal phagocytosis were evaluated. T60 extract showed a higher concentration of polyphenols, anthocyanins, and antioxidant activity than T0 extract. ROS were inhibited using the 1:800 and 1:1,600 (v:v) dilutions from both extracts, even used as pretreatments. IL‐1β levels and MSU crystal phagocytosis were reduced. Cherry is a source of polyphenolic compounds with antioxidant and anti‐inflammatory activity.
Practical applications
The cherries and a cherry extract obtained via MAE has benefits as a possible coadjuvant to conventional gout therapy due to attenuate the inflammation and the oxidative stress triggered by monosodium urate crystals in THP‐1 cells, which mimic an acute episode of gout.
Microwave assisted extraction allows higher concentration of polyphenols from cherry.
Cherry extracts attenuates the oxidative and inflammatory responses in the gout.
The cherry extracts inhibiting the MSU crystal phagocytosis.
Osteoarthritis (OA) is a complex disease with a multifactorial etiology. The genetic component is one of the main associated factors, resulting from interactions between genes and environmental ...factors. The aim of this study was to identify gene-gene interactions (epistasis) of the articular cartilage extracellular matrix (ECM) in knee OA. Ninety-two knee OA patients and 147 healthy individuals were included. Participants were genotyped in order to evaluate nine variants of eight genes associated with ECM metabolism using the OpenArray technology. Epistasis was analyzed using the multifactor dimensionality reduction (MDR) method. The MDR analysis showed significant gene-gene interactions between MMP3 (rs679620) and COL3A1 (rs1800255), and between COL3A1 (rs1800255) and VEGFA (rs699947) polymorphisms, with information gain values of 3.21% and 2.34%, respectively. Furthermore, in our study we found interactions in high-risk genotypes of the HIF1AN, MMP3 and COL3A1 genes; the most representative were AA+CC+GA, AA+CT+GA and AA+CT+GG, respectively; and low-risk genotypes AA+CC+GG, GG+TT+GA and AA+TT+GA, respectively. Knowing the interactions of these polymorphisms involved in articular cartilage ECM metabolism could provide a new tool to identify individuals at high risk of developing knee OA.
Several countries around the world have faced an important obesity challenge for the past four decades as the result of an obesogenic environment. This disease has a multifactorial origin and it is ...associated with multiple comorbidities including type 2 diabetes, hypertension, osteoarthritis, metabolic syndrome, cancer, and dyslipidemia. With regard to dyslipidemia, hypertriglyceridemia is a well-known activator of the NLRP3 inflammasome, triggering adipokines and cytokines secretion which in addition induce a systemic inflammatory state that provides an adequate scenario for infections, particularly those mediated by viruses such as HIV, H1N1 influenza, and SARS-CoV-2. The SARS-CoV-2 infection causes the coronavirus disease 2019 (COVID-19) and it is responsible for the pandemic that we are currently living. COVID-19 causes an aggressive immune response known as cytokine release syndrome or cytokine storm that causes multiorgan failure and in most cases leads to death. In the present work, we aimed to review the molecular mechanisms by which obesity-associated systemic inflammation could cause a more severe clinical presentation of COVID-19. The SARS-CoV-2 infection could potentiate or accelerate the pre-existing systemic inflammatory state of individuals with obesity,
the NLRP3 inflammasome activation and the release of pro-inflammatory cytokines from cells trough Gasdermin-pores commonly found in cell death by pyroptosis.
Recent studies have identified AKNA as a potential susceptibility gene for several inflammatory diseases. Here, we aimed to assess the potential association of
AKNA
polymorphisms with knee ...osteoarthritis (KOA) susceptibility in a Mexican population, following STREGA recommendations. From a DNA bank of 181 KOA patients and 140 healthy controls, two
AKNA
SNPs were genotyped using TaqMan probes. The association between KOA susceptibility and
AKNA
polymorphisms genotypes was evaluated by multivariated logistic regression analysis. Information regarding patients’ inflammatory biomarkers levels was obtained and their association with
AKNA
polymorphisms genotypes was assessed by lineal regression. We found a positive association with the recessive inheritance model of both
AKNA
polymorphisms (A/A genotype for both) and KOA susceptibility adjusting by age, body mass index (BMI), gender and place of birth (OR = 2.48, 95% CI 1.09–5.65 for rs10817595 polymorphism; and OR = 4.96; 95% CI 2.421–10.2 for rs3748176 polymorphism). Additionally these associations were also seen after stratifying patients by KOA severity and age. Furthermore the total leukocyte count was positively associated with rs10817595
AKNA
polymorphism (β = 1.39; 95% CI 0.44–2.34) adjusting by age, BMI, gender, place of birth and disease severity. We suggest that regulatory and coding polymorphisms of the inflammatory modulator gene
AKNA
can influence the development of KOA. Further structural and functional studies might reveal the role of AKNA in OA and other rheumatic diseases.
Humans do not produce uricase, an enzyme responsible for degrading uric acid. However, some bacteria residing in the gut can degrade one-third of the dietary and endogenous uric acid generated daily. ...New insights based on metagenomic and metabolomic approaches provide a new interest in exploring the involvement of gut microbiota in gout. Nevertheless, the exact mechanisms underlying this association are complex and have not been widely discussed. In this study, we aimed to review the evidence that suggests uric acid extrarenal excretion and gut microbiome are potential risk factors for developing gout. A literature search was performed in PubMed, Web of Science, and Google Scholar using several keywords, including “gut microbiome AND gout”. A remarkable intestinal dysbiosis and shifts in abundance of certain bacterial taxa in gout patients have been consistently reported among different studies. Under this condition, bacteria might have developed adaptive mechanisms for de novo biosynthesis and salvage of purines, and thus, a concomitant alteration in uric acid metabolism. Moreover, gut microbiota can produce substrates that might cross the portal vein so the liver can generate de novo purinogenic amino acids, as well as uric acid. Therefore, the extrarenal excretion of uric acid needs to be considered as a factor in gout development. Nevertheless, further studies are needed to fully understand the role of gut microbiome in uric acid production and its extrarenal excretion, and to point out possible bacteria or bacterial enzymes that could be used as probiotic coadjutant treatment in gout patients.
Dysregulation of joint tissue homeostasis induces articular degenerative changes and musculoskeletal diseases such as osteoarthritis. This pathology represents the first cause of motor disability in ...individuals over 60 years of age, impacting their quality of life and the costs of health systems. Nowadays, pharmacological treatments for cartilage disease have failed to achieve full tissue regeneration, resulting in a functional loss of the joint; therefore, joint arthroplasty is the gold standard procedure to cure this pathology in severe cases of Osteoarthritis. A different treatment is the use of anti-inflammatory drugs which mitigate pain and inflammation in some degree, but without significant inhibition of disease progression. In this sense, new therapeutic alternatives based on natural compounds have been proposed to delay osteoarthritis progression, particularly those agents that regulate articular homeostasis. Preclinical studies have shown a therapeutic application of honey and its bioactive compounds, ranging from treating wounds, coughs, skin infections, and are also used as a biological stimulant by exerting antioxidant and anti-inflammatory properties. In this article, we reviewed the current medicinal applications of honey with particular emphasis on its use regulating articular homeostasis by inhibiting inflammation and oxidative stress.
Currently, two pathogenic pathways describe the role of obesity in osteoarthritis (OA); one through biomechanical stress, and the other by the contribution of systemic inflammation. The aim of this ...study was to evaluate the effect of free fatty acids (FFA) in human chondrocytes (HC) expression of proinflammatory factors and reactive oxygen species (ROS).
HC were exposed to two different concentrations of FFA in order to evaluate the secretion of adipokines through cytokines immunoassays panel, quantify the protein secretion of FFA-treated chondrocytes, and fluorescent cytometry assays were performed to evaluate the reactive oxygen species (ROS) production.
HC injury was observed at 48 h of treatment with FFA. In the FFA-treated HC the production of reactive oxygen species such as superoxide radical, hydrogen peroxide
and the reactive nitrogen species increased significantly in a at the two-dose tested (250 and 500 μM). In addition, we found an increase in the cytokine secretion of IL-6 and chemokine IL-8 in FFA-treated HC in comparison to the untreated HC.
In our in vitro model of HC, a hyperlipidemia microenvironment induces an oxidative stress state that enhances the inflammatory process mediated by adipokines secretion in HC.
Celotno besedilo
Dostopno za:
DOBA, IZUM, KILJ, NUK, PILJ, PNG, SAZU, SIK, UILJ, UKNU, UL, UM, UPUK
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