Lipid-lowering Effects Research Articles

LDL cholesterol-lowering effect of Daeshiho-tang in patients with dyslipidemia: A pilot randomized, double-blind, placebo-controlled trial

BackgroundDyslipidemia, a major risk factor for atherosclerotic cardiovascular disease, can be prevented by lowering low-density lipoprotein cholesterol (LDL-C) levels. The lipid improvement effects of Daeshiho-tang (DSHT), a herbal formula, have been proven through various preclinical studies based on anti-obesity and anti-inflammatory properties, however, clinical trials were few. This preliminary study aimed to assess the lipid-lowering effect of DSHT in patients with dyslipidemia and examine its safety profile. The study was a randomized, double-blind, placebo-controlled trial. The trial included 60 patients with untreated dyslipidemia: total cholesterol (TC) > 200 mg/dL, triglyceride (TG) > 150 mg/dL, LDL-C >130 mg/dL, or high-density lipoprotein cholesterol (HDL-C) <40 mg/dL. Participants (mean age, 44.7 ± 13.7 years) consumed DSHT extract or an equivalent placebo at a dose of 3 g, thrice a day for 8 weeks. Participants underwent blood tests assessing serum lipid and apolipoprotein (apo) levels, including LDL-C, HDL-C, TC, TG, apoA1, and apoB, at baseline and 4 and 8 weeks. Levels of biochemical safety markers, including AST, ALT, GGT, creatinine, and eGFR, were assessed throughout the study. Between the two groups, significant differences were observed in the changes of LDL-C, TC, and apoB concentrations from baseline to post-intervention. Compared with the placebo group, DSHT-administered participants showed significantly reduced LDL-C by 14.0 ± 4.66 mg/dL (p < 0.01), TC by 13.7 ± 4.73 mg/dL (p < 0.01) and apolipoprotein-B by 7.03 ± 3.23 mg/dL (p < 0.05). No significant changes were observed in the safety biochemical parameters in either group. DSHT treatment for 8 weeks improved LDL-C levels and reduced apoB concentrations without severe adverse events.

Molecular Drug Simulation and Experimental Validation of the CD36 Receptor Competitively Binding to Long-Chain Fatty Acids by 7-Ketocholesteryl-9-carboxynonanoate.

Long-chain fatty acids (LCFAs) are one of the main energy-supplying substances in the body. LCFAs with different lengths and saturations may have contrasting biological effects that exacerbate or alleviate progress against a variety of systemic disorders of lipid metabolism in organisms. Nonalcoholic fatty liver disease is characterized by chronic inflammation and steatosis, mainly caused by the ectopic accumulation of lipids in the liver, especially LCFAs. CD36 is a scavenger receptor that recognizes and mediates the transmembrane absorption of LCFAs and is expressed in a variety of cells throughout the body. In previous studies, our group found that 7-ketocholesteryl-9-carboxynonanoate (oxLig-1) has the biological effect of targeting CD36 to inhibit oxidized low-density lipoprotein lipotoxicity-induced lipid metabolism disorder; it has an ω-carboxyl physiologically active center and is structurally similar to LCFAs. However, the biological mechanism of oxLig-1 binding to CD36 and competing for binding to different types of LCFAs is still not clear. In this study, molecular docking and molecular dynamics simulation were utilized to simulate and analyze the binding activity between oxLig-1 and different types of LCFAs to CD36 and confirmed by the enzyme-linked immunosorbent assay (ELISA) method. Absorption, distribution, metabolism, excretion, and toxicity (ADMET) platform was applied to predict the drug-forming properties of oxLig-1, and HepG2 cells model of oleic acid and nonalcoholic fatty liver disease (NAFLD) model mice were validated to verify the biological protection of oxLig-1 on lipid lowering. The results showed that there was a co-binding site of LCFAs and oxLig-1 on CD36, and the binding driving forces were mainly hydrogen bonding and hydrophobic interactions. The binding abilities of polyunsaturated LCFAs, oxLig-1, monounsaturated LCFAs, and saturated LCFAs to CD36 showed a decreasing trend in this order. There was a similar decreasing trend in the stability of the molecular dynamics simulation. ELISA results similarly confirmed that the binding activity of oxLig-1 to CD36 was significantly higher than that of typical monounsaturated and saturated LCFAs. ADMET prediction results indicated that oxLig-1 had a good drug-forming property. HepG2 cells model of oleic acid and NAFLD model mice study results demonstrated the favorable lipid-lowering biological effects of oxLig-1. Therefore, oxLig-1 may have a protective effect by targeting CD36 to inhibit the excessive influx and deposition of lipotoxicity monounsaturated LCFAs and saturated LCFAs in hepatocytes.

Nutraceutical support in the prevention and treatment of cardiovascular diseases

Cardiovascular disease is the most common cause of death worldwide. In this regard, there is a need to find and implement effective methods for the prevention and treatment of such diseases. Lifestyle modification is an important component of a complex of preventive and therapeutic measures, including nutrition optimization, increased physical activity, and breaking bad habits. Currently, an actively developing area is the use of biologically active additives to food, in order to replenish the missing nutrients in the diet and maintain health. In the course of the present review, an analysis was made of randomized clinical trials performed over the past 5 years. The studies investigated both the short-term effects of taking omega-3 polyunsaturated fatty acids (effect on the blood lipid spectrum, blood pressure levels) and longterm results (development of myocardial infarction, stroke, cardiovascular mortality). This supplement has demonstrated a positive effect on immediate outcomes, namely the reduction of total cholesterol, low-density lipoprotein, triglycerides (lipid-lowering effect). However, there was no significant effect on long-term results. It also provides information on studies that have examined the cardioprotective effects of supplements such as resveratrol, red yeast rice, L-arginine, and curcumin. An analysis of publications has shown that these supplements have the potential to reduce the risk of development and progression of cardiovascular diseases due to possible hypolipidemic, endothelial protective, and antihypertensive effects. Nutraceutical support can be an effective addition to the basic treatment and help reduce morbidity and mortality due to cardiovascular disease.

Chitosan Oligosaccharides Alleviate Heat-Stress-Induced Lipid Metabolism Disorders by Suppressing the Oxidative Stress and Inflammatory Response in the Liver of Broilers.

Heat stress has been reported to induce hepatic oxidative stress and alter lipid metabolism and fat deposition in broilers. Chitosan oligosaccharides (COSs), a natural oligosaccharide, has anti-oxidant, anti-inflammatory, and lipid-lowering effects. This study is conducted to evaluate dietary COS supplementation on hepatic anti-oxidant capacity, inflammatory response, and lipid metabolism in heat-stressed broilers. The results indicate that heat-stress-induced poor (p < 0.05) growth performance and higher (p < 0.05) abdominal adiposity are alleviated by COS supplementation. Heat stress increases (p < 0.05) serum AST and ATL activity, serum and liver MDA, TG, TC, and LDL-C levels, and the expression of hepatic IL-1β, IL-6, SREBP-1c, ACC, and FAS, while it decreases (p < 0.05) serum SOD and CAT activity, liver GSH-Px and SOD activity, and the expression of hepatic Nrf2, GPX1, IL-10, MTTP, PPARα, and CPT1. Nevertheless, COS supplementation decreases (p < 0.05) serum AST and ATL activity, serum and liver MDA, TG, TC, and LDL-C levels, and the expression of hepatic IL-1β, IL-6, SREBP-1c, ACC, and FAS, while it increases (p < 0.05) serum SOD and CAT activity, liver GSH-Px activity, and the expression of hepatic Nrf2, CAT, IL-10, LPL, MTTP, PPARα, and CPT1. In conclusion, COS could alleviate heat-stress-induced lipid metabolism disorders by enhancing hepatic anti-oxidant and anti-inflammatory capacity.

Extraction and characterization of polysaccharide from fermented mycelia of Coriolus versicolor and its efficacy for treating nonalcoholic fatty liver disease

Coriolus versicolor, a popular traditional Chinese medicinal herb, is widely used in China to treat spleen and liver diseases; however, the beneficial effects of C. versicolor polysaccharides (CVPs) on nonalcoholic fatty liver disease (NAFLD) remain elusive. Herein we isolated and purified a novel CVP (molecular weight, 17,478 Da) from fermented mycelium powder. This CVP was composed of mannose, galacturonic acid, glucose, galactose, xylose, and fucose at a molar ratio of 22:1:8:15:10:3. Methylation, gas chromatography–mass spectrometry, and nuclear magnetic resonance analyses indicated that the CVP backbone consisted of →1)-β-D-Man-(6,4→1)-α-D-Gal-(3→1)-α-D-Man-(4→1)-α-D-Gal-(6→, with branches of →1)-α-D-Glc-(6→1)-α-D-Man-(4,3→1)-β-D-Xyl-(2→1)-β-D-Glc on the O-6 position of →1)-β-D-Man-(6,4→ of the main chain. The secondary branches linked to the O-4 position of →1)-α-D-Man-(4,3→ with the chain of →1)-α-D-Fuc-(4→1)-α-D-Man. Further, CVP treatment alleviated the symptoms of NAFLD in an HFD-induced mice model. CVP altered gut microbiota, predominantly suppressing microbes associated with bile acids both in the serum and cecal contents. In vitro data showed that CVP reduced HFD-induced hyperlipidemia via farnesoid X receptor. Our results improve our understanding of the mechanisms underlying the cholesterol- and lipid-lowering effects of CVP and indicate that CVP is a promising candidate for NAFLD therapy.

Molecular pharmacology of coenzyme Q10 in the context of treatment of hyperlipidemic conditions

Background. Therapy of hyperlipidemia with synthetic statin drugs is characterized by a number of side effects. In particular, statin-dependent myopathy occurs as a result of statin inhibition of biosynthesis of cofactor coenzyme Q10 (CoQ10), which plays a central role in the electron transport chains during adenosine triphosphate (ATP) synthesis in mitochondria.Objective: systematic analysis of scientific publications on CoQ10 pharmacology with an emphasis on its effect on the lipid profile.Material and methods. The analysis included 16,788 articles found by “coenzyme Q10 OR ubiquinone" query in the PubMed/MEDLINE biomedical publications database. Topological and metric big data analysis methods were used developed in the scientific school of Academician of the Russian Academy of Sciences Yu.I. Zhuravlev.Results. A much wider range of CoQ10 pharmacological effects was established than simply supporting ATP biosynthesis. Coenzyme Q10 exhibits pronounced lipid-lowering, anti-asthenic, and anti-inflammatory effects and can be successfully used in the treatment of asthenic conditions, cardiovascular pathology (including hyperlipidemia and statin-induced myopathy), carbohydrate metabolism disorders (insulin resistance), and diverse neurological diseases. CoQ10 supplements reduce mortality by 50% in patients with cardiovascular diseases, improve glycemic control in insulin resistance, kidney function, and are useful in the treatment of migraine and neurodegenerative pathologies (Parkinson's disease, etc.).Conclusion. Experimental data and evidence base indicate the potential of using CoQ10 in patients with hyperlipidemia and other cardiovascular system diseases.

Bio-Assay-Guided Isolation of Fractions and Constituents with Antioxidant and Lipid-lowering Activity from Allium cepa.

Active fractions and constituents with antioxidant and lipid-lowering activities were investigated using bio-assay-guided isolation and identification. The data showed that the antioxidant fraction of A. cepa was AC50%, the main constituents of which were quercetin and isoquercitrin, by way of both ultra-high performance liquid chromatography-mass spectrometry (UPLC-MS) and bio-assay-guided purification and elucidation. Similarly, the lipid-lowering active fraction of A. cepa was AC30% with the main constituents of 3,4-dihydroxybenzoic acid and quercetin 3,4'-O-diglucoside. Also, bio-assay-guided isolation led to the isolation and identification of five known compounds with a purity of more than 98%, and quercetin was both the best free radical scavenger and lipid-lowering constituent. Moreover, the mechanism of the lipid-lowering effect of AC30% might be its reduction in mRNA expression levels of sterol regulatory element binding protein 2 (SREBP2) and FAS gene in lipid synthesis. Otherwise, reducing the mRNA expression level of lipid synthesis genes, including SREBP1, SREBP2, fatty acid synthetase (FASN), β-Hydroxy β-methylglutaryl-CoA (HMGCR), stearoyl CoA desaturase 1 (SCD1), and increasing the mRNA expression level of lipid decomposition gene, such as carnitine palmitoyl transferease-1 (CPT1), might be involved in the lipid-lowering activity of quercetin. This study suggested that Allium cepa might be used to prevent and treat oxidative stress and dislipidemia-related disorders, including NAFLD.

Bioactive Compounds from Artichoke and Application Potential.

Cynara cardunculus L. var. scolymus, known as the artichoke, originated in the Mediterranean region and is now cultivated in several countries. The artichoke has leaves, a stem, and a head, also called a floral capitulum, covered with green and pointed bracts. It is rich in polyphenols, flavonoids, anthocyanins, phenolic compounds, inulin, coumarins, terpenes, dietary fibre, enzymes, polysaccharides, minerals and vitamins, and therefore has a wide range of uses, including in the food industry, medicine and biofuels. Several studies have shown that artichokes have properties such as antioxidant, anti-inflammatory, antimicrobial, anticancer, hypocholesterolaemic, anti-HIV, cardioprotective, hepatoprotective and lipid-lowering effects. The aim of this study is to provide a literature review on the phytochemical composition, bioactivity and applications, focusing on the methods of extraction, purification and concentration of enzymes present in artichoke.

Evaluation of the safety and potential lipid-lowering effects of oral hydrogen-rich coral calcium (HRCC) capsules in patients with metabolic syndrome: a prospective case series study.

Metabolic syndrome is characterized by a cluster-like occurrence of conditions such as hypertension, hyperglycaemia, elevated low-density lipoprotein (LDL) cholesterol or triglycerides (TG) and high visceral fat. Metabolic syndrome is linked to the build-up of plaque within the artery, which leads to disorders of the circulatory, nervous and immune systems. A variety of treatments target the regulation of these conditions; nevertheless, they remain dominant risk factors for the development of type 2 diabetes (T2DM) and cardiovascular disease (CVD), which affect 26.9% of the US population. Management and intervention strategies for improving cholesterol and/or TG are worthwhile, and recent studies on hydrogen treatment are promising, particularly as molecular hydrogen is easily ingested. This study aimed to investigate the lipid-lowering effects and quality of life (QOL) improvement of hydrogen-rich coral calcium (HRCC) in patients with metabolic syndrome. The patients, all Taiwanese, were randomly assigned to 3 different doses (low, medium, and high) of HRCC capsules. The primary outcome was the adverse effects/symptoms during this 4-week use of HRCC capsules. The secondary outcome was lipid profile changes. Complete blood count, inflammatory biomarkers, and QOL were also measured before and after the course of HRCC. Sixteen patients with metabolic syndrome completed this study (7 males, 9 females; mean age: 62 years; range: 32-80). No obvious adverse effects were recorded. Only changes in blood TG reached significance. The baseline TG value was 193.19 μL (SD = 107.44), which decreased to 151.75 μL (SD = 45.27) after 4 weeks of HRCC (p = 0.04). QOL showed no significant changes. This study is the first human clinical trial evaluating HRCC capsules in patients with metabolic syndrome. Based on the safety and potential TG-lowering effects of short-term HRCC, further long-term investigations of HRCC are warranted. [ClinicalTrials.gov], identifier [NCT05196295].

Evaluation of the intracellular lipid-lowering effect of polyphenols extract from highland barley in HepG2 cells

Active ingredients from highland barley have received considerable attention as natural products for developing treatments and dietary supplements against obesity. In practical application, the research of food combinations is more significant than a specific food component. This study investigated the lipid-lowering effect of highland barley polyphenols via lipase assay in vitro and HepG2 cells induced by oleic acid (OA). Five indexes, triglyceride (TG), total cholesterol (T-CHO), low density lipoprotein-cholesterol (LDL-C), aspartate aminotransferase (AST), and alanine aminotransferase (ALT), were used to evaluate the lipid-lowering effect of highland barley extract. We also preliminary studied the lipid-lowering mechanism by Real-time fluorescent quantitative polymerase chain reaction (qPCR). The results indicated that highland barley extract contains many components with lipid-lowering effects, such as hyperoside and scoparone. In vitro, the lipase assay showed an 18.4 % lipase inhibition rate when the additive contents of highland barley extract were 100 µg/mL. The intracellular lipid-lowering effect of highland barley extract was examined using 0.25 mM OA-induced HepG2 cells. The results showed that intracellular TG, LDL-C, and T-CHO content decreased by 34.4 %, 51.2 %, and 18.4 %, respectively. ALT and AST decreased by 51.6 % and 20.7 % compared with the untreated hyperlipidemic HepG2 cells. qPCR results showed that highland barley polyphenols could up-regulation the expression of lipid metabolism-related genes such as PPARγ and Fabp4.

Liraglutide attenuates palmitate-induced apoptosis via PKA/β-catenin/Bcl-2/Bax pathway in MC3T3-E1 cells.

Liraglutide (LRG), one agonist of glucagon-like peptide-1 receptor (GLP1R), has multiple lipid-lowering effects in type 2 diabetes mellitus, however, studies on the role of LRG in saturated fatty acid-induced bone loss are limited. Therefore, our aim was to investigate whether LRG reduces palmitate (PA)-induced apoptosis and whether the mechanism involves PKA/β-catenin/Bcl-2/Bax in osteoblastic MC3T3-E1 cells. MC3T3-E1 cells were treated with different concentrations of PA, LRG, or pretreated with Exendin 9-39 and H89, cell viability, intracellular reactive oxygen species (ROS), cAMP levels, apoptosis and the expression of protein kinase A (PKA) and phosphorylation of PKA (p-PKA), β-catenin and phosphorylation of β-catenin (Ser675)(p-β-catenin), GLP1R, cleaved-capase 3, Bcl2-Associated X Protein (Bax) and B-cell lymphoma-2 (Bcl-2) along with expression of Osteoprotegerin (OPG) and receptor activator of nuclear factor-κB ligand (RANKL) were evaluated. PA treatment inhibited cell proliferation and cAMP levels, elevated intracellular ROS levels and promoted apoptosis, increased protein expressions of RANKL, Bax and cleaved-caspase3, meanwhile decreased protein expression of OPG and Bcl-2 in a dose-dependent manner. LRG inverted PA-induced apoptosis, increased cAMP levels, promoted expression of p-PKA, p-β-catenin (Ser675) and reversed these gene expressions via increasing GLP1R expression. Pretreatment of the cells with Exendin 9-39 and H89 partially eradicated the protective effect of LRG on PA-induced apoptosis and gene expressions. Therefore, these findings indicated that LRG attenuates PA-induced apoptosis possibly by GLP1R-mediated PKA/β-catenin/Bcl-2/Bax pathway in MC3T3-E1 cells. Our results point to LRG as a new strategy to attenuate bone loss associated with high fat diet beyond its lipid-lowering actions. LRG inhibits PA-mediated apoptosis via GLP1R-mediated PKA/β-catenin/Bcl-2/ Bax pathway, while possibly enhances PA-inhibited differentiation by regulating the expression of OPG and RANKL.

Hepatic Steatosis Alleviated by a Novel Metformin and Quercetin Combination Activating Autophagy Through the cAMP/AMPK/SIRT1 Pathway.

Non-alcoholic fatty liver disease (NAFLD) incidence and prevalence are rapidly increasing globally. The combined effects of metformin and quercetin (Que) have yet to be investigated. However, both have demonstrated the potential to reduce triglyceride (TG) levels and treat NAFLD by promoting autophagy. The objective of the present study was to elucidate the mechanism of action and assess the role of autophagy in the lipid-lowering effects of Que, both individually and in combination with metformin, in a HepG2 cell model of hepatic steatosis. Triglyceride levels and lipogenic gene expression were reduced in HepG2 cells exposed to palmitic acid (PA) when treated with Que-metformin, as evidenced by triglyceride measurements and real-time PCR. The LDH release assay also showed that this combination induced autophagy to protect HepG2 cells from PA-induced cell death. According to the Western blot analysis outcomes, Que-metformin increased LC3-I and LC3-II protein levels while decreasing p62 expression to induce autophagy. In HepG2 cells, the co-administration of Que-metformin elevated cAMP, phosphorylated AMP-activated protein kinase (p-AMPK), and Beclin-1 levels. Additionally, the inhibition of SIRT1 reversed the autophagy induced by Que-metformin. The findings of this study demonstrated for the first time that Que-metformin reduced hepatosteatosis by stimulating autophagy through the cAMP/AMPK/SIRT1 signaling pathway and diminishing inflammatory cytokines.

Dry beans (Phaseolus vulgaris L.) modulate the kinetics of lipid digestion in vitro: Impact of the bean matrix and processing

The lipid-lowering effect of dry beans and their impact on lipid and cholesterol metabolism have been established. This study investigates the underlying mechanisms of this effect and explore how the structural integrity of processed beans influences their ability to modulate lipolysis using the INFOGEST static in vitro digestion model. Dietary fiber (DF) fractions were found to decrease lipolysis by increasing the digesta viscosity, leading to depletion-flocculation and/or coalescence of lipid droplets. Bean flours exhibited a more pronounced reduction in lipolysis compared to DF. Furthermore, different levels of bean structural integrity showed varying effects on modulating lipolysis, with medium-sized bean particles demonstrating a stronger reduction. Hydrothermal treatment compromised the ability of beans to modulate lipid digestion, while hydrostatic-pressure treatment (600 MPa/5min) enhanced the effect. These findings highlight that the lipid-lowering effect of beans is not solely attributed to DF but also to the overall bean matrix, which can be manipulated through processing techniques.

Combined GIP receptor and GLP1 receptor agonism attenuates NAFLD in male APOE∗3-Leiden.CETP mice.

Combined glucose-dependent insulinotropic polypeptide receptor (GIPR) and glucagon-like peptide-1 receptor (GLP1R) agonism is superior to single GLP1R agonism with respect to glycemic control and weight loss in obese patients with or without type 2 diabetes. As insulin resistance and obesity are strong risk factors for nonalcoholic fatty liver disease (NAFLD), in the current study we investigated the effects of combined GIPR/GLP1R agonism on NAFLD development. Male APOE∗3-Leiden.CETP mice, a humanized model for diabetic dyslipidemia and NAFLD when fed a high-fat high-cholesterol diet, received subcutaneous injections with either vehicle, a GIPR agonist, a GLP1R agonist, or both agonists combined every other day. GIPR and GLP1R agonism reduced body weight and additively lowered fasting plasma levels of glucose, triglycerides and total cholesterol. Strikingly, we report an additive reduction in hepatic steatosis as evidenced by lower hepatic lipid content and NAFLD scores. Underlying the lipid-lowering effects were a reduced food intake and intestinal lipid absorption and an increased uptake of glucose and triglyceride-derived fatty acids by energy-combusting brown adipose tissue. Combined GIPR/GLP1R agonism also attenuated hepatic inflammation as evidenced by a decreased number of monocyte-derived Kupffer cells and a reduced expression of inflammatory markers. Together, the reduced hepatic steatosis and inflammation coincided with lowered markers of liver injury. We interpretate that GIPR and GLP1R agonism additively attenuate hepatic steatosis, lower hepatic inflammation, ameliorate liver injury, together preventing NAFLD development in humanized APOE∗3-Leiden.CETP mice. We anticipate that combined GIPR/GLP1R agonism is a promising strategy to attenuate NAFLD progression in humans. This work was supported by a grant from the Netherlands CardioVascular Research Initiative: the Dutch Heart Foundation, Dutch Federation of University Medical Centers, the Netherlands Organization for Health Research and Development, and the Royal Netherlands Academy of Sciences [CVON-GENIUS-II] to P.C.N.R., a Lilly Research Award Program [LRAP] Award to P.C.N.R. and S.K., a Dutch Heart Foundation [2017T016] grant to S.K., and an NWO-VENI grant [09150161910073] to M.R.B.; J.F.D.B. is supported by the Nutrition and Health initiative of the University of Groningen; Z.Y. is supported by a full-time PhD scholarship from the China Scholarship Council (201806850094 to Z.Y.).

Hypolipidemic effects of microencapsulated powder fraction from Hibiscus sabdariffa. L calyx in hyperlipidic rats

The lipid-lowering activity of microencapsulated and nonmicroencapsulated Hibiscus sabdariffa L. powder fractions in rats rendered hyperlipidemic by a hyperlipid diet (HLD) was determined. Dried calyces of H. sabdariffa were finely ground and fractionated on a sieve column to retain particle sizes ϕ &lt; 315 µm, and were microencapsulated with maltodextrin (MD). Rats were randomly divided into four groups: normal control group, hyperlipid diet group (negative control groups), hyperlipid diet group supplemented with atorvastatin, non-microencapsulated (NMEPHS) and microencapsulated (MEPHS) powders from H. sabdariffa calyces groups. Rats received atorvastatin, NMEPHS and MEPHS for three weeks. Atorvastatin (10 mg/kg) and individual powders were dissolved in water and administered to rats at a dose of 250 mg/kg body weight for three weeks. Body weight, total cholesterol (TC), triglycerides (TG), low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C), aspartate transferase (AST), alanine transferase (ALT), superoxide dismutase (SOD), catalase (CAT) and malondialdehyde (MDA) were measured. Very low-density lipoprotein cholesterol (VLDL-C), hepatosomatic index (HSI), and adiposomatic index (ASI) were calculated. Lipid profil, and MDA were increased in the negative control rat groups compared with the negative control rat group. NMEPHS and MEPHS significantly reduced body weight gain, ASI, HSI, TC, TG, LDL-C, ALT, AST, and MDA and increased HDL-C level significantly. Moreover, SOD and CAT activities were reduced with HLD and significantly increased with HSCP intake. however, the most significant activities were revealed by MEPHS. These results suggest that MEPHS exerts potent lipid-lowering effects, promotes hepatic fat breakdown, and regulates antioxidant enzymes in a more efficient manner.

Protective effects and molecular mechanisms of tea polyphenols on cardiovascular diseases.

Aging is the most important factor contributing to cardiovascular diseases (CVDs), and the incidence and severity of cardiovascular events tend to increase with age. Currently, CVD is the leading cause of death in the global population. In-depth analysis of the mechanisms and interventions of cardiovascular aging and related diseases is an important basis for achieving healthy aging. Tea polyphenols (TPs) are the general term for the polyhydroxy compounds contained in tea leaves, whose main components are catechins, flavonoids, flavonols, anthocyanins, phenolic acids, condensed phenolic acids and polymeric phenols. Among them, catechins are the main components of TPs. In this article, we provide a detailed review of the classification and composition of teas, as well as an overview of the causes of aging-related CVDs. Then, we focus on ten aspects of the effects of TPs, including anti-hypertension, lipid-lowering effects, anti-oxidation, anti-inflammation, anti-proliferation, anti-angiogenesis, anti-atherosclerosis, recovery of endothelial function, anti-thrombosis, myocardial protective effect, to improve CVDs and the detailed molecular mechanisms.

Durvillaea antarctica: A Seaweed for Enhancing Immune and Cardiometabolic Health and Gut Microbiota Composition Modulation.

Durvillaea antarctica is the seaweed that is the most consumed by the Chilean population. It is recognized worldwide for its high nutritional value in protein, vitamins, minerals, and dietary fiber. This is a narrative review in which an extensive search of the literature was performed to establish the immunomodulator, cardiometabolic, and gut microbiota composition modulation effect of Durvillaea antarctica. Several studies have shown the potential of Durvillaea antarctica to function as prebiotics and to positively modulate the gut microbiota, which is related to anti-obesity, anti-inflammatory, anticancer, lipid-lowering, and hypoglycemic effects. The quantity of Bacteroides was negatively correlated with that of inflammatory monocytes and positively correlated with the levels of several gut metabolites. Seaweed-derived polysaccharides modulate the quantity and diversity of beneficial intestinal microbiota, decreasing phenol and p-cresol, which are related to intestinal diseases and the loss of intestinal function. Additionally, a beneficial metabolic effect related to this seaweed was observed, mainly promoting the decrease in the glycemic levels, lower cholesterol levels and cardiovascular risk. Consuming Durvillaea antarctica has a positive impact on the immune system, and its bioactive compounds provide beneficial effects on glycemic control and other metabolic parameters.

Antiatherogenic Potential of Transcranial Electrical Stimulation in a High-Fructose/High-Fat Diet: Experimental Randomized Trial

Background. Transcranial electrical stimulation is a promising method for correction of malnutrition-induced hyperlipidemia, in the absence of indications for drug hypolipidemic therapy in young and middle-aged patients with low and moderate cardiovascular risk. Objectives — to study the effect of transcranial electrical stimulation on lipid metabolism in a high-fructose/high-fat (HFHF) diet in rats.Methods. An experimental randomized trial was performed to study the effect of transcranial electrical stimulation on lipid metabolism in a high-calorie diet enriched with fructose and saturated animal fat in rats. The experiments involved 180 outbred male rats and were carried out on the basis of the vivarium of Kuban State Medical University. The animals were divided into three groups: group 1 (control group, n = 60) — followed a standard diet; group 2 (comparison group, n = 60) — followed a HFHF diet; group 3 (experimental group, n = 60) — underwent transcranial electrical stimulation against the background of a HFHF diet. According to the target reference point of the study, the groups were divided into three equal subgroups of 20 rats each: subgroup A — day 30, subgroup B — day 60, and subgroup C — day 90 (biomaterial sampling and euthanasia were carried out on those days). In the obtained blood samples, the following lipid metabolism parameters were evaluated: total cholesterol, triglycerides, low-density lipoprotein cholesterol, high-density lipoprotein cholesterol, and atherogenic index. Statistical analysis was performed using Microsoft Office Excel 2021 (Microsoft, USA), GraphPadPrism 9 (GraphPad Software, USA) and Statistica 13.3 (StatSoft, USA).Results. On the 30th day of the study, it was noted that in group 3, the concentration of low-density lipoprotein cholesterol was 14.9% lower and the atherogenic index was 30.8% lower (p &lt; 0.05) than in group 2, while total cholesterol concentration, triglycerides, and high-density lipoprotein cholesterol had no statistically significant differences (p &gt; 0.05). On the 60th day of the study, in group 3, when compared to group 2, the concentration of total cholesterol was 18.7% lower, low-density lipoprotein cholesterol was 42.9% lower, high-density lipoprotein cholesterol was 16.7% higher, and the atherogenic index was 56.3% lower (p &lt; 0.05), while triglycerides had no statistically significant differences (p &gt; 0.05). On the 90th day of the study, in group 3, when compared to group 2, the concentration of total cholesterol was 29.2% lower, the concentration of triglycerides was 36.0% lower, low-density lipoprotein cholesterol was 42.8% lower, and the atherogenic index was 57.0% lower (p &lt; 0.05), while the concentration of high-density lipoprotein cholesterol had no statistically significant differences (p &gt; 0.05).Conclusion. High-fructose/high-fat diet leads to a progressive increase in the serum concentration of low-density lipoprotein cholesterol, total cholesterol, triglycerides, as well as to a moderate decrease in high-density lipoprotein cholesterol and a growth in the atherogenic index. Transcranial electrical stimulation has a moderate lipid-lowering effect, manifested in the form of a decrease in the serum concentration of low-density lipoprotein cholesterol, total cholesterol and atherogenic index, while the effect on the concentration of triglycerides and high-density lipoprotein cholesterol is insignificant.

Aqueous extract of Polygala japonica Houtt. ameliorated nonalcoholic steatohepatitis in mice through restoring the gut microbiota disorders and affecting the metabolites in feces and liver

BackgroundPolygala japonica Houtt. (PJ) has been demonstrated with several biological potentials such as lipid-lowering and anti-inflammatory effects. However, the effects and mechanisms of PJ on nonalcoholic steatohepatitis (NASH) remain unclear. PurposeThe aim of this study was to evaluate the effects of PJ on NASH and illustrate the mechanism based on modulating gut microbiota and host metabolism. Materials and methodsNASH mouse model was induced using methionine and choline deficient (MCD) diet and orally treated with PJ. The therapeutic, anti-inflammatory, and anti-oxidative effects of PJ on mice with NASH were firstly assessed. Then, the gut microbiota of mice was analyzed using 16S rRNA sequencing to assess the changes. Finally, the effects of PJ on the metabolites in liver and feces were explored by untargeted metabolomics. ResultsThe results indicated that PJ could improve hepatic steatosis, liver injury, inflammatory response, and oxidative stress in NASH mice. PJ treatment also affected the diversity of gut microbiota and changed the relative abundances of Faecalibaculum. Lactobacillus, Muribaculaceae, Dubosiella, Akkermansia, Lachnospiraceae_NK4A136_group, and Turicibacter in NASH mice. In addition, PJ treatment modulated 59 metabolites both in liver and feces. Metabolites involved in histidine, and tryptophan metabolism pathways were identified as the key metabolites according to the correlation analysis between differential gut microbiota and metabolites. ConclusionOur study demonstrated the therapeutic, anti-inflammatory and anti-oxidative potentials of PJ on NASH. The mechanisms of PJ treatment were related to the improvement of gut microbiota dysbiosis and the regulation of histidine and tryptophan metabolism.

Three arms, double-blind, non-inferiority, randomized clinical study testing the lipid-lowering effect of a novel dietary supplement containing red yeast rice and artichoke extracts compared to Armolipid Plus® and placebo.

There is growing interest in head-to-head comparison between different lipid-lowering nutraceuticals. The aim of our study was to test the lipid-lowering effect of dietary supplementation with low-dose monacolins from red yeast rice (2.8 mg per daily dose) combined with berberine (Armolipid Plus®) or highly standardized artichoke extract versus placebo. 60 overall healthy adult volunteers with polygenic hypercholesterolemia (baseline low-density lipoprotein cholesterol (LDL-C) = 160.2 ±9.2 mg/dl) were enrolled in a 3-arm, double-blind, non-inferiority, randomized, parallel-group clinical trial. After 4-week diet standardization, enrolled individuals were randomized to be treated for 8 weeks with red yeast rice and highly standardized artichoke extracts (ATC group), Armolipid Plus®, or placebo. At the enrolment visit, LDL-C values were similar in the compared groups. After 8 weeks, all actively treated subjects experienced significant improvements in baseline total cholesterol (TC), LDL-C and apolipoprotein B (Apo-B) (all p < 0.01) (ATC group: TC = -18.9%, LDL-C = -26.7% (placebo-corrected: -12.4%), Apo-B = -19.6%; Armolipid Plus®: TC = -18.4%, LDL-C = -25.8% (placebo-corrected: -12.1%), Apo-B = -23.2%; placebo: TC = -6.2%, LDL-C = -8%, Apo-B = -8.4%). Participants in the ATC group attained significantly lower body mass index (BMI) values (-2.1%), while individuals treated with Armolipid Plus® showed improvements in baseline high-density lipoprotein cholesterol (HDL-C) (+8.7%) and triglyceride (TG) (+17.5%) levels. Finally, baseline hepatic steatosis index (HSI) values significantly decreased in both actively treated groups (by -2.4% and -2.4% in ATC and in Armolipid Plus®, respectively). Patients with polygenic hypercholesterolemia experienced a significant improvement in several cardiovascular risk factors in both ATC and Armolipid Plus® groups.