BackgroundElevated remnant cholesterol (RC) is associated with a higher risk of various cardiac diseases. Heart failure (HF) usually occurs at the end stage of various cardiac diseases. However, there is limited research on the association between RC and the risk of HF. Therefore, we aimed to provide relevant evidence by determining whether a high RC level also influences the risk of HF.Materials and methodsIn this secondary analysis of the Atherosclerosis Risk in Communities (ARIC) study, we included 12,595 participants without coronary heart disease. We determined the association of the RC level as a continuous or categorical variable with the risk of HF using the multivariable-adjusted Cox proportional hazards models and restricted cubic spline curve.ResultsDuring a median follow-up of 22.5 years, 2,029 (16.1%) cases of HF occurred in all included participants. Compared with participants in the RC < 0.50 mmol/L group, the adjusted hazard ratio (HR) for HF increased progressively in participants with the RC level of 0.50 to 0.99 mmol/L, 1.00 to 1.49 mmol/L, and ≥1.50 mmol/L, from 1.17 (95% confidence interval [CI]: 1.05–1.30) to 1.27(95% CI: 1.08–1.49) and to 1.50 (95% CI: 1.14–1.97) (P for trend < 0.001). Cubic spline curves also revealed that the risk of HF increased with the RC level.ConclusionIn the general population without coronary heart disease, a higher level of RC was significantly associated with a higher risk of HF, indicating that a higher RC level might be a potential risk factor for HF. Therefore, the management of blood cholesterol to reduce the risks of HF should focus not only on the traditional blood lipid parameters but also on the RC level.

Baclground The present study aimed to investigate whether N- acetylcysteine (NAC) protects human umbilical vein endothelial cells (HUVECs) against high glucose (HG)-induced injury by inhibiting leptin/leptin receptor (LEPR).Methods HUVECs were treated with 40 mmol/L glucose for 24 h to establish a model of HG-induced endothelial cell injury; The cell viability was examined by cell counter kit-8(CCK-8) assay; The expression levels of leptin, LEPR, cleaved caspase-3 and endothelial nitric oxide synthase (eNOS) were detected by western blot. The intracellular levels of reactive oxygen species (ROS) were tested by DCFH-DA staining followed by photofluorography. Tumor necrosis factor-α (TNF-α)、nuclear factor-kappa B (NF-κB) and intercellular adhesion molecule-1 (ICAM-1) were detected by enzyme-linked immunosorbent assay (ELISA). The number of apoptotic cells was observed by photofluorograph with Hoechst 33258 nuclear staining. Mitochondrial membrane potential (MMP) was obtained using JC-1. Results The expression of leptin and LEPR began to significantly increase after exposure to 40 mmol/L HG for 24 h. Pretreatment of HUVECs with 7 mmol/L NAC or 50 ng/mL leptin antagonists (LA) for 30min inhibited the increased expression of leptin and LEPR induced by HG in HUVECs. Furthermore, pretreatment with 7 mmol/L NAC or 50 ng/mL LA for 30 min also inhibited HG-induced injury, by increasing the cell viability and eNOS expression, and decreasing the inflammatory response and cleaved caspase-3 expression, the apoptotic cells and generation of intracellular ROS and a loss of MMP. Conclusions NAC protects the HUVECs against HG-induced injury by inhibiting leptin/LEPR.

Background The present study aimed to investigate whether N-acetylcysteine (NAC) protects human umbilical vein endothelial cells (HUVECs) against high glucose (HG)-induced injury by inhibiting leptin/leptin receptor (LEPR).Methods HUVECs were treated with 40 mmol/L glucose for 24 h to establish a model of HG-induced endothelial cell injury; The cell viability was examined by cell counter kit-8 (CCK-8) assay; The expression levels of leptin, LEPR, cleaved caspase-3 and endothelial nitric oxide synthase (eNOS) were detected by western blot. The intracellular levels of reactive oxygen species (ROS) were tested by DCFH-DA staining followed by photofluorography. Tumor necrosis factor-α (TNF-α) nuclear factorkappa B (NF-κB) and intercellular adhesion molecule-1 (ICAM-1) were detected by enzyme-linked immunosorbent assay (ELISA). The number of apoptotic cells was observed by photofluorograph with Hoechst 33258 nuclear staining. Mitochondrial membrane potential (MMP) was obtained using JC-1. ResultsThe expression of leptin and LEPR began to significantly increase after exposure to 40 mmol/L HG for 24 h. Pretreatment of HUVECs with 7 mmol/L NAC or 50 ng/mL leptin antagonists (LA) for 30min inhibited the increased expression of leptin and LEPR induced by HG in HUVECs.Furthermore, pretreatment with 7 mmol/L NAC or 50 ng/mL LA for 30 min also inhibited HG-induced injury, by increasing the cell viability and eNOS expression, and decreasing the inflammatory response and cleaved caspase-3 expression, the apoptotic cells and generation of intracellular ROS and a loss of MMP.Conclusions NAC protects the HUVECs against HG-induced injury by inhibiting leptin/LEPR.