scholarly journals Influence of Short-Term Consumption of Hericium erinaceus on Serum Biochemical Markers and the Changes of the Gut Microbiota: A Pilot Study

Nutrients ◽  
2021 ◽  
Vol 13 (3) ◽  
pp. 1008
Author(s):  
Xiao-Qian Xie ◽  
Yan Geng ◽  
Qijie Guan ◽  
Yilin Ren ◽  
Lin Guo ◽  
...  
Keyword(s):  
Gut Microbiota ◽  
Biochemical Markers ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Alpha Diversity ◽  
Streptococcus Thermophilus ◽  
Protective Effects ◽  
Hericium Erinaceus ◽  
Blood Indices ◽  
Serum Biochemical

Hericium erinaceus (H. erinaceus) is widely studied as a medicinal and edible fungus. Recent studies have shown that H. erinaceus has protective effects for diseases, such as inflammatory bowel disease and cancer, which are related to gut microbiota. To investigate the benefits of H. erinaceus intake on gut microbiota and blood indices in adulthood, we recruited 13 healthy adults to consume H. erinaceus powder as a dietary supplement. Blood changes due to H. erinaceus consumption were determined by routine hematological examination and characterized by serum biochemical markers. Microbiota composition was profiled by 16S ribosomal RNA gene sequencing. Results showed that daily H. erinaceus supplementation increased the alpha diversity within the gut microbiota community, upregulated the relative abundance of some short-chain fatty acid (SCFA) producing bacteria (Kineothrix alysoides, Gemmiger formicilis, Fusicatenibacter saccharivorans, Eubacterium rectale, Faecalibacterium prausnitzii), and downregulated some pathobionts (Streptococcus thermophilus, Bacteroides caccae, Romboutsia timonensis). Changes within the gut microbiota were correlated with blood chemical indices including alkaline phosphatase (ALP), low-density lipoprotein (LDL), uric acid (UA), and creatinine (CREA). Thus, we found that the gut microbiota alterations may be part of physiological adaptations to a seven-day H. erinaceus supplementation, potentially influencing beneficial health effects.

Lactobacillus reuteri A9 and Lactobacillus mucosae A13 isolated from Chinese superlongevity people modulate lipid metabolism in a hypercholesterolemia rat model

2019 ◽  
Vol 366 (24) ◽  
Author(s):  
Jinchi Jiang ◽  
Ninghan Feng ◽  
Chengcheng Zhang ◽  
Fengping Liu ◽  
Jianxin Zhao ◽  
...  
Keyword(s):  
Gut Microbiota ◽  
Mrna Expression ◽  
Lactobacillus Reuteri ◽  
Cholesterol Metabolism ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Bile Salt Hydrolase ◽  
Low Density ◽  
Cholesterol Levels ◽  
Lactobacillus Mucosae

ABSTRACT While there is strong evidence showing that many food-borne probiotics regulate cholesterol metabolism, few studies have examined how probiotics of human origin affect cholesterol metabolism. Because people living in so-called ‘longevity villages’ are unlikely to have hypercholesterolemia, we hypothesized that probiotics isolated from the residents would have cholesterol-reducing effects on rats with hypercholesterolemia. We isolated 16 strains of Lactobacillus from four longevity populations in China. The strains were tested in vitro for bile salt hydrolase (BSH) activity and two isolates, Lactobacillus reuteri A9 and Lactobacillus mucosae A13, were screened out. These two strains were then administered daily for 28 d to rats fed a cholesterol-rich diet. The serum total cholesterol levels in the L. reuteri A9 and L. mucosae A13 groups decreased by 24.3% and 21.6%, respectively. The serum low density lipoprotein cholesterol levels decreased by 23.8% and 25.2%, respectively. The L. reuteri A9 and L. mucosae A13 groups also exhibited upregulated hepatic mRNA expression of Sterol regulatory element-binding protein 2 (Srebp2) by 2.71-fold and 2.54-fold, respectively. The mRNA expression levels of hepatic low-density lipoprotein receptor (Ldlr) in the two groups were significantly up-regulated by 1.28-fold and 2.17-fold, respectively. The composition of gut microbiota was recovered by oral gavage in both experimental groups, and the destroyed diversity of gut microbiota was relieved.

scholarly journals ChREBP-Mediated Regulation of Lipid Metabolism: Involvement of the Gut Microbiota, Liver, and Adipose Tissue

2020 ◽  
Vol 11 ◽  
Author(s):  
Katsumi Iizuka ◽  
Ken Takao ◽  
Daisuke Yabe
Keyword(s):  
Adipose Tissue ◽  
Fatty Acid ◽  
Lipid Metabolism ◽  
Gut Microbiota ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Acid Synthesis ◽  
Whole Body ◽  
Acetyl Coa ◽  
Alcoholic Fatty Liver

Carbohydrate response element-binding protein (ChREBP) plays an important role in the development of type 2 diabetes, dyslipidemia, and non-alcoholic fatty liver disease, as well as tumorigenesis. ChREBP is highly expressed in lipogenic organs, such as liver, intestine, and adipose tissue, in which it regulates the production of acetyl CoA from glucose by inducing Pklr and Acyl expression. It has recently been demonstrated that ChREBP plays a role in the conversion of gut microbiota-derived acetate to acetyl CoA by activating its target gene, Acss2, in the liver. ChREBP regulates fatty acid synthesis, elongation, and desaturation by inducing Acc1 and Fasn, elongation of long-chain fatty acids family member 6 (encoded by Elovl6), and Scd1 expression, respectively. ChREBP also regulates the formation of very low-density lipoprotein by inducing the expression of Mtp. Furthermore, it plays a crucial role in peripheral lipid metabolism by inducing Fgf21 expression, as well as that of Angptl3 and Angptl8, which are known to reduce peripheral lipoprotein lipase activity. In addition, ChREBP is involved in the production of palmitic-acid-5-hydroxystearic-acid, which increases insulin sensitivity in adipose tissue. Curiously, ChREBP is indirectly involved in fatty acid β-oxidation and subsequent ketogenesis. Thus, ChREBP regulates whole-body lipid metabolism by controlling the transcription of lipogenic enzymes and liver-derived cytokines.

scholarly journals Reversal of age-associated oxidative stress in mice by PFT, a novel kefir product

2020 ◽  
Vol 34 ◽  
pp. 205873842095014
Author(s):  
Mamdooh Ghoneum ◽  
Shaymaa Abdulmalek ◽  
Deyu Pan
Keyword(s):  
Oxidative Stress ◽  
Low Density Lipoprotein ◽  
Redox Homeostasis ◽  
Density Lipoprotein ◽  
Antioxidant Enzyme Activities ◽  
Protective Effects ◽  
Oxidative Stress Biomarkers ◽  
Age Related ◽  
Total Antioxidant ◽  
The Brain

Introduction: Oxidative stress is a key contributor to aging and age-related diseases. In the present study, we examine the protective effects of PFT, a novel kefir product, against age-associated oxidative stress using aged (10-month-old) mice. Methods: Mice were treated with PFT orally at a daily dose of 2 mg/kg body weight over 6 weeks, and antioxidant status, protein oxidation, and lipid peroxidation were studied in the brain, liver, and blood. Results: PFT supplementation significantly reduced the oxidative stress biomarkers malondialdehyde (MDA) and nitric oxide; reversed the reductions in glutathione (GSH) levels, total antioxidant capacity (TAC), and anti-hydroxyl radical (AHR) content; enhanced the antioxidant enzyme activities of glutathione peroxidase (GPx), catalase (CAT), and superoxide dismutase (SOD); inhibited the liver enzyme levels of aspartate aminotransferase (AST) and alanine aminotransferase (ALT); significantly reduced triglyceride (TG), total cholesterol (TC), and low density lipoprotein (LDL) levels; and significantly elevated high density lipoprotein (HDL) levels. Interestingly, PFT supplementation reversed the oxidative changes associated with aging, thus bringing levels to within the limits of the young control mice in the brain, liver, and blood. We also note that PFT affects the redox homeostasis of young mice and that it is corrected post-treatment with PFT. Conclusion: Our findings show the effectiveness of dietary PFT supplementation in modulating age-associated oxidative stress in mice and motivate further studies of PFT’s effects in reducing age-associated disorders where free radicals and oxidative stress are the major cause.

Protective Effects of Berberine against Low-Density Lipoprotein (LDL) Oxidation and Oxidized LDL-Induced Cytotoxicity on Endothelial Cells

2007 ◽  
Vol 55 (25) ◽  
pp. 10437-10445 ◽  
Author(s):  
Yih-Shou Hsieh ◽  
Wu-Hsien Kuo ◽  
Ta-Wei Lin ◽  
Horng-Rong Chang ◽  
Teseng-His Lin ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Oxidized Ldl ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Ldl Oxidation ◽  
Low Density ◽  
Protective Effects

scholarly journals Changes in Mouse Gut Microbial Community in Response to the Different Types of Commonly Consumed Meat

2019 ◽  
Vol 7 (3) ◽  
pp. 76 ◽  
Author(s):  
Zhimin Zhang ◽  
Dapeng Li ◽  
Rong Tang
Keyword(s):  
Gut Microbiota ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Blood Lipid ◽  
Chow Group ◽  
Red Meat ◽  
White Meat ◽  
Different Types ◽  
Lipid Metabolites ◽  
Gut Microbial Community

The consumption of various meats prevalent throughout the world affects host health probably by associating with compositional shifts of gut microbiota. However, the responses of gut microbiota to different types of meat are not well understood. In this study, we explored the effects of cooked fish (white meat), and pork and beef (red meat) on gut microbiota and blood lipid metabolism in male C57BL/6 mice by comparing to those fed laboratory chow. Significant differences in microbial communities were observed among meat- and chow-fed mice. Compared with the chow group, the red and white meat groups obviously increased in abundance of Clostridium, and decreased in Prevotella abundance. The richness and diversity of gut microbiota were markedly decreased in the two red meat groups, with lower abundance of Oscillospira and higher abundance of Escherichia. Meanwhile, there were significant meat-related differences in blood lipid metabolites, with lower levels of high-density lipoprotein, low-density lipoprotein, cholesterol, and in mice fed white, compared with red, meat. Lipopolysaccharide-binding protein was significantly lower in fish-fed mice. Our results indicate that different types of meat potentially influence gut microbial compositions and blood metabolic profiles, suggesting a need to focus on clinically relevant bacteria in gut microbiota associated with increasing meat consumption.

scholarly journals Myricetin Ameliorates Ox-LDL-induced HUVECs Apoptosis and Inflammation via lncRNA GAS5 Upregulating the Expression of miR-29a-3p

2020 ◽  
Author(s):  
Yunpeng Bai ◽  
Qingliang Chen ◽  
Nan Jiang ◽  
zhigang guo
Keyword(s):  
Western Blot ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Cell Counting ◽  
Protective Effects ◽  
Cell Dysfunction ◽  
Rna Immunoprecipitation ◽  
Induced Apoptosis ◽  
Apoptosis And Inflammation ◽  
Relationship Of

Abstract BackgroundOxidized low-density lipoprotein (ox-LDL)-induced an endothelial cell dysfunction is a significant event in the progression of atherosclerosis[1]. Even myricetin (Myr) has been exhibited strong antioxidant potency, the effect on atherosclerosis is still elusive. MethodsHUVECs were subjected to ox-LDL, before which cells were preconditioned with Myr. Cell Counting Kit-8 (CCK-8) assay, flow cytometry, quantitative real-time polymerase chain reaction (qRT-PCR) and Western blot were carried out to assess the impacts of ox-LDL and Myr on HUVECs. The expression of EndMT markers was determined by Western blot analysis and immunocytochemistry. In addition, the relationship of GAS5 and miR-29a-3p was evaluated by RNA Fluorescent in Situ Hybridization (FISH) and RNA immunoprecipitation (RIP) assay. ResultsMyr preconditioning prevented ox-LDL-induced apoptosis, inflammatory response, and EndMT. GAS5 was upregulated in response to ox-LDL while it was down-regulated by Myr preconditioning. GAS5 over-expression attenuates Myr protective effects against ox-LDL–mediated HUVEC injury. Besides, miR-29a-3p is a target of GAS5 and down-regulated miR-29a-3p could further resuced the effects of GAS5 in ox-LDL–mediated HUVEC. Furthermore, Myr inactivated the TLR4/NF-κB signaling pathway in ox-LDL-treated HUVEC by down-regulating GAS5 or upregulating miR-26a-5p. ConclusionMyr possessed an anti-inflammatory and anti-EndMT function against ox-LDL-induced HUVEC injury by regulating the GAS5/miR-29a-3p, indicating that Myr may have an important therapeutic function for atherosclerosis.

scholarly journals Potential Benefits of Probiotics and Prebiotics for Coronary Heart Disease and Stroke

Nutrients ◽  
2021 ◽  
Vol 13 (8) ◽  
pp. 2878
Author(s):  
Haicui Wu ◽  
Jiachi Chiou
Keyword(s):  
Coronary Heart Disease ◽  
Heart Disease ◽  
Gut Microbiota ◽  
Inflammatory Responses ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
High Sensitivity ◽  
Therapeutic Interventions ◽  
Functional Changes ◽  
Hs Crp

Among cardiovascular diseases (CVDs), a major cause of morbidity and mortality worldwide, coronary heart disease and stroke are the most well-known and extensively studied. The onset and progression of CVD is associated with multiple risk factors, among which, gut microbiota has received much attention in the past two decades. Gut microbiota, the microbial community colonizing in the gut, plays a prominent role in human health. In particular, gut dysbiosis is directly related to many acute or chronic dysfunctions of the cardiovascular system (CVS) in the host. Earlier studies have demonstrated that the pathogenesis of CVD is strongly linked to intestinal microbiota imbalance and inflammatory responses. Probiotics and prebiotics conferring various health benefits on the host are emerging as promising therapeutic interventions for many diseases. These two types of food supplements have the potential to alleviate the risks of CVD through improving the levels of several cardiovascular markers, such as total and low-density lipoprotein (LDL) cholesterol, high sensitivity C-reactive protein (hs-CRP), and certain cytokines involved in the inflammatory response. In this review, we focus mainly on the preventive effects of probiotics and prebiotics on CVD via rebalancing the structural and functional changes in gut microbiota and maintaining immune homeostasis.

scholarly journals Myricetin ameliorates ox-LDL-induced HUVECs apoptosis and inflammation via lncRNA GAS5 upregulating the expression of miR-29a-3p

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Yunpeng Bai ◽  
Xiankun Liu ◽  
Qingliang Chen ◽  
Tongyun Chen ◽  
Nan Jiang ◽  
...  
Keyword(s):  
Western Blot ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Cell Counting ◽  
Protective Effects ◽  
Cell Dysfunction ◽  
Rna Immunoprecipitation ◽  
Induced Apoptosis ◽  
Apoptosis And Inflammation ◽  
Relationship Of

AbstractOxidized low-density lipoprotein (ox-LDL)-induced endothelial cell dysfunction is a significant event in the progression of atherosclerosis. Even Myricetin (Myr) has been exhibited strong antioxidant potency, the effect on atherosclerosis is still elusive. HUVECs were subjected to ox-LDL, before which cells were preconditioned with Myr. Cell Counting Kit-8 assay, flow cytometry, quantitative real-time polymerase chain reaction and Western blot were carried out to assess the impacts of ox-LDL and Myr on HUVECs. The expression of EndMT markers was determined by Western blot analysis and immunocytochemistry. In addition, the relationship of GAS5 and miR-29a-3p was evaluated by RNA Fluorescent in Situ Hybridization and RNA immunoprecipitation assay. Myr preconditioning prevented ox-LDL-induced apoptosis, inflammatory response, and EndMT. GAS5 was upregulated in response to ox-LDL while it was down-regulated by Myr preconditioning. GAS5 over-expression attenuates Myr protective effects against ox-LDL–mediated HUVEC injury. Besides, miR-29a-3p is a target of GAS5 and down-regulated miR-29a-3p could further reduce the effects of GAS5 in ox-LDL–mediated HUVEC. Furthermore, Myr inactivated the TLR4/NF-κB signalling pathway in ox-LDL-treated HUVEC by down-regulating GAS5 or upregulating miR-26a-5p. Myr possessed an anti-inflammatory and anti-EndMT function against ox-LDL-induced HUVEC injury by regulating the GAS5/miR-29a-3p, indicating that Myr may have an important therapeutic function for atherosclerosis.

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