Fulminant hepatic failure (FHF) is a clinical syndrome characterized by sudden and severe liver dysfunction. Apoptosis and inflammation are essential for the pathogenesis of FHF. Crocetin, the major component present in saffron, has been reported to possess anti-inflammatory and antioxidant functions; however, its role in FHF is poorly understood. The aim of this study was to explore the protective effects of crocetin against lipopolysac § §charide (LPS)/D-galactosamine (D-GalN)-induced FHF and the underlying mechanisms in a rat model. For the in vivo study, rats were assigned to the LPS/D-GalN group or to the crocetin pre-treatment+LPS/D-GalN group. Each group was then further divided according to the different LPS/D-GalN treatment times of 0, 6, 12 or 48 h. The results demonstrated that crocetin pre-treatment efficiently protected against LPS/D-GalN-induced FHF by improving liver tissue morphology, reducing total bilirubin generation and decreasing the activities of alanine transaminase and aspartate aminotransferase. Moreover, crocetin pre-treatment significantly decreased hepatocyte apoptosis, p53 mRNA expression and the expression of proteins in the caspase family and the Bcl-2 pro-apoptotic family following LPS/D-GalN treatment. Furthermore, crocetin also decreased the secretion of pro-inflammatory cytokines in the serum and in the liver via suppression of NF-κB activation, and also suppressed hepatic oxidative stress. In conclusion, crocetin protected against LPS/D-GalN-induced FHF and inhibited apoptosis, inflammation and oxidative stress. The underlying mechanisms may be related to the regulation of apoptotic proteins in the caspase family and the Bcl-2 family, as well as the modulation of NF-κB expression. Therefore, crocetin may be used as a novel therapy for preventing FHF.
Cellular senescence is described as the state where the cell cycle is arrested irreversibly, which occurs in response to various forms of stress factors in cells, leading to the senescence-associated secretory phenotype (SASP). We can assess the accumulation of senescent cells in tissues or organs through biomarkers of cellular senescence such as p16INK4a, p53, p21, and SA-β-GAL. In recent decades, a large number of studies have reported the biomarkers of increased cell senescence in pathogenic tissues, demonstrating the possible connection between cell senescence and various diseases. Kidney damage often occurs in the pathophysiological process of certain metabolic diseases, resulting in metabolic-associated kidney diseases. For example, hypertension causes systemic arteriosclerosis, and the kidney can be seriously affected by abundant blood vessels, which may lead to a decreased glomerular filtration rate (GFR) and proteinuria, resulting in hypertension-related kidney diseases. The accumulation of senescent cells may also be observed in some metabolic-associated kidney diseases (such as obesity-related nephropathy, hypertension-related nephropathy, and diabetic nephropathy). In this paper, we review existing knowledge regarding the influence of cellular senescence on metabolic-associated kidney diseases, providing new ideas for future treatment.
Patients with chronic kidney disease treated by dialysis (CKD-G5D) are characterized by a high prevalence of coronary artery disease (CAD). Such patients differ from non-uremic CAD patients and have been excluded from several clinical CAD trials. CKD-G5D patients may be asymptomatic for their CAD, making their risk stratification and management challenging. This review will focus on the incidence, epidemiology, pathophysiology, screening tools, and management/treatment of CAD in CKD-G5D patients. It will also review recent studies concerning the screening tools and management strategies available for these patients. The need for improved evaluation of cardiovascular risk factors, screening and early intervention for symptomatic CAD in CKD-G5D patients will be highlighted.
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