Aim: We aimed to evaluate the circulating thrombospondin-1 (TSP-1) and nuclear factor kappa B (NF-κB) in nonalcoholic fatty liver disease (NAFLD) in order to integrate these signaling pathways in the inflammatory and fibrogenic processes of this liver disorder. Methods: Ninety-five NAFLD patients were recruited in the study. The study also included 83 age-sex matched healthy controls. Results: The number of patients with metabolic syndrome (MetS) criteria was 57 (60%). TSP-1 level was found to be statistically significantly lower in the NAFLD group compared to the control group (p=0.037). However, NF-κB level was found to be significantly higher in the NAFLD group compared to the control group (p=0.004). There was a significant negative correlation between plasma TSP-1 levels with glucose (r=-0.235, p=0.022), alanine aminotransferase (r=-0.261, p=0.011) and aspartate transaminase (r=-0.328, p=0.001) levels. In addition, a significant negative correlation was found between plasma TSP-1 and NF-κB levels (r=-0.729, p<0.001). Conclusions: Our results suggest a close relationship between increased NF-κB and reduced TSP-1 in NAFLD. TSP-1 and NF-κB signaling pathways might have a role in the inflammatory and fibrogenic processes. Furthermore, they may be used as a noninvasive marker and could assist as a therapeutic target for NAFLD.
Metformin has been suggested to have protective effects on the central nervous system with an unclari ed mechanism. The similarity between the effects of metformin and the inhibition of glycogen synthase kinase (GSK)-3β suggests that metformin may inhibit GSK-3β. In addition, zinc is an important element that inhibits GSK-3β by phosphorylation. In this study, it was investigated whether the effects of metformin on neuroprotection and neuronal survival were mediated by zinc-dependent inhibition of GSK-3β in rats with glutamate-induced neurotoxicity. Forty adult male rats were divided into 5 groups; Control, Glutamate, Metformin + Glutamate, Zinc De ciency + Glutamate, Zinc De ciency + Metformin + Glutamate. Zinc de ciency was induced with a zinc-poor pellet. Metformin was given orally for 35 days. D-glutamic acid was administered intraperitonally on the 35th day. On the 38th day, neurodegeneration was examined histopathologically and effects on neuronal protection and survival were evaluated via intracellular S-100β immunohistochemical staining. The ndings were examined in relation to nonphosphorylated (active) GSK-3β levels and oxidative stress parameters observed in brain tissue and blood. Neurodegeneration was higher (p < 0.05) in rats fed with an inadequate zinc diet. Active GSK-3β levels were increased in groups with neurodegeneration (p < 0.01). Decreased neurodegeneration and increased neuronal survival (p < 0.01); decreased active GSK-3β (p < 0.01) levels and oxidative stress parameters, and increased antioxidant parameters were observed in groups treated with metformin (p < 0.01). Metformin had less protective effects in rats fed with an inadequate zinc diet. Metformin may demonstrate its neuroprotective effects and may increase S-100β mediated neuronal survival by a zincdependent inhibition of GSK-3β in glutamate neurotoxicity.
The etiopathogenesis of metabolic syndrome (MetS) has not been fully understood yet, and chronic low-grade inflammation is thought to be associated with the development of complications related to MetS. We aimed to investigate the role of Nuclear factor Kappa B ( NF-κB ), Peroxisome Proliferator-Activated Receptor- α and γ (PPAR-α, and PPAR-γ) which are the main markers of inflammation in older adults with MetS. A total of 269 patients aged ≥18, 188 patients with MetS who met the diagnostic criteria of the International Diabetes Federation, and 81 controls who applied to geriatrics and general internal medicine outpatient clinics for various reasons were included in the study. Patients were separated into four groups: young with MetS (˂60, n = 76), elderly with MetS (≥60, n = 96), young control (˂60, n = 31), elderly controls (≥60, n = 38). Carotid intima-media thickness (CIMT) and NF-κB , PPAR-α, and PPAR-γ plasma levels were measured in all of the participants. Age and sex distribution were similar between MetS and control groups. C-reactive protein (CRP), NF-κB levels (p = 0.001) and CIMT (p<0,001) of MetS group were significantly higher than in the control groups. On the other hand, the PPAR-γ (p=0.008) and PPAR-α (p=0.003) levels were significantly lower in MetS. ROC analysis revealed that the NF-κB, PPAR-α, and PPAR-γ could be used to indicate MetS in younger adults (AUC: 0.735, p<0.000; AUC: 0.653, p=0.003), whereas it could not be an indicator in older adults (AUC: 0.617, p=0.079; AUC:0.530, p=0.613). It seems that these markers have important roles in MetS-related inflammation. In our results, suggest that the indicator feature of NF-κB , PPAR-α and PPAR-γ in recognizing MetS in young individuals is lost in older adults with Mets.
Biomarker research has become increasingly interesting in many areasnowadays. Biomarkers are indicators of the biological process that can show changes indisease and health status and reveal pathological conditions. There is always a need formarkers that divide patients into risk categories that can help in early diagnosis, detectcomplications ahead of time, guide treatment, and predict adverse outcomes in achronic complex and certain diseases such as cancer. microRNAs (miRNAs) are ~ 22nt long npcRNAs involved in post-transcriptional arrangements. miRNAs regulatemessenger RNAs (mRNA), especially through negative regulation of gene expression.The fact that miRNAs have come to the fore in many disease mechanisms brings uptheir use as biomarkers in the early stage. The purpose of this review is to gather thelatest information on this subject by bringing together recent articles and reviews tocontribute to understanding the role of miRNAs, which act as biomarkers in differentways in vital processes, in the formation, early diagnosis, and treatment of diseases.miRNAs have an important potential to become a next-generation biomarker andtherapeutic. But, each miRNA molecule can bind to a large number of differentmRNAs, and different miRNAs in each mRNA. Therefore, new findings are needed todetermine the expression activities and targets of miRNAs.
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