Chronic alcohol intake can affect both liver and intestinal barrier function. The goal of this investigation was to evaluate the function and mechanism of lutein administration on the chronic ethanol-induced liver and intestinal barrier damage in rats. During the 14-week experimental cycle, seventy rats were randomly divided into seven groups, with 10 rats in each group: a normal control group (Co), a control group of lutein interventions (24 mg/kg/day), an ethanol model group (Et, 8–12 mL/kg/day of 56% (v/v) ethanol), three intervention groups with lutein (12, 24 and 48 mg/kg/day) and a positive control group (DG). The results showed that liver index, ALT, AST and TG levels were increased, and SOD and GSH-Px levels were reduced in the Et group. Furthermore, alcohol intake over a long time increased the level of pro-inflammatory cytokines TNF-α and IL-1β, disrupted the intestinal barrier, and stimulated the release of LPS, causing further liver injury. In contrast, lutein interventions prevented alcohol-induced alterations in liver tissue, oxidative stress and inflammation. In addition, the protein expression of Claudin-1 and Occludin in ileal tissues was upregulated by lutein intervention. In conclusion, lutein can improve chronic alcoholic liver injury and intestinal barrier dysfunction in rats.

Chronic excessive alcohol intake may lead to male reproductive damage. Lutein is a carotenoid compound with antioxidant activity. The purpose of this study was to observe the effect of lutein supplementation on male reproductive damage caused by excessive alcohol intake. In this study, an animal model of excessive drinking (12 mL/(kg.bw.d)) for 12 weeks was established and supplemented with different doses of lutein (12, 24, 48 mg/(kg.bw.d)). The results showed that the body weight, sperm quality, sex hormones (FSH, testosterone), and antioxidant markers (GSH-Px) decreased significantly, while MDA and inflammatory factors (IL-6, TNF-α) increased significantly in the alcohol model group when compared to the normal control group. After 12 weeks of high-dose lutein supplementation with 48mg/(kg.bw.d), the spermatogenic ability, testosterone level, and the activity of marker enzymes reflecting testicular injury were improved. In addition, high-dose lutein supplementation downregulated the NF-κB and the pro-apoptosis biomarkers (Bax, Cytc and caspase-3), whereas it upregulated the expression of Nrf2/HO-1 and the anti-apoptotic molecule Bcl-2. These findings were fully supported by analyzing the testicular histopathology and by measuring germ cell apoptosis. In conclusion, lutein protects against reproductive injury induced by excessive alcohol through its antioxidant, anti-inflammatory, and anti-apoptotic properties.

Food is an important factor affecting the treatment of patients with early gastric cancer (EGC). We have established a hospital cohort to guide dietary patterns and observe the health status of patients with EGC after endoscopic submucosal dissection (ESD) after dietary modification. A total of 273 patients with EGC who underwent ESD were recruited to the cohort. They were given dietary instruction and education through a dietary manual and were followed up for 12 months. If the dietary pattern changed to the “traditional food” pattern (high consumption of vegetables, wheat products, and red meat) after the nutritional guidance, subjects were defined as the improvement diet group. Dietary patterns focused on “alcohol and fish” (drink a lot of wine and beer and eating freshwater and marine fish) or “coarse cereals” (mainly whole grains, beans and poultry) were the main ones in the unimproved diet group. The nutritional status, gastric mucosa, and gastrointestinal symptoms of the two groups of patients before and after the dietary instruction were compared. Compared with the unimproved diet group, the endoscopic performance score and the symptom score in the improved diet group were decreased by an average of 1.31 and 1.90, respectively. Except for lymphocyte count (P = 0.227), total protein (P < 0.000), albumin (P = 0.003), globulin (P = 0.014), red blood cell count (P < 0.000), and hemoglobin (P < 0.000) values were improved to varying degrees. After changing the diet, the intake of wheat products and vegetables in the improved diet group increased by 15.58 and 17.52%, respectively, while the intake of alcohol, fish, and pickled products was reduced by 43.36, 36.43, and 31.41%, respectively. After 1 year of dietary adjustment, the nutritional status, gastric mucosa, and gastrointestinal symptoms of patients with EGC after ESD eating the "traditional food" diet were all improved.

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IntroductionBackground: Considering the poorly understood mechanism of lysine demethylase 1A (KDM1A) in osteosarcoma (OS), we here commence our investigation to fill the blank.Material and methodsMethods: Following the transfection as appropriate, 3-[4,5-dimethylthiazol-2-yl]-2,5 diphenyl tetrazolium bromide (MTT) and flow cytometry assays were used to determine the viability and apoptosis of OS cells MG-63, in which the generation of reactive oxygen species (ROS) and the binding between KDM1A and Bcl-2/ cellular Myc (c-Myc) were separately confirmed via DCF-DA method and chromatin immunoprecipitation-PCR. Reverse-transcription quantitative PCR and western blot were finally introduced to quantify the levels of KDM1A/Bcl-2/c-Myc and endoplasmic reticulum (ER) stress-related factors.ResultsResults: Overexpressed KDM1A enhanced the viability (48 hours) yet repressed the apoptosis and ROS generation, with the downregulation on ER stress-related factors (C/EBP homologous protein [CHOP]; proline-rich extensin-like receptor kinase (PERK) and activating transcription factor 4 [ATF4]) yet the elevation of Bcl-2/c-Myc, while its depletion exerted contrary effects. More importantly, KDM1A could act as the demethylase of Bcl-2/c-Myc, as reflected by the results that the depletion of KDM1A decreased the enrichment of Bcl-2/c-Myc promoter using the antibody against KDM1A yet increased the enrichment by the antibody targeting H3K9me2. Bcl-2/c-Myc silencing, conversely, promoted the ROS generation and apoptosis, elevated the levels of ER stress-related factors and abolished the effects of KDM1A on OS cells.ConclusionsConclusion: KDM1A exerts a repressive effect on the apoptosis of OS cells MG-63 by inhibiting the ROS generation and ER stress via demethylation of Bcl-2 and c-Myc.