Effectiveness and safety of red yeast rice predominated by monacolin K ß-hydroxy acid form for hyperlipidemia treatment and management.

OBJECTIVE: To assess the lipid-lowering activity and safety of a dietary supplement containing monacolin K ß-hydroxy acid form (MKA), Heye (), and Cangzhu (), compared to lifestyle modifications. METHODS: Totally 117 subjects with moderate to severe dyslipidemia (according to Chinese guidelines) and low CV risk were randomly assigned into three treatment groups: lifestyle modification (LM), LM plus a low dosage of MKA, LM plus a high dosage of MKA, and treated for 60 d. The primary endpoint was the reduction of low density lipoprotein cholesterol (LDL-C) and total cholesterol (TC). Safeties along with Traditional Chinese Medicine Syndromes were assessed through the study. RESULTS: A low dosage of MKA along with lifestyle modifications caused a significant decrease in LDL-C by 15.6% on average (95% , 9.6% to 21%) with, a decrease in TC by 15.3% on average (95% CI, 9.26% to 21.4%), and a decrease in non-HDL-C by 35.4% (95% CI, 25.76% to 41.34%). Weak evidence of a reduction of triglycerides but an increment of HDL-C was observed in patients with severe hyperlipidemia. No severe adverse events occurred during the study. CONCLUSION: Our results confirm the LDL-C and TC lowering properties of MKA is clinically meaningful. It also produces a significant reduction of non-HDL-C, and slightly effects on TG and HDL-C as well.

MiR-144-3p targets STC1 to activate PI3K/AKT pathway to induce cell apoptosis and cell cycle arrest in selenium deficiency broilers.

Selenium (Se) is an indispensable trace element in vertebrate. Se deficiency can damage the immune system. Studies have shown that Se deficiency can cause immune organ damage by regulating the expression of microRNA. Bursa of Fabricius is a special immune organ in poultry. In order to explore the mechanism of bursa of Fabricius injury caused by Se deficiency and the role of miRNA in this process. Firstly, we established the Se deficient model of broilers in vivo and found that Se deficiency could induce apoptosis and cell cycle arrest of bursa of Fabricius cells through Phosphoinositide 3-kinase (PI3K)/Protein Kinase B (AKT) pathway. Secondly, we inferred miRNA (miR-144-3p) and target gene Stanniocalcin 1 (STC1) that may regulate PI3K/AKT pathway through biological analysis system, and further predicted and determined the targeting relationship between them through dual luciferase, it was found that miR-144-3p was highly expressed in the process of cell apoptosis and cell cycle arrest induced by Se deficiency. Finally, in order to further understand whether miR-144-3p/STC1 axis is involved in the process, miR-144-3p knockdown and overexpression experiments were carried out, it was found that miR-144-3p inhibitor can reduce the occurrence of cell apoptosis and cell cycle arrest. In conclusion, Se deficiency can induce apoptosis and cell cycle arrest of bursa of Fabricius in Broilers by up regulating miR-144-3p targeting STC1 and activating PI3K/AKT pathway, leading to injury of bursa of Fabricius in broilers.

Yeast Selenium Exerts an Antioxidant Effect by Regulating the Level of Selenoprotein to Antagonize Cd-Induced Pyroptosis of Chicken Liver.

Cadmium (Cd) exposure can cause multiple organ damage in humans and animals by causing oxidative stress. Organic selenium can antagonize the toxic damage of heavy metals by exerting antioxidant effects. Oxidative stress can activate NLRP3/Caspase1-dependent pyroptosis, but it is not clear whether yeast selenium (Se Y) can antagonize Cd-induced pyroptosis in the chicken liver. In this experiment, we studied the effects of CdCl2 single, Se Y single, and combined exposure on the pyroptosis of chicken liver. The results showed that Cd exposure induced oxidative stress in the chicken liver, and the expression of Sepx1, SelU, SelT, GPx1, GPx4, Dio1, Dio2, Dio3, TrxR1, TrxR2, TrxR3, SelH, SelI, SelO, SelK, SelPb, Selpp, and Sel15 decreased. In addition, NLRP3 inflammasome complex (NOD-like receptor protein 3 (NLRP3), apoptosis-associated speck-like protein containing (ASC), and pro-Caspase1), Cysteinyl aspartate specific proteinase (Caspase1), Interleukin-ß (IL-1ß), and Interleukin-18 (IL-18) were upregulated. The combined treatment of Se Y and Cd found that the antioxidant level and the expression level of selenoprotein recovered to the Se group, and the liver pyroptosis decreased. Principal component analysis and correlation analysis screened out that selenoprotein O (SelO) is negatively correlated with pyroptosis-related genes. In short, our data shows that Se Y exerts an antioxidant effect by increasing the expression of selenoproteins and antagonizing the pyroptosis of chicken liver induced by Cd. This study provides new ideas for the field of heavy metal toxicology research. And the selected SelO has an important reference significance for follow-up research.