Astaxanthin Protects Dendritic Cells from Lipopolysaccharide-Induced Immune Dysfunction.

Astaxanthin, originating from seafood, is a naturally occurring red carotenoid pigment. Previous studies have focused on its antioxidant properties; however, whether astaxanthin possesses a desired anti-inflammatory characteristic to regulate the dendritic cells (DCs) for sepsis therapy remains unknown. Here, we explored the effects of astaxanthin on the immune functions of murine DCs. Our results showed that astaxanthin reduced the expressions of LPS-induced inflammatory cytokines (TNF-α, IL-6, and IL-10) and phenotypic markers (MHCII, CD40, CD80, and CD86) by DCs. Moreover, astaxanthin promoted the endocytosis levels in LPS-treated DCs, and hindered the LPS-induced migration of DCs via downregulating CCR7 expression, and then abrogated allogeneic T cell proliferation. Furthermore, we found that astaxanthin inhibited the immune dysfunction of DCs induced by LPS via the activation of the HO-1/Nrf2 axis. Finally, astaxanthin with oral administration remarkably enhanced the survival rate of LPS-challenged mice. These data showed a new approach of astaxanthin for potential sepsis treatment through avoiding the immune dysfunction of DCs.

Non-alcoholic fatty liver disease with reduced myocardial FDG uptake is associated with coronary atherosclerosis.

BACKGROUND: Non-alcoholic fatty liver disease (NAFLD) has a significant role in the development of coronary atherosclerosis, independent of traditional cardiovascular and metabolic risk factors. However, the role of myocardial glucose uptake in NAFLD patients who develop coronary atherosclerosis was unclear. The aim of the present study thus was to investigate the association between NAFLD with characteristic of coronary atherosclerotic plaque and myocardial glucose uptake measured by using 18F-fluorodeoxyglucose positron emission tomography (18F-FDG PET). METHODS AND RESULTS: A total of 418 consecutive subjects who had undergone FDG PET/computed tomography (CT) and coronary computed tomography angiography (CCTA) were retrospectively investigated. Fatty liver was assessed by unenhanced CT. Coronary atherosclerotic plaques and stenosis on CCTA were evaluated. The metabolic parameters were measured on PET images. The ratio of the maximum myocardium FDG value to the mean standardized uptake value of liver (SUVratio) was calculated to estimate myocardial glucose uptake. The association of myocardial glucose uptake with NAFLD and coronary atherosclerosis was determined by multivariate logistic regression analysis. The proportion of low SUVratio in patients with NAFLD was significantly higher compared to those without NAFLD (45.00% vs 19.82%, P < .001). There was a significantly negative correlation between myocardial FDG uptake and hepatic steatosis in association trend analysis (P < .001). When the proportion of individuals with non-calcified plaque on CCTA is stratified by quartiles of SUVratio, patients with low quartiles of SUVratio were more likely to have higher proportion of non-calcified plaque than those with high quartiles of SUVratio (Q1 and Q2 vs Q3 and Q4, P = .003). The trend analysis presented correlated inversely relationship between non-calcified plaque and myocardial SUVratio (P = .001). Moreover, multivariate regression analysis showed that the low SUVratio was independently associated with NAFLD, non-calcified plaque, and significant stenosis after adjusting for clinically important factors. CONCLUSION: We demonstrated that the presence of reduced myocardial glucose uptake in patients with NAFLD was independently associated with non-calcified plaque and significant stenosis, suggesting an increased risk of coronary atherosclerosis and future cardiovascular events.