RESUMO
Coupled with the ageing population, frailty, characterized by high prevalence and difficult treatment, has progressively evolved into a significant public health concern. Frail individuals can often observe serious metabolic disorders and sleep-wake cycle disruption, which may be caused by the decline in physiological reserve and increased vulnerability. Moreover, sleep-wake cycle disruptions and metabolic dysfunctions associated with circadian rhythm disorders are considered to be a central part of the disorder. Previous studies have documented a correlation between frailty and sleep-wake disruptions; nevertheless, the association between circadian rhythm disorders and frailty has not yet been definitively established. Hence, we hypothesize a bidirectional link between circadian rhythm disorders and frailty, with each condition exerting a significant influence on the progression of the other's disease trajectory.
RESUMO
The effect of thymic stromal lymphopoietin (TSLP) on macrophage-derived foam cell formation and the underlying mechanism were studied. Macrophages isolated from C57BL/6 mice were co-cultured in vitro with different concentrations of TSLP or TSLPR-antibody in the presence of oxidized low density lipoprotein (ox-LDL). The effects of TSLP on macrophage-derived foam cell formation were observed by using oil red O staining and intracellular lipid determination. The expression levels of foam cell scavenger receptors (CD36 and SRA) as well as ABCA1 and TSLPR were detected by using RT-PCR and Western blotting. As compared with the control group, TSLP treatment significantly promoted lipid accumulation in macrophages, significantly increased protein expression of CD36 and TSLPR in a dose-dependent manner, and significantly reduced the expression of ABCA1 protein in a dose-dependent manner. No significant differences were noted between the TSLPR-antibody group and the control group. TSLP may down-regulate the expression of cholesterol efflux receptor ABCA1 and up-regulate scavenger receptor expression via the TSLPR signaling pathway, thereby promoting macrophage-derived foam cell formation.