Assuntos
Doença Pulmonar Obstrutiva Crônica , Choque Séptico , Pressão Venosa Central , Hidratação , Objetivos , HumanosRESUMO
Many natural polysaccharides have been proven to have ameliorative effects on high-fat diet-induced hyperlipidemia with fewer side effects. However, similar data on Gougunao tea polysaccharides remain obscure. In this study, we aimed to investigate the role of Gougunao tea polysaccharides (GTP40) in the alleviation of hyperlipidemia and regulation of gut microbiota in C57BL/6J mice induced by a high-fat diet. The results indicated that GTP40 intervention inhibited the abnormal growth of body weight and the excessive accumulation of lipid droplets in the livers and ameliorated the biochemical parameters of serum/liver related to lipid metabolism in hyperlipidemia mice. The elevated levels of antioxidant enzyme and anti-inflammation cytokine in serum, as well as the up-regulating anti-inflammation gene in the liver, reflected that GTP40 might mitigate the oxidative and inflammatory stress induced by a high-fat diet. In addition, GTP40 could modulate the composition, abundance, and diversity of gut microbiota in hyperlipidemia mice. Besides, Spearman's correlation analysis implied that GTP40 intervention could enrich beneficial bacteria (e.g., Akkermansia, Bacteroides, Roseburia, and Alistipes), and decrease harmful bacteria (e.g., Blautia, Faecalibaculum, Streptococcus, and norank_f_Desulfovibrionaceae), which were correlated with the lipid metabolic parameters associated with hyperlipidemia. Moreover, it also indicated that there was a significant correlation between gut microbiota and SCFAs. Thus, GTP40 may be a novel strategy against fat accumulation, oxidative stress, and inflammation, as well as restoring the normal microbial balance of the gut in hyperlipidemia mice.
Assuntos
Microbioma Gastrointestinal , Hiperlipidemias , Doenças Metabólicas , Camundongos , Animais , Hiperlipidemias/tratamento farmacológico , Dieta Hiperlipídica/efeitos adversos , Camundongos Endogâmicos C57BL , Chá , Polissacarídeos/farmacologiaRESUMO
Biomass-derived raw bamboo charcoal (BC), NaOH-impregnated bamboo charcoal (BC-I), and magnetic bamboo charcoal (BC-IM) were fabricated and used as bio-adsorbents and Fenton-like catalysts for methylene blue removal. Compared to the raw biochar, a simple NaOH impregnation process significantly optimized the crystal structure, pore size distribution, and surface functional groups and increase the specific surface area from 1.4 to 63.0 m2/g. Further magnetization of the BC-I sample not only enhanced the surface area to 84.7 m2/g, but also improved the recycling convenience due to the superparamagnetism. The maximum adsorption capacity of BC, BC-I, and BC-IM for methylene blue at 328 K was 135.13, 220.26 and 497.51 mg/g, respectively. The pseudo-first-order rate constants k at 308 K for BC, BC-I, and BC-IM catalytic degradation in the presence of H2O2 were 0.198, 0.351, and 1.542 h-1, respectively. A synergistic mechanism between adsorption and radical processes was proposed.
RESUMO
OBJECTIVE: Sepsis is a systemic inflammatory response syndrome that results in severe myocardial injury. This study aimed to explore the role and mechanism of long non-coding RNA (lncRNA) small nucleolar RNA host gene 1 (SNHG1) in sepsis-induced myocardial injury in vitro. METHODS: Embryonic rat ventricular myocardial cell line (H9c2) was treated with lipopolysaccharide (LPS) to simulate sepsis-induced myocardial injury in vitro. A quantitative real-time polymerase chain reaction was executed to determine the expression of SNHG1 and microRNA (miR)-181a-5p. 3-(4, 5-dimethyl-2-thiazolyl)-2, 5-diphenyl-2-h-tetrazolium bromide assay was employed to measure cell viability. The levels of inflammatory factors (tumor necrosis factor alpha [TNF-α], interleukin 6 [IL-6], and IL-1ß) were measured by enzyme-linked immunosorbent assay. Oxidative stress was assessed by measuring malondialdehyde, superoxide dismutase, and lactate dehydrogenase. The targeted interrelations among SNHG1, miR-181a-5p, and X-linked inhibitor of apoptosis protein (XIAP) were verified by dual-luciferase reporter assay. Relative protein expression of XIAP was detected by western blot. RESULTS: SNHG1 and XIAP were down-regulated, and miR-181a-5p was up-regulated in LPS-induced H9c2 cells. Overexpression of SNHG1 or inhibition of miR-181a-5p facilitated cell viability and repressed inflammation and oxidative stress in LPS-treated H9c2 cells. MiR-181a-5p was a target of and negatively regulated by SNHG1. At the same time, XIAP was a target gene of and inversely modulated by miR-181a-5p. In addition, XIAP was positively regulated by SNHG1. Up-regulation of miR-181a-5p or silencing of XIAP reversed the inhibitory effects of SNHG1 on inflammation and oxidative stress, as well as the promoting effects on cell viability in LPS-induced H9c2 cells. CONCLUSION: SNHG1 protected H9c2 cells against LPS-induced injury through modulating the miR-181a-5p/XIAP axis.
Assuntos
Traumatismos Cardíacos/genética , RNA Longo não Codificante/genética , Animais , Apoptose/efeitos dos fármacos , Linhagem Celular , Proliferação de Células/efeitos dos fármacos , Sobrevivência Celular/efeitos dos fármacos , Regulação Neoplásica da Expressão Gênica/efeitos dos fármacos , Traumatismos Cardíacos/metabolismo , Humanos , Interleucina-1beta/metabolismo , Interleucina-6/metabolismo , MicroRNAs/genética , Miocárdio/metabolismo , RNA Longo não Codificante/metabolismo , RNA Nucleolar Pequeno/farmacologia , Ratos , Sepse/complicações , Sepse/genética , Fator de Necrose Tumoral alfa/metabolismo , Proteínas Inibidoras de Apoptose Ligadas ao Cromossomo X/genéticaRESUMO
OBJECTIVE: This double-blind and randomized placebo-controlled trial evaluated the safety and efficacy of Danhong injection combined with Naoxintong capsule in patients with acute coronary syndrome (ACS) after percutaneous coronary intervention (PCI). METHODS: ACS patients scheduled to undergo PCI (n = 130) were equally and randomly apportioned to either a treatment or control group. After PCI, the treatment group received Danhong injection combined with Naoxintong capsule for 12 weeks, while the control group was given placebo. Both groups were otherwise treated with conventional secondary prevention of coronary artery disease. The groups were primarily evaluated for clinical efficacy and cardiovascular events. Evaluative indicators of safety included adverse events, platelet count, and liver, renal, and blood coagulation functions. RESULT: No cardiovascular events or adverse reactions were observed in either group. The treatment group demonstrated better signs of clinical efficacy, including left ventricular ejection fraction, higher nitric oxide levels, and lower levels of endothelin-1 (ET-1) and von Willebrand factor (VWF). CONCLUSION: ACS patients treated with Danhong injection combined with Naoxintong capsule after PCI demonstrated better improvement with regard to markers associated with atherosclerosis and adverse cardiovascular events, without apparent adverse effects. Thus, Danhong injection combined with Naoxintong capsule was safe and effective for treating ACS patients after PCI.