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Purpose Blueberry and cranberry are rich in anthocyanins. The present study was to investigate the effects of anthocyanin extracts from blueberry and cranberry on body weight and gut microbiota. Methods C57BL/6 J Mice were divided into six groups ( n  = 9 each) fed one of six diets namely low-fat diet (LFD), high-fat diet (HFD), HFD with the addition of 1% blueberry extract (BL), 2% blueberry extract (BH), 1% cranberry extract (CL), and 2% cranberry extract (CH), respectively. Results Feeding BL and BH diets significantly decreased body weight gain by 20–23%, total adipose tissue weight by 18–20%, and total liver lipids by 16–18% compared with feeding HFD. Feeding CH diet but not CL diet reduced the body weight by 27%, accompanied by a significant reduction of total plasma cholesterol by 25% and tumor necrosis factor alpha (TNF-α) by 38%. The metagenomic analysis showed that the supplementation of blueberry and cranberry anthocyanin extracts reduced plasma lipopolysaccharide concentration, accompanied by a reduction in the relative abundance of Rikenella and Rikenellaceae . Dietary supplementation of berry anthocyanin extracts promoted the growth of Lachnoclostridium , Roseburia , and Clostridium _ innocuum_group in genus level, leading to a greater production of fecal short-chain fatty acids (SCFA). Conclusions It was concluded that both berry anthocyanins could manage the body weight and favorably modulate the gut microbiota at least in mice.

Background Trimethylamine- N -oxide (TMAO) is an independent risk factor for atherosclerosis. Consumption of hawthorn fruit is believed to be cardio-protective, yet whether it is able to suppress the TMAO-induced atherosclerosis remains unexplored. The present study was to investigate the effects of hawthorn fruit extract (HFE) on TMAO-exacerbated atherogenesis. Methods Five groups of male Apolipoprotein E knock-out (ApoE −/− ) mice were fed a low-fat diet (LFD), a Western high-fat diet (WD), or one of the three WDs containing 0.2% TMAO (WD + TMAO), 0.2% TMAO plus 1% HFE (WD + TMAO + L-HFE), or 0.2% TMAO plus 2% HFE (WD + TMAO + H-HFE), respectively. After 12-weeks of intervention, plasma levels of TMAO, lipid profile, inflammatory biomarkers, and antioxidant enzyme activities were measured. Atherosclerotic lesions in the thoracic aorta and aortic sinus were evaluated. The sterols and fatty acids in the liver and feces were extracted and measured. Hepatic expressions of inflammatory biomarkers and antioxidant enzymes were analyzed. Results Dietary TMAO accelerated atherogenesis, exacerbated inflammation, and reduced antioxidant capacities in the plasma and the liver. TMAO promoted hepatic cholesterol accumulation by inhibiting fecal excretion of acidic sterols. HFE could dose-dependently reduce the TMAO-aggravated atherosclerosis and inflammation. HFE was also able to reverse the TMAO-induced reduction in antioxidant capacity by up-regulating the expression of antioxidant enzymes including superoxide dismutase 1 (SOD1), SOD2, glutathione peroxidase 3 (GSH-Px3), and catalase (CAT) in the liver. Moreover, the hepatic cholesterol content was lowered by HFE via enhanced fecal excretion of neutral and acidic sterols. Conclusions The present results indicated that HFE was able to reduce the TMAO-exacerbated atherogenesis by attenuating inflammation and improving antioxidant capacity at least in mice. Graphic abstract

This paper designs a ratio consistency algorithm based on event triggering mechanism aiming at the frequency recovery deviation caused by traditional droop control in microgrid. It achieves secondary frequency modulation in microgrid by adjusting the active power setting value. The max-min consistency algorithm is proposed to realize asymptotic consistency of distributed power supply in a finite time. Communication delay is added to ensure the accuracy of frequency update and verifies the robustness of the algorithm against itself. Meanwhile, the validity of event triggering conditions is verified. Finally, the simulation examples are carried out to prove the correctness and superiority of the proposed finite-time control strategy.

Background Hypercholesterolemia and gut microbiota dysbiosis are associated with the risk of cardiovascular diseases. Hawthorn fruits has shown to be cardioprotective and hypocholesterolemic. However, no studies to date have studied the biological activity of hawthorn seed oil (HSO). The present study was to investigate if HSO could favourably reduce plasma cholesterol and modulate gut microbiota in hypercholesterolemia hamsters. Methods Golden Syrian hamsters (age, 8 weeks) were randomly divided into five groups ( n  = 8, each) and fed one of the following five diets, namely a non-cholesterol diet, a high cholesterol diet containing 0.15% cholesterol (HCD); a HCD diet with addition of 4.75% HSO (LHSO), a HCD diet with addition of 9.5% HSO (HHSO), a HCD diet with addition of 0.50% cholestyramine as positive control diet. After 6-week dietary intervention, plasma lipids, inflammatory markers, atherosclerosis plaque, hepatic and fecal lipids were quantified. Microbiota in fresh feces were analysed by sequencing 16S rRNA genes, while RT-PCR and Western blot analyses were employed to quantify the expression of genes involved in cholesterol homeostasis. Results HSO at a dose of 9.5% HSO could decrease plasma cholesterol and non-HDL-cholesterol by 15%. Additionally, both HSO experimental groups also suppressed mRNA of 3-Hydroxy-3-Methylglutaryl-CoA Reductase (HMG-CoA-R). Supplementation of HSO at 4.75% could significantly increase the excretion of fecal acidic sterols, accompanied by elevation of short-chain fatty acid levels in feces. The analyses of gut microbiome indicated that HSO supplementation could selectively alter the genera abundance of gut bacteria that were correlated with cholesterol metabolism including unclassified_f__Christensenellaceae, Ruminococcaceae_NK4A214_ group, norank_o_Gastranaerophilales, Faecalibaculum, Peptococcus, norank_f__Clostridiales_vadinBB60_group and Ruminococcus_2. Conclusions HSO supplementation was able to decrease plasma cholesterol by favourably modulating gut microbiota composition and gut-derived metabolites associated with cholesterol regulation. Graphical Abstract

Rutin (R) and quercetin (Q) are two widespread dietary flavonoids. Previous studies regarding the plasma cholesterol-lowering activity of R and Q generated inconsistent results. The present study was therefore carried out to investigate the effects of R and Q on cholesterol metabolism in both HepG2 cells and hypercholesterolemia hamsters. Results from HepG2 cell experiments demonstrate that both R and Q decreased cholesterol at doses of 5 and 10 µM. R and Q up-regulated both the mRNA and protein expression of sterol regulatory element binding protein 2 (SREBP2), low-density lipoprotein receptor (LDLR), and liver X receptor alpha (LXRα). The immunofluorescence study revealed that R and Q increased the LDLR expression, while only Q improved LDL-C uptake in HepG2 cells. Results from hypercholesterolemia hamsters fed diets containing R (5.5 g/kg diet) and Q (2.5 g/kg diet) for 8 weeks demonstrate that both R and Q had no effect on plasma total cholesterol. In the liver, only Q reduced cholesterol significantly. The discrepancy between the in vitro and in vivo studies was probably due to a poor bioavailability of flavonoids in the intestine. It was therefore concluded that R and Q were effective in reducing cholesterol in HepG2 cells in vitro, whereas in vivo, the oral administration of the two flavonoids had little effect on plasma cholesterol in hamsters.

Soybean germ phytosterols (SGP) largely exist in soybean germ oil. Our previous study demonstrated that soybean germ oil was effective in reducing plasma cholesterol. However, it remains unknown if its phytosterols are the active ingredients responsible for the plasma cholesterol-lowering activity. The present study aimed to test the effect of SGP on plasma cholesterol and to investigate its associated underlying mechanisms using hamsters as animal model. Male hamsters (n = 40) were randomly divided into five groups (n = 8/group) and fed one of the five diets: a non-cholesterol diet (NCD), a high cholesterol diet (HCD), a HCD diet containing 0.5% cholestyramine (PC), and two HCD diets containing 0.1% (LP) and 0.2% (HP) SGP, respectively, for six weeks. Results showed that SPG reduced plasma cholesterol level in a dose-dependent manner, whereas it dose-dependently increased the excretion of both fecal neutral and acidic sterols. SGP was also effective in displacing cholesterol from micelles. It was concluded that SGP possessed hypocholesterolemic activity, likely by inhibiting cholesterol absorption in the intestine and promoting fecal sterol excretion.

Repeated reuse of frying oil raises health concerns due to the accumulation of oxidative products after each frying cycle. Gut microbiota is integral in lipid metabolism and immune regulation. The present study was designed to investigate the effects of thermally-oxidized corn oil and lard on gut microbiota in relation to atherosclerosis, inflammatory cytokines, and plasma lipids. Male Golden Syrian hamsters were randomly divided into four groups and fed one of four diets containing fresh corn oil (CF), oxidized corn oil (CO), fresh lard (LF), and oxidized lard (LO), for six weeks. CO and LO were prepared by deep-frying potatoes in corn oil or lard for seven days. Results indicated that oxidized oil and lard caused the loss of species diversity and richness of gut microbiota. Feeding CO and LO also reduced the body and adipose tissue weights, associated with genus Acetatifactor and Allobaculum. Plasma triacylglycerols significantly increased by 51% in the CO and 35% in the LO group compared with that in their CF and LF counterparts, respectively. CO could also affect the abundance of specific bacteria genera: Bacteroides, Barnesiella, Acetatifactor, Allobaculum, Clostridium_IV, Clostridium_XIVa, Coprococcus, Lactococcus, Paraprevotella, Parasutterella, and Oscillibacter. In addition, CO and LO could adversely remodel gut composition and affect intestinal production of short-chain fatty acids, pro-inflammatory biomarkers (LPS and IL-6), anti-inflammatory biomarker IL-10, and atherosclerotic progression. It was concluded that frying oil could adversely modulate the gut microbiota and exacerbate the atherosclerosis at least in a hypercholesterolemia hamster model.

PurposePeony (Paeonia spp.) seed oil (PSO) contains a high amount of α-linolenic acid. The effects of PSO on hypercholesterolemia and gut microbiota remains unclear. The present study was to investigate effects of PSO supplementation on cholesterol metabolism and modulation of the gut microbiota.MethodsMale Golden Syrian hamsters (n = 40) were randomly divided into five groups (n = 8, each) fed one of the following diets namely low-cholesterol diet (LCD); high cholesterol diet (HCD); HCD with PSO substituting 50% lard (LPSO), PSO substituting 100% lard (HPSO) and HCD with addition of 0.5% cholestyramine (PCD), respectively, for 6 weeks.ResultsPSO supplementation dose-dependently reduced plasma total cholesterol (TC) by 9–14%, non-high-density lipoprotein cholesterol (non-HDL-C) by 7–18% and triacylglycerols (TG) by 14–34% (p < 0.05). In addition, feeding PSO diets reduced the formation of plaque lesions by 49–61% and hepatic lipids by 9–19% compared with feeding HCD diet (p < 0.01). PSO also altered relative genus abundance of unclassified_f__Coriobacteriaceae, unclassified_f__Erysipelotrichaceae, Peptococcus, unclassified_f__Ruminococcaceae, norank_o__Mollicutes_RF9 and Christensenellaceae_R-7_group.ConclusionsIt was concluded that PSO was effective in reducing plasma cholesterol and hepatic lipids and favorably modulating gut microbiota associated with cholesterol metabolism.

Cardiovascular disease (CVD) is the leading cause of mortality worldwide, and hypercholesterolemia is recognized as one of the primary risk factors. Dietary intervention to manage hypercholesterolemia is generally considered to be a safe and effective strategy to prevent the incidence of heart diseases. The gut microbiota has been noted to influence host blood lipids and potentially impact the development of cardiovascular diseases. The purpose of the present study was (i) to evaluate the effects of sea buckthorn seeds oil (SBSO), wild melon seeds oil (CO) and ursolic acids (UA) on plasma cholesterol; (ii) to explore the potency of SBSO, CO and UA in modulating gut microbiota; and (iii) to investigate the related underlying mechanisms in hypercholesterolemic hamsters. Sea buckthorn is one of the most important shrubs grown widely in China. It has been traditionally used as a natural remedy for the prevention of heart diseases, diabetes, and cancer. Recent studies have also indicated that SBSO may possess a variety of health benefits. The first part of the thesis research aimed to examine the effect of SBSO on blood cholesterol in hypercholesterolemic hamsters. Four groups of hamsters (n=8 each) were given one of four diets, namely a non-cholesterol control diet (NCD), a high-cholesterol diet (HCD) containing 0.1% cholesterol, and HCD diet with sea buckthorn seed oil replacing 50% lard (SL) or replacing 100% lard (SH). Feeding SL and SH diets could reduce blood total cholesterol by 20-22%. This was accompanied by downregulation on gene expression of 3-hydroxy-3-methylglutaryl-CoA reductase (HMG-CoA-R), acyl-CoA: cholesterol acyltransferase 2 (ACAT2), microsomal triacylglycerol transport protein (MTP), and ATP-binding cassette transporter subfamily G member 8 (ABCG8). SBSO supplementation also increased the production of intestinal short-chain fatty acids (SCFAs) and fecal outputs of neutral sterols. The metagenomic analysis demonstrated that feeding SL and SH diets could favorably modulate the relative abundance of Bacteroidales_S24- 7_group, Ruminococcaceae, and Eubacteriaceae. It was therefore concluded that SBSO was effective in reducing blood cholesterol in hypercholesterolemic hamsters via inhibiting hepatic cholesterol synthesis, increasing intestinal cholesterol excretion and promoting the growth of SCFAs-producing bacteria. CO is rich in polyunsaturated fatty acids and phytosterols. The second part of the present study was to investigate the effects of CO on blood cholesterol and gut microbiota in hamsters fed a high cholesterol diet. Hamsters (n=32) were randomly divided into four groups fed one of the four diets namely NCD, HCD, HCD diet containing 4.75% CO, and HCD diet containing 9.5% CO for 6 weeks respectively. Results showed that supplementation of CO at 9.5% reduced plasma cholesterol by 24% and increased the excretion of fecal bile acids by 150%. This was accompanied by up-regulation on the gene expression of hepatic cholesterol 7α-hydroxylase (CYP7A1). In addition, CO supplementation remarkably increased the production of fecal short-chain fatty acids and favorably altered the relative abundance of Eubacteriaceae, Clostridiales_vadinBB60_group, Ruminococcaceae, Streptococcaceae and Desulfovibrionaceae at a family level. It was concluded that CO could favorably reduce plasma cholesterol via promoting the excretion of fecal acidic sterols and modulating gut microbiota. UA, a pentacyclic triterpenoid acid, is abundantly present in fruits and vegetables. Most previous researches have focused on its anti-cancer, antiinflammatory and antioxidant properties. The third part of the thesis was to examine the effect of UA on cholesterol metabolism and gut microbiota in hamsters. Thirty-two hamsters were assigned into four groups receiving an NCD, an HCD and two HCD diets containing 0.2% and 0.4%, respectively, for 6 weeks. Results suggested that the UA administration significantly reduced plasma TC by 15%-16%, and non-HDL-C by 26%-30%, respectively. This was accompanied by the reduction in liver cholesterol and down-regulation on the gene expression of hepatic 3-hydroxy-3-methylglutaryl-CoA reductase (HMG-CoA-R). Meanwhile, UA supplementation significantly increased the fecal short chain fatty acids concentration and favorably changed the proportion of Bacteroidales_S24-7_group, Ruminococcaceae and Bifidobacterium. In conclusion, the present study clearly demonstrated UA exhibited the cholesterol lowering activity by regulating cholesterol synthesis in the liver and altering gut microbiota. Taken together, it can be summarized that sea buckthorn seeds oil, wild melon seeds oil and ursolic acid were effective in the prevention of hypercholesterolemia and modulation of gut microbiota in hamsters.

Using the dielectric loss property of carbon black , cement-based composites were prepared by introducing carbon black into cement. The reflection losses were studied using arched testing method in the frequency range of 2~18 GHz. The results showed that the absorption properties were improved in high frequency. The filling ratio of carbon black as well as the thickness of samples had influence on the absorption properties. The lowest reflection loss of-10.6 dB was obtained at 18 GHz of 5wt.% carbon black filled cement with thickness of 20mm. The new material can be used for building indoor electromagnetic radiation protection.