The process of cardiac aging can be illuminated through the biological estimation of heart age. Existing research, however, overlooks the differing rates of aging throughout the various cardiac areas.
Magnetic resonance imaging radiomics phenotypes will be utilized to ascertain the biological age of the left ventricle (LV), right ventricle (RV), myocardium, left atrium, and right atrium, along with investigating determinants of cardiac aging stratified by anatomical region.
The study utilized a cross-sectional methodology.
From the UK Biobank's dataset of healthy participants, a cohort of 18,117 was ascertained, further delineated as 8,338 men (average age 64.275 years) and 9,779 women (average age 63.074 years).
A 15T, balanced, steady-state free precession.
To extract radiomic features, an automated algorithm first segmented the five cardiac regions. Chronological age, as the output, was used alongside radiomics features, as predictors, for the estimation of the biological age of each cardiac region via Bayesian ridge regression. The difference in age was a result of the divergence between a person's biological and chronological age. Linear regression analysis was conducted to explore the relationships between age differences across cardiac regions and socioeconomic factors, lifestyle, body composition, blood pressure, arterial stiffness, blood biomarkers, mental well-being, multi-organ health, and exposure to sex hormones (n=49).
Multiple comparisons were corrected using a false discovery rate method, with a 5% threshold applied.
The model's greatest inaccuracy was observed in RV age estimations, while LV age predictions exhibited the least error (mean absolute error of 526 years for men versus 496 years). There were 172 statistically significant age gap relationships, according to the findings. Visceral adipose tissue levels demonstrated the strongest correlation with wider age discrepancies, including differences in myocardial age for women (Beta=0.85, P=0.0001691).
Poor mental health is often associated with significant age differences, including disinterest and myocardial age discrepancies in men (Beta=0.25, P=0.0001). Furthermore, a history of dental problems, like left ventricular hypertrophy in men, also demonstrate this association (Beta=0.19, P=0.002). Higher bone mineral density was found to be the strongest predictor of smaller age gaps, especially in the context of myocardial age in men, with a beta coefficient of -152 and a highly significant p-value of 74410.
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By employing image-based heart age estimation, a novel approach, this work contributes to a deeper understanding of cardiac aging.
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Various chemicals have been developed due to the advancement of industrialization, including endocrine-disrupting chemicals (EDCs), which are essential for plastic production and are utilized as plasticizers and flame retardants. The convenience and hence widespread use of plastics in modern life unfortunately increases human exposure to endocrine-disrupting chemicals. The endocrine-disrupting effects of EDCs manifest as reproductive impairments, cancer, and neurological abnormalities, thereby classifying them as hazardous substances. Additionally, they pose a threat to a spectrum of organs, yet they remain in practical application. Thus, examining the contamination status of EDCs, choosing potentially harmful substances for management, and closely monitoring safety standards are required. Correspondingly, it is important to discover substances that can protect against EDC toxicity and actively study the protective impact of these compounds. Korean Red Ginseng (KRG), according to recent research, demonstrates protective properties against multiple toxicities arising from human exposure to EDCs. This review explores the influence of endocrine-disrupting chemicals (EDCs) on human physiology, and investigates the part played by keratinocyte growth regulation (KRG) in offering protection from the toxic effects of EDCs.
The alleviation of psychiatric disorders is facilitated by red ginseng (RG). Stress-induced gut inflammation is mitigated by fermented red ginseng (fRG). Dysbiosis in the gut, combined with inflammation of the gastrointestinal tract, may be a factor in the development of psychiatric disorders. To determine how RG and fRG affect anxiety/depression (AD) through their interaction with the gut microbiota, we studied the influence of RG, fRG, ginsenoside Rd, and 20(S),D-glucopyranosyl protopanaxadiol (CK) on gut microbiota-induced AD and colitis in mice.
Mice concurrently afflicted with AD and colitis were subjected to either immobilization stress or fecal matter transplant from patients exhibiting ulcerative colitis and depression. Assessment of AD-like behaviors included the use of the elevated plus maze, light/dark transition, forced swimming, and tail suspension tests.
Following oral UCDF treatment, mice displayed an augmentation in AD-like behaviors, accompanied by neuroinflammation, gastrointestinal inflammation, and disruptions within the gut microbiota. Oral fRG or RG treatment ameliorated the UCDF-induced behavioral changes characteristic of Alzheimer's disease, suppressed interleukin-6 levels in the hippocampus and hypothalamus, lowered blood corticosterone levels, while UCDF reduced hippocampal BDNF levels.
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Dopamine, hypothalamic serotonin, and cell populations exhibited an upward trend. Their treatments effectively suppressed the UCDF-induced colonic inflammation, while partially reinstating the normal fluctuations in the UCDF-induced gut microbiota. Oral administration of fRG, RG, Rd, or CK mitigated IS-induced AD-like behaviors, reducing blood IL-6 and corticosterone, as well as colonic IL-6 and TNF- levels, and alleviating gut dysbiosis; conversely, IS-suppressed hypothalamic dopamine and serotonin levels were elevated.
In mice, oral gavage with UCDF resulted in the development of AD, neuroinflammation, and gastrointestinal inflammation. fRG successfully countered AD and colitis in UCDF-exposed mice through modifications to the intricate microbiota-gut-brain axis, and in mice exposed to IS, by adjustments to the hypothalamic-pituitary-adrenal axis.
In mice, oral UCDF administration resulted in the appearance of AD, neuroinflammation, and gastrointestinal inflammation. fRG's impact on AD and colitis in UCDF-exposed mice was achieved by modulating the microbiota-gut-brain axis, while in IS-exposed mice, it regulated the hypothalamic-pituitary-adrenal axis.
Advanced pathological manifestations of many cardiovascular diseases, myocardial fibrosis (MF), can lead to heart failure and malignant arrhythmias. Nevertheless, the current medical approach to MF is devoid of targeted pharmaceutical interventions. Rats treated with ginsenoside Re show an anti-MF effect, but the exact mechanism by which this effect is produced is not yet understood. Consequently, we explored ginsenoside Re's anti-myocardial fibrosis (MF) properties by establishing a mouse model of acute myocardial infarction (AMI) and an Ang II-induced cardiac fibroblast (CF) model.
By transfecting CFs with miR-489 mimic and inhibitor, the study sought to understand the anti-MF effect of miR-489. A comprehensive study examined the effect of ginsenoside Re on MF and its underlying mechanisms in a mouse model of AMI and an Ang-induced CFs model, utilizing various techniques including ultrasonography, ELISA, histopathological staining, transwell assays, immunofluorescence, Western blot, and qPCR.
In normal and Ang-treated CFs, MiR-489 led to a decrease in the expression of -SMA, collagen, collagen and myd88, and an inhibition of NF-κB p65 phosphorylation. AZD7648 Cardiac function may be enhanced by ginsenoside Re, along with its inhibitory effect on collagen buildup and the migration of cardiac fibroblasts. This compound also encourages miR-489 transcription and reduces MyD88 expression and NF-κB p65 phosphorylation.
Through regulation of the myd88/NF-κB pathway, MiR-489 effectively controls the pathological process of MF. The amelioration of AMI and Ang-induced MF by Ginsenoside Re is probably, in part, associated with the regulation of the miR-489/myd88/NF-κB signaling pathway. antibiotic-bacteriophage combination Therefore, miR-489 potentially represents a target for anti-MF treatments, and ginsenoside Re may represent a powerful drug for MF.
Inhibition of MF's pathological processes by MiR-489 is at least partly explained by its impact on the regulation of the myd88/NF-κB pathway. Ginsenoside Re alleviates AMI and Ang-induced MF, possibly through influencing the miR-489/myd88/NF-κB signaling pathway. In summary, miR-489 may be a promising therapeutic target for MF, and ginsenoside Re may be an effective medicine for MF's management.
In clinical trials involving myocardial infarction (MI) patients, QiShen YiQi pills (QSYQ), a Traditional Chinese Medicine (TCM) formula, has demonstrated a strong therapeutic impact. The molecular underpinnings of QSYQ's role in regulating pyroptosis post-myocardial infarction are still largely unknown. Thus, the design of this study was to determine the working principle of the active constituent in QSYQ.
Using a synergistic approach of network pharmacology and molecular docking, researchers sought to pinpoint active components and shared target genes of QSYQ to inhibit pyroptosis in the wake of myocardial infarction. Subsequently, STRING and Cytoscape were leveraged to establish a PPI network, enabling the isolation of candidate active compounds. fine-needle aspiration biopsy To probe the binding potential of candidate components with pyroptosis proteins, molecular docking simulations were executed. The safeguarding effect and the mechanistic underpinnings of the candidate drug were explored using oxygen-glucose deprivation (OGD) induced cardiomyocyte damage.
Initially, two drug-likeness compounds were chosen, and the hydrogen bonding capacity between Ginsenoside Rh2 (Rh2) and the critical target High Mobility Group Box 1 (HMGB1) was established. 2M Rh2's administration prevented H9c2 cell death triggered by OGD, accompanied by a decrease in both IL-18 and IL-1 levels, possibly by inhibiting NLRP3 inflammasome activation, suppressing p12-caspase-1 expression, and lowering the concentration of the pyroptosis-associated protein GSDMD-N.