No abstract

Non-alcoholic fatty liver disease (NAFLD), ranging from simple steatosis to non-alcoholic steatohepatitis (NASH), hepatic fibrosis and even hepatocellular carcinoma, is a liver disease worldwide without approved therapeutic drugs. Baicalein (BAL), a flavonoid compound extracted from the Traditional Chinese Medicine (TCM) Scutellariae Radix (Scutellaria baicalensis Georgi.), has been used in TCM clinical practice for thousands of years to treat liver diseases due to its “hepatoprotective effect”. However, the underlying liver-protecting mechanisms remain largely unknown. Here, we found that oral administration of BAL significantly decreased excess serum levels of triglyceride (TG), low-density lipoprotein cholesterol (LDL-C), aspartate aminotransferase (AST) as well as hepatic TG in fructose-fed rats. Attenuation of the increased vacuolization and Oil Red O staining area was evident on hepatic histological examination in BAL-treated rats. Mechanistically, results of RNA-sequencing, western-blot, real-time quantitative PCR (RT-qPCR) and hepatic metabolomics analyses indicated that BAL decreased fructose-induced excessive nuclear expressions of mature sterol regulatory element-binding protein 1c (mSREBP1c) and carbohydrate response element-binding protein (ChREBP), which led to the decline of lipogenic molecules [including fatty acid synthase (FASN), stearoyl-CoA desaturase 1 (SCD1), elongation of very long chain fatty acids 6 (ELOVL6), acetyl-CoA carboxylase (ACC)], accompanying with the alternation of hepatic fatty acids composition. Meanwhile, BAL enhanced fatty acid oxidation by activating AMPK/PGC1α signaling axis and PPARα signal pathway, which elicited high expression of carnitine palmitoyl transferase 1α (CPT1α) and Acyl-CoA oxidase 1 (ACO1) in livers of fructose-fed rats, respectively. BAL ameliorated fructose-induced hepatic steatosis, which is associated with regulating fatty acid synthesis, elongation and oxidation.

Previous observational studies have inconsistently suggested that poor sleep is a novel risk factor for breast cancer (BC). However, these studies mainly focused on sleep duration; other sleep domains were rarely reported. The aim of this study was to evaluate the association of a broad range of sleep domains with the risk of BC incidence. We used a community-based 1 : 1 individual matched case-control design that included 401 female patients with incident BC and 401 age-matched and area-matched female controls in Jiujiang, China. Long-term sleep habits were assessed comprehensively using a validated 17-item Sleep Factors Questionnaire. Adjusted odds ratios (aORs) and 95% confidence intervals (CIs) were calculated using conditional logistic regression. Light exposure at night (highest vs. lowest level, aOR=1.19, 95% CI: 1.06-2.68), habitual timing of sleep (after 12 a.m. midnight vs. before 22 p.m., aOR=1.12, 95% CI: 1.03-2.62), night/shift work (yes vs. no, aOR=1.38, 95% CI: 1.04-2.71), and frequency of night-time wakings (>2 per night vs. never, aOR=1.21, 95% CI: 1.10-2.96) were associated with an increased risk of BC after mutually adjusting for other sleep parameters. These positive associations remained irrespective of menopausal status and tumor estrogen receptor status. There was no association between sleep duration, sleep quality, sleep medication use, insomnia frequency, daytime nap, and the risk of BC. Our results indicate that sleep problems including light exposure at night, night/shift work, late sleeping, and frequent night waking could increase the risk of BC development, independent of other sleep factors.

No abstract

This study aimed to investigate the absorption mechanism of three curcumin constituents in rat small intestines. Self-emulsification was used to solubilize the three curcumin constituents, and the rat in situ intestinal perfusion method was used to study factors on drug absorption, including drug mass concentration, absorption site, and the different types and concentrations of absorption inhibitors. Within the scope of experimental concentrations, three curcumin constituents were absorbed in rat small intestines through the active transport mechanism.