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Selenium is a trace element that provides protection against cellular damage and death. Previous research using several types of cells identified anti-oxidant, anti-inflammatory, and anti-apoptotic effects for selenium. One of the diseases related to selenium is cardiovascular disease, as low selenium intake has been linked to cardiomyopathy. However, the mechanism of the cardioprotective effects of selenium is not thoroughly understood. Several studies supported the possible effects of selenium on heart cell survival. In this review, we analyzed recent research (2015-2020) on the roles and mechanism of action of selenium in cell survival and its cardioprotective effects. Furthermore, the prevention of apoptosis through both intrinsic and extrinsic pathways is discussed in this review. Signalling pathways that regulate cell survival such as the p-AMPK, poly (ADP-ribose) polymerase-1, nuclear factor-erythroid 2-related factor-2, AKT/PI3K, and STAT pathways are involved in the protective effects of selenium. In addition, signaling pathways that affect heart cell survival include the AKT and STAT pathways. It also affects autophagy through the PPAR-γ pathway. These findings should facilitate further research on the cardioprotective effects of selenium.Intestinal flora plays a major role in cardiovascular diseases, like atherosclerosis (AS). Ginkgolide B (GB), a natural substance extracted from Ginkgo biloba L., is recently acknowledged as a potential therapeutic drug of AS. However, the underlying mechanism of GB is not fully clear. Thus, we evaluated whether the antiatherosclerotic effect of GB was related to alterations in gut microbial structure and if so, whether specific bacterial taxa contributed to the beneficial effects of GB. We constructed a high fat diet (HFD)-induced ApoE-/- mice model to explore the antiatherosclerotic effects of GB. The effects of GB on lipid metabolism, hypoglycemia, inflammation and gut barrier integrity were also investigated. Then HFD inventories and high throughput sequencing of the V3-V4 region of the bacterial 16S ribosomal RNA gene were used to characterize how GB modulated gut microbiome composition. We found that HFD-induced dyslipidemia, inflammation, increased atherosclerotic plaque and gut barrier dysfunction were reduced by GB treatment. Moreover, GB treatment obviously inhibited the mRNA level and protein expression of FMO3, and then decreased the concentrations of TMA and TMAO, which was related to changes of gut microbiota in HFD-fed mice. Modulation of gut microbiota, specifically the increased abundance of Bacteroides and decreased abundance of Helicobacter, might contribute to the antiatherosclerotic effects of GB. Our findings first support the therapeutic value of GB on gut microbiota manipulation in treating AS, which still need to further study.Salidroside is a kind of phenylethanoid glycoside and widespread in the plants from Rhodiola and Ligustrum species. Our previous study has reported that salidroside can prevent atherosclerosis progression by ameliorating glyerolipid and glycerophospholipid metabolism in apoE-deficient (apoE-/-) mice. MG-101 order However, its effect on neutral lipids and underlying mechanism remains largely unclear. Here we investigated the molecular mechanism of salidroside action from the perspective of metabolic regulation by integrating metabonomics and transcriptomics pattern. The results showed that salidroside significantly reduced cholesterols, esterified cholesterols, fatty acids, unsaturated fatty acids and triacylclycerols biosynthesis in liver through down-regulating the genes expressions of sterol regulatory element-binding proteins (Srebf1 and Srebf2). The expressions of SREBPs targeted and downstream genes, such as the encoding genes of fatty acid synthase (Fasn), glycerol-3-phosphate acyltransferase (Gpam), stearoyl-CoA desaturase (Scd), 3-hydroxy-3-methylglutaryl-CoA reductase (Hmgcr), and proprotein convertase subtilisin/kexin type 9 (Pcsk9), were also inhibited after salidroside administration. ATP citrate lyase gene (Acly) that encodes an important enzyme producing acetyl-CoA for cholesterol and fatty acid biosynthesis significantly decreased after treatment as well. Moreover, one of ketone body products, 3-hydroxybutyrate, was significantly up-regulated in drug-treated group, indicating that fatty acid degradation was accelerated by salidroside at the same time. Our findings identify salidroside as a regulator of lipid homeostasis in atherosclerotic mice, suggesting its potential to be an alternative medicine for lowering the risks of atherosclerosis-related diseases.Doxorubicin (DOX) is an anthracycline antibiotic widely used in the treatment of cancer, however, it is associated with the occurrence of adverse reactions that limits its clinical use. In this context, the encapsulation of DOX in micelles responsive to pH variations has shown to be a strategy for tumor delivery of the drug, with the potential to increase therapeutic efficacy and to reduce the toxic effects. In addition, radiolabeling nanoparticles with a radioactive isotope is of great use in preclinical studies, since it allows the in vivo monitoring of the nanostructure through the acquisition of quantitative images. Therefore, this study aimed to develop, characterize, and evaluate the antitumor activity of a pH-sensitive micelle composed of DSPE-PEG2000, oleic acid, and DOX. The micelles had a diameter of 13 nm, zeta potential near to neutrality, and high encapsulation percentage. The critical micellar concentration (CMC) was 1.4 × 10-5 mol L-1. The pH-sensitivity was confirmed in vitro through a drug release assay. Cytotoxicity studies confirmed that the encapsulation of DOX into the micelles did not impair the drug cytotoxic activity. Moreover, the incorporation of DSPE-PEG2000-DTPA into the micelles allowed it radiolabeling with the technetium-99 m in high yield and stability, permitting its use to monitor antitumor therapy. In this sense, the pH-sensitive micelles were able to inhibit tumor growth significantly when compared to non-pH-sensitive micelles and the free drug. in vivo toxicity evaluation in the zebrafish model revealed significantly lower toxicity of pH-sensitive micelles compared to the free drug. These results indicate that the developed formulation presents itself as a promising alternative to potentiate the treatment of tumors.