Rice bran active peptide (RBAP) inhibited macrophage differentiation to foam cell and atherosclerosis in mice via regulating cholesterol efflux.

BACKGROUND: Atherosclerosis is a long-lasting inflammatory condition affecting the walls of arteries, marked by the buildup of fats, plaque formation, and vascular remodeling. Recent findings highlight the significance of cholesterol removal pathways in influencing atherosclerosis, yet the connection between cholesterol removal and regulation of macrophage inflammation remains poorly understood. RBAP could serve as an anti-inflammatory agent; however, its role in atherosclerosis and the mechanism behind it are still not well understood. PURPOSE: The objective of this research is to explore how RBAP impacts cholesterol efflux, which is a considerable element in the advancement of atherosclerosis. METHODS: An atherosclerosis mouse model was established by using an ApoE KO strain mouse on a high-fat diet (HFD) to assess the effects of RBAP, conducted either orally or through injection. Additionally, in vitro experiments were conducted where the induction of THP-1 cells was conducted for the differentiation towards macrophages, and along with mouse RAW264.7 cells, were challenged with ox-LDL to evaluate the impact of RBAP. RESULTS: In this study, RBAP was found to reduce the production and downregulate TNF-α, IL-1ß, and IL-6 levels and inhibited the activation of the TLR4/MyD88/NF-κB signaling in atherosclerosis model mice, as well as in ox-LDL-challenged THP-1 cells and mouse RAW264.7 macrophages. RBAP's effectiveness also improved the enhancement of reverse cholesterol transport (RCT) and cholesterol removal to HDL and apoA1 by increasing the activity of genes related to cholesterol removal PPARγ/LXRα/ABCA1/ABCG1, both in ApoE-/- mice and in THP-1 cells and mouse RAW264.7 macrophages. Notably, RBAP exerted similar effects on atherosclerosis model mice and macrophages to those of TAK-242, an inhibitor of the TLR4 signaling. When RBAP and TAK-242 were applied simultaneously, the improvement was not enhanced compared with either RBAP or TAK-242 treatment alone. CONCLUSION: These findings suggest that RBAP, as a TLR4 inhibitor, has anti-atherosclerotic effects by improving inflammation and promoting cholesterol effection, indicating its therapeutic potential in intervening atherosclerosis.

The Nutritional Intervention of Ingredients from Food Medicine Homology Regulating Macrophage Polarization on Atherosclerosis.

The polarization of macrophages plays a crucial regulatory role in a range of physiological and pathological processes involving macrophages. There are numerous concerns with macrophage polarization in atherosclerosis; however, most focus on modulating macrophage polarization to improve the microenvironment, and the mechanism of action remains unknown. In recent years, the advantages of natural and low-toxicity side effects of food medicine homology-derived substances have been widely explored. Few reports have started from ingredients from food medicine homology to regulate the polarization of macrophages so that early intervention can reduce or delay the process of atherosclerosis. This review summarizes the classification of macrophage polarization and related markers in the process of atherosclerosis. It summarizes the regulatory role of ingredients from food medicine homology in macrophage polarization and their possible mechanisms to provide ideas and inspiration for the nutritional intervention in vascular health.

Diabetic macrophage small extracellular vesicles-associated miR-503/IGF1R axis regulates endothelial cell function and affects wound healing.

Diabetic foot ulcer (DFU) is a break in the skin of the foot caused by diabetes. It is one of the most serious and debilitating complications of diabetes. The previous study suggested that dominant M1 polarization during DFU could be the leading reason behind impaired wound healing. This study concluded that macrophage M1 polarization predominates in DFU skin tissue. iNOS was increased in HG-induced M1-polarized macrophages; conversely, Arg-1 was decreased. Macrophage pellets after HG stimulation can impair endothelial cell (EC) function by inhibiting cell viability, tube formation and cell migration, indicating M1 macrophage-derived small extracellular vesicles (sEVs) -mediated HUVEC dysfunction. sEVs miR-503 was significantly upregulated in response to HG stimulation, but inhibition of miR-503 in HG-stimulated macrophages attenuated M1 macrophage-induced HUVEC dysfunction. ACO1 interacted with miR-503 and mediated the miR-503 package into sEVs. Under HG stimulation, sEVs miR-503 taken in by HUVECs targeted IGF1R in HUVECs and inhibited IGF1R expression. In HUVECs, miR-503 inhibition improved HG-caused HUVEC dysfunction, whereas IGF1R knockdown aggravated HUVEC dysfunction; IGF1R knockdown partially attenuated miR-503 inhibition effects on HUVECs. In the skin wound model in control or STZ-induced diabetic mice, miR-503-inhibited sEVs improved, whereas IGF1R knockdown further hindered wound healing. Therefore, it can be inferred from the results that the M1 macrophage-derived sEVs miR-503 targets IGF1R in HUVECs, inhibits IGF1R expression, leads to HUVEC dysfunction, and impedes wound healing in diabetic patients, while packaging miR-503 as an M1 macrophage-derived sEVs may be mediated by ACO1.

Proteins, polysaccharides and their derivatives as macromolecular antioxidant supplements: A review of in vitro screening methods and strategies.

Owing to the implications of oxidative stress in disease and ageing process, antioxidant research has been a research hotspot. Antioxidants are derived from among the active components of plant and animal extracts, including macromolecular proteins, peptides and polysaccharides, and some small molecule peptides, phenols and flavonoids, among others. Exogenous antioxidant supplementation is effective in combating oxidative stress and promoting recovery from diseases and disease-associated processes, such as inflammation, atherosclerosis, and neurodegeneration. In clinical studies, antioxidant supplementation has been shown to mitigate disease exacerbation. Therefore, screening of antioxidants and the active substances in natural biological macromolecules is crucial. In vitro studies of antioxidant properties represent the first step in screening. Selection of a suitable method to evaluate the properties of antioxidant substances from biological macromolecules sources is particularly important. However, a critique of existing methods for comparing the antioxidant activities of macromolecular antioxidants is lacking. The aim of this review is to provide a set of redox reaction-based methods and application strategies to evaluate the antioxidant properties of natural biological macromolecules components. The paper describes the mechanisms, advantages, disadvantages and applicability of different in vitro methods for assessing antioxidant properties. In particular, a set of strategies for screening antioxidant supplements are discussed.

An update on the effects of food-derived active peptides on the intestinal microecology.

The intestinal microecology is a research hotspot, and neologisms related to the gut such as gut-brain axis, gut-lung axis, gut-bone axis, gut-skin axis, gut-renal axis, and gut-liver axis have emerged from recent research. Meticulous investigation has discovered that food-derived active peptides (FDAPs) are bioactive substances that optimize the structure of the gut microbiota to improve human health. However, few reviews have summarized and emphasized the nutritional value of FDAPs and their mechanisms of action in regulating the composition of the gut microbiota. We aim to provide an update on the latest research on FDAPs by comparing, summarizing, and discussing the potential food sources of FDAPs, their physiological functions, and regulatory effects on the intestinal microecology. The key findings are that few studies have analyzed the potential mechanisms and molecular pathways through which FDAPs maintain intestinal microecological homeostasis. We found that an imbalance in the ratio of Bacteroidetes and Firmicutes in the gut microbiota and abnormal production of short-chain fatty acids are key to the occurrence and development of various diseases. This review provides theoretical support for future comprehensive research on the digestion, distribution, metabolism, and excretion of FDAPs and the mechanisms underlying the interactions between FDAPs and the intestinal microecology.

Inhibitory Effect of Lactobacillus delbrueckii subsp. bulgaricus KSFY07 on Kappa-Carrageenan-Induced Thrombosis in Mice and the Regulation of Oxidative Damage.

A mouse thrombosis model was established by kappa-carrageenan to observe the inhibitory effect of Lactobacillus delbrueckii subsp. bulgaricus KSFY07 (LDSB-KSFY07) on thrombosis and the oxidative stress response. Mouse serum, liver tissue-related indicators, and intestinal microbial composition were measured by examining the expression of microbes in mouse faeces using a biochemical kit, slice observations, and quantitative polymerase chain reaction (qPCR) experiments. The results showed that LDSB-KSFY07 effectively reduced the degree of black tail in thrombotic mice, increased activated partial thromboplastin time (APTT), and decreased thrombin time (TT), fibrinogen (FIB), and prothrombin time (PT) in thrombotic mice. LDSB-KSFY07 was also able to reduce malondialdehyde (MDA) levels and increase superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GSH-Px) levels in the serum and liver tissues of thrombotic mice. Pathological observations showed that LDSB-KSFY07 reduced liver tissue lesions and tail vein thrombosis. Further, experimental results showed that LDSB-KSFY07 was able to upregulate the mRNA expression of copper/zinc-SOD (Cu/Zn-SOD), manganese-SOD, and GSH-Px in the liver tissue of thrombotic mice. Moreover, LDSB-KSFY07 was also able to downregulate the mRNA expression of NF-κB p65, intercellular cell adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1), and E-selectin in tail vein vascular tissue. Meanwhile, LDSB-KSFY07 could raise plasminogen activator inhibitor-1 (PAI-1) mRNA expression and reduce tissue plasminogen activator (t-PA) expression in heart and tail vein vascular tissues of thrombotic mice. A mouse faeces examination revealed that LDSB-KSFY07 could also upregulate Bacteroides, Lactobacterium, and Bifidobacterium microbial expression and downregulate Firmicutes expression in the gut. These results indicate that LDSB-KSFY07 was able to inhibit mouse thrombosis and reduce liver oxidative stress damage in thrombus mice and show that high concentrations of LDSB-KSFY07 provided a better response similar to that of the drug heparin.

Lactobacillus fermentum ZS40 Ameliorates Inflammation in Mice With Ulcerative Colitis Induced by Dextran Sulfate Sodium.

Ulcerative colitis is an inflammatory disease of the intestine caused by many reasons, and it may even develop into colon cancer. Probiotics are normal bacteria that exist in the human body and have been proven to regulate the balance of intestinal flora and alleviate inflammation. The current study aimed to study the effect of Lactobacillus fermentum ZS40 (ZS40) on dextran sulfate sodium (DSS)-induced ulcerative colitis mice. The length and weight of the colon were measured, and the histopathological morphological changes of colon tissue were observed to evaluate the effects of ZS40 on colitis. Biochemical kits, ELISA kits, real-time quantitative PCR (RT-qPCR), and western blot were also used to detect the effects of ZS40 on serum and colon tissue related oxidative indicators and pro-inflammatory and anti-inflammatory cytokines. We found that ZS40 could reduce colonic inflammatory cell infiltration and goblet cell necrosis, increase total superoxide dismutase and catalase in mouse serum, and reduce myeloperoxidase and malondialdehyde levels. ZS40 could down-regulate the level of proinflammatory cytokines and up-regulate the level of anti-inflammatory cytokines. More importantly, ZS40 down-regulated the relative expression of nuclear factor-κB p65 (NF-κBp65), IL-6, and TNF-α mRNA and protein, up-regulated the relative expression of inhibitor kapa B alpha (IκB-α). By regulating the NF-κB and MAPK pathways to down-regulated the relative expression of p38 and JNK1/2 mRNA and p38, p-p38, JNK1/2, and p-JNK1/2 proteins. Our study suggested that ZS40 may serve as a potential therapeutical strategy for ulcerative colitis.

Lactobacillus plantarum ZS62 Alleviates Alcohol-Induced Gastric Injury in Mice via an Anti-Oxidative Mechanism.

AIM: Gastric mucosal injury is a typical characteristic of gastric diseases. The prevalence of gastric mucosal injury caused by alcohol has been on the rise, which has been considered a serious problem. The purpose of this study is to explore the protective effect on gastric injury of Lactobacillus plantarum ZS62 (LP-ZS62) isolated from naturally fermented yak yoghurt. METHODS: We established a gastric injury model through alcohol and evaluated the protective effect of LP-ZS62 on gastric injury in mice. The injury to the gastric mucosa, histopathological sections, related biochemical indicators, and related genes were examined to evaluate the protective effect of LP-ZS62. RESULTS: LP-ZS62 effectively alleviated alcohol-induced gastric injury according to visual observations of gastric tissue and pathological tissue sections. The experimental results revealed that LP-ZS62 decreased malondialdehyde (MDA) level, and elevated superoxide dismutase (SOD) and glutathione (GSH) levels in gastric tissues. Additionally, LP-ZS62 increased glutathione peroxidase (GSH-Px), prostaglandin E2 (PGE2), and somatostatin (SS) levels. LP-ZS62 also decreased inflammatory cytokines interleukin (IL)-1ß, tumor necrosis factor-α (TNF-α) and IL-6 levels, and increased the anti-inflammatory cytokine IL-10 level. The quantitative polymerase chain reaction results showed that LP-ZS62 upregulated mRNA expression of nuclear factor E2-related factor 2 (Nrf2), copper/zinc superoxide dismutase (SOD1), manganese superoxide dismutase (SOD2), catalase (CAT), gamma-glutamylcysteine synthetase (GSH1), and glutathione peroxidase (GSH-Px). CONCLUSION: This study confirmed that LP-ZS62 alleviated alcohol-induced gastric injury by regulating antioxidant capacity. Therefore, LP-ZS62 could be developed as a probiotic product to treat alcoholic gastric injury.

Lactobacillus plantarum HFY09 alleviates alcohol-induced gastric ulcers in mice via an anti-oxidative mechanism.

The protective effect of Lactobacillus plantarum HFY09 (LP-HFY09) on alcohol-induced gastric ulcers was investigated. Gastric morphology observation and pathological tissue sections showed that LP-HFY09 effectively relieved gastric tissue injury. The biochemical indicator detection showed that LP-HFY09 increased superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), glutathione (GSH), prostaglandin E2 (PGE2), and somatostatin (SS) levels, and decreased malondialdehyde (MDA) levels. Moreover, LP-HFY09 inhibited the levels of inflammatory cytokines interleukin (IL)-1ß, IL-6, and tumor necrosis factor-α (TNF-α), and elevated the level of anti-inflammatory cytokine IL-10. The quantitative polymerase chain reaction (q-PCR) examination revealed that LP-HFY09 enhanced the mRNA expression of nuclear factor E2-related factor 2 (Nrf2) and downstream genes, including copper/zinc superoxide dismutase (SOD1), heme oxygenase-1 (HO-1), gamma-glutamylcysteine synthetase (GSH1), manganese superoxide dismutase (SOD2), catalase (CAT), and GSH-Px. This study indicated that LP-HFY09 alleviated alcohol-induced gastric ulcers by increasing gastric mucosa defense factor, and inhibiting oxidative stress and the inflammatory response. PRACTICAL APPLICATIONS: LP-HFY09 has the potential to be investigated as a treatment for gastric injury induced by alcohol.

The Impact of Antarctic Ice Microalgae Polysaccharides on D-Galactose-Induced Oxidative Damage in Mice.

Antarctic ice microalgae (Chlamydomonas sp.) are a polysaccharide-rich natural marine resource. In this study, we evaluated the impact of Antarctic ice microalgae polysaccharides (AIMP) on D-galactose-induced oxidation in mice. We conducted biological and biochemical tests on tissue and serum samples from mice treated with AIMP. We found that AIMP administration was associated with improved thymus, brain, heart, liver, spleen, and kidney index values. We also found that AIMP treatment inhibited the reduced aspartate aminotransferase, alanine aminotransferase, alkaline phosphatase, superoxide dismutase, glutathione peroxidase, and glutathione levels as well as the increased serum, splenic, and hepatic nitric oxide and malondialdehyde levels arising from oxidation in these animals. Pathological examination revealed that AIMP also inhibited D-galactose-induced oxidative damage to the spleen, liver, and skin of these animals. AIMP was additionally found to promote the upregulation of neuronal nitric oxide synthase, endothelial nitric oxide synthase, cuprozinc-superoxide dismutase, manganese superoxide dismutase, catalase, heme oxygenase-1, nuclear factor erythroid 2-related factor 2, γ-glutamylcysteine synthetase, and NAD(P)H dehydrogenase [quinone] 1 as well as the downregulation of inducible nitric oxide synthase in these animals. High-performance liquid chromatography analysis revealed AIMP to be composed of five monosaccharides (mannitol, ribose, anhydrous glucose, xylose, and fucose). Together, these results suggest that AIMP can effectively inhibit oxidative damage more readily than vitamin C in mice with D-galactose-induced oxidative damage, which underscores the value of developing AIMP derivatives for food purposes.

Lactobacillus fermentum CQPC07 attenuates obesity, inflammation and dyslipidemia by modulating the antioxidant capacity and lipid metabolism in high-fat diet induced obese mice.

BACKGROUND: Obesity is an epidemic disease in the world, the treatment and prevention of obesity methods have gained great attention. Lactobacillus is the main member of probiotics, and the physiological activity of it is specific to different strains. This study systematically explored the anti-obesity effect and possible mechanism of Lactobacillus fermentum CQPC07 (LF-CQPC07), which was isolated from pickled vegetables. RESULTS: LF-CQPC07 effectively controlled the weight gain of mice caused by a high-fat diet. The results of pathological sections indicated that LF-CQPC07 alleviated hepatocyte damage and fat accumulation in adipocytes. The detection of biochemical indictors revealed that LF-CQPC07 decreased the levels of total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C), and triglycerides (TG), and increased the level of high-density lipoprotein cholesterol (HDL-C). Additionally, LF-CQPC07 caused the decrease in the amounts of inflammatory cytokines interleukin (IL)-1ß, tumor necrosis factor-α (TNF-α), IL-6, and interferon-γ (IFN-γ), and the increase in the amounts of the anti-inflammatory cytokines IL-10 and IL-4. LF-CQPC07 also decreased the amounts of alanine aminotransferase (ALT), aspartate transaminase (AST), and alkaline phosphatase (ALP). Confirmed by qPCR, LF-CQPC07 enhanced the mRNA expression of catalase (CAT), gamma glutamylcysteine synthetase 1 (GSH1), copper/zinc superoxide dismutase (SOD1), manganese superoxide dismutase (SOD2), and glutathione peroxidase (GSH-Px). It also increased the mRNA expression levels of carnitine palmitoyltransferase 1 (CPT1), peroxisome proliferator-activated receptor alpha (PPAR-α), lipoprotein lipase (LPL), and cholesterol 7 alpha hydroxylase (CYP7A1), and decreased that of PPAR-γ and CCAAT/enhancer binding protein alpha (C/EBP-α) in the liver of mice. CONCLUSION: This research confirmed that LF-CQPC07 is capable of ameliorating obesity, improving hyperlipemia, and alleviating chronic low-grade inflammation and liver injury accompanied with obesity. Its mechanism may be the regulation of antioxidant capacity and lipid metabolism. Therefore, LF-CQPC07 has enormous potential to serve as a potential probiotic for the prevention or treatment of obesity.

Protective effect of Lactobacillus plantarum YS3 on dextran sulfate sodium-induced colitis in C57BL/6J mice.

The protective effect of Lactobacillus plantarum YS3 (LP-YS3) on ulcerative colitis (UC) was assessed using a mouse model of dextran sodium sulfate (DSS)-induced colitis. Different concentrations of LP-YS4 were administered to the experimental mice by daily gavage. Several inflammatory and biochemical indices, such as interleukin-2 (IL-2), interleukin-10 (IL-10), interleukin-6 (IL-6), interleukin-1 beta (IL-1ß), tumor necrosis factor-alpha (TNF-α), glutathione (GSH), malondialdehyde (MDA), myeloperoxidase (MPO), and nitric oxide (NO), were examined in mouse serum and colon tissue. The mRNA and protein expression levels of c-Kit, CXC chemokine receptor type 2 (CXCR2), interleukin-8 (IL-8), and stem cell factor (SCF) in mouse colon tissue were assessed using Western blot and quantitative polymerase chain reaction (qPCR) assays. The findings indicated that LP-YS3 remarkably decreased the disease activity index (DAI) of UC mice (p < .05), inhibited colon length shortening induced by UC, and elevated the value of colon weight/length ratio. LP-YS3 could also markedly reduce (p < .05) the activities of MDA, MPO, and NO; while an increase in the GSH content in the colonic tissue of UC mice. Moreover, LP-YS3 remarkably increased (p < .05) the serum level of IL-2 in UC mice, while reduced those of IL-10, IL-6, IL-1ß, TNF-α cytokines. qPCR data revealed that LP-YS3 could markedly upregulate the expression levels of c-Kit and SCF, while downregulate those of CXCR2 and IL-8 in the colonic tissue of UC mice (p < .05). LP-YS3 exerted an outstanding protective effect on DSS-induced colitis in C57BL/6J mice, especially at higher concentrations. PRACTICAL APPLICATIONS: Lactobacillus plantarum YS3 is a newly isolated and identified lactic acid bacteria. This study confirmed that L. plantarum YS3 can inhibit colitis and has good probiotic potential, which needs further development and utilization.

Preventive Effect of Lactobacillus acidophilus XY27 on DSS-Induced Ulcerative Colitis in Mice.

INTRODUCTION: Lactobacillus acidophilus is widely used as probiotic supplement in functional foods due to its beneficial regulatory effects on host, such as immune regulation, anti-inflammatory, and antioxidant activities. AIM: This study aimed to determine the preventive effect of Lactobacillus acidophilus XY27 (L. acidophilus XY27) on colitis induced by dextran sodium. METHODS: The mice were randomly divided into five groups. Except for the control group, the other four groups were induced for ulcerative colitis (UC) with dextran sodium sulfate (DSS), and three groups in DSS-groups were treated with L. acidophilus XY27, L. bulgaricus, and salicylazosulfapyridine. The weight change, DAI score, colon length, and length to weight ratio were tested. The oxidation index and the levels of inflammatory cytokines in the serum were measured. Subsequently, the gene expression levels of inflammatory factors in the colon tissue were determined by the Real-Time quantitative polymerase chain reaction (qRT-PCR) method. RESULTS: The results showed that the mice in the L. acidophilus XY27 group performed better in terms of weight, DAI score, colon length, and length to weight ratio or colonic pathological sections compared with the DSS-induced group. Further, the levels of tumor necrosis factor α (TNF-α), Interleukin-6 (IL-6), Interleukin-12 (IL-12) and Interleukin-1ß (IL-1ß), malondialdehyde (MDA) content, and myeloperoxidase activity in the serum of UC mice treated with L. acidophilus XY27 significantly decreased, while the levels of Interferon-γ (IFN-γ), Interleukin-10 (IL-10), Catalase (CAT), and total superoxide dismutase (SOD) significantly increased. The gene expression levels of Ets-like transcription factor-1 (EIK-1), IL-12, IL-1ß, Cyclooxygenase 2 (COX-2), TNF-α, Escherichia coli, Lipopolysaccharide (LPS), and p100 in the colon significantly decreased while those of tight junction protein 1 (ZO-1), nuclear factor kappa B (NF-kB), p53, and NF-kappa-B inhibitor alpha (IκB-α) increased in the L. acidophilus XY27 group. CONCLUSION: The results of the experiment suggested that L. acidophilus XY27 prevented colitis and alleviated symptoms in mice with DSS-induced UC, and also repaired the intestinal barrier function.

Effects of Lactobacillus fermentum CQPC04 on Lipid Reduction in C57BL/6J Mice.

Probiotics are functional foods that can effectively regulate lipid reduction and maintain body health. In this study, a strain of Lactobacillus fermentum CQPC04 (LF-CQPC04) isolated from traditional naturally fermented vegetables (Sichuan pickles) was studied, and its effects on lipid reduction in mice, as well as its mechanism of action, were observed. The results of this experiment show that LF-CQPC04 can reduce the abnormal weight gain and abnormal visceral index of mice caused by a high-fat diet. LF-CQPC04 can decrease TG (triglycerides), TC (total cholesterol), LDL-c (low-density lipoprotein cholesterol), AST (aspartate transaminase), ALT (alanine aminotransferase), and AKP (alkaline phosphatase) levels and increase HDL-c (high-density lipoprotein cholesterol) levels in the serum of high-fat mice. LF-CQPC04 can also decrease the levels of inflammatory cytokines, such as IL-6 (interleukin-6), IL-1ß (interleukin-1 beta), TNF-α (tumor necrosis factor alpha), and IFN-γ (interferon gamma), and increase IL-4 and IL-10 levels in the serum of high-fat mice. The results of RT-qPCR (real-time quantitative polymerase chain reaction) and western blot experiments show that LF-CQPC04 can also down-regulate the expression of PPAR-γ (peroxisome proliferator-activated receptor gamma), C/EBP-α (CCAAT/enhances binding protein alpha) mRNA, and protein in the liver tissue of high-fat mice, while up-regulating the expression of Cu/Zn-SOD (copper/zinc superoxide dismutase), Mn-SOD (manganese superoxide dismutase), CAT (catalase), CYP7A1 (cholesterol 7 alpha hydroxylase), PPAR-α (peroxisome proliferator-activated receptor alpha), CPT1 (carnitine palmitoyl transferase 1), LPL (lipoprotein lipase), and ABCA1 (ATP-binding cassette transporter A1). Moreover, LF-CQPC04 shows stronger effects in regulating lipid reduction in mice than L-carnitine and commercial LB (Lactobacillus delbrueckii subsp. Bulgaricus) bacteria. LF-CQPC04 is beneficial for lipid reduction in animals and has good probiotic potential.

Lactobacillus Plantarum HFY15 Helps Prevent Retinoic Acid-Induced Secondary Osteoporosis in Wistar Rats.

A rat model of secondary osteoporosis was constructed using retinoic acid as an inducer, and the genes, proteins, and bone mass of the rats were analyzed. qPCR detection of the Wnt/ß-catenin and OPG/RANK/RANKL signaling pathway-related gene expression levels showed that Lactobacillus plantarum HFY15 played a positive role in regulating both pathways. HFY15 significantly increased ß-catenin, Lrp5, Lrp6, Wnt10b, OPG, RANKL, and Runx2 expression and downregulated DKK1, RANK, CTSK, TRACP, and ALP expression. Enzyme-linked immunosorbent assays further confirmed the qPCR results. Tartrate-resistant acid phosphatase staining showed that HFY15 slowed retinoic acid-induced osteoclast formation. Microcomputed tomography showed that HFY15 reduced trabecular separation and increased the percent bone volume, trabecular numbers, trabecular thickness, and bone mineral density in the rats in vivo. These findings indicate that HFY15 may help prevent retinoic acid-induced secondary osteoporosis in vivo.

Antioxidant Capacity-Related Preventive Effects of Shoumei (Slightly Fermented Camellia sinensis) Polyphenols against Hepatic Injury.

Shoumei is a kind of white tea (slightly fermented Camellia sinensis) that is rich in polyphenols. In this study, polyphenols were extracted from Shoumei. High-performance liquid chromatography (HPLC) showed that the polyphenols included mainly gallic acid, catechin, hyperoside, and sulfuretin. In an in vitro experiment, H2O2 was used to induce oxidative damage in human normal hepatic L-02 cells. In an animal experiment, CCl4 was used to induce liver injury. The in vitro results showed that Shoumei polyphenols inhibited oxidative damage in normal hepatic L-02 cells, and the in vivo results showed that the polyphenols effectively reduced liver index values in mice with liver injury. The polyphenols also decreased aspartate aminotransferase (AST), alanine aminotransferase (ALT), alkaline phosphatase (ALP), triglyceride (TG), total cholesterol (TC), blood urea nitrogen (BUN), nitric oxide (NO), malondialdehyde (MDA), interleukin 6 (IL-6), interleukin 12 (IL-12), tumour necrosis factor alpha (TNF-α), and interferon gamma (IFN-γ) levels and increased albumin (ALB), superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GSH-Px) levels in the serum of mice with liver injury. Furthermore, pathological observation showed that the Shoumei polyphenols reduced CCl4-induced hepatocyte damage. qRT-PCR and Western blotting showed that the polyphenols upregulated the mRNA and protein expression of neuronal nitric oxide synthase (nNOS), endothelial nitric oxide synthase (eNOS), manganese- (Mn-) SOD, copper/zinc- (Cu/Zn-) SOD, CAT, and inhibitor of nuclear factor kappa B (NF-κB) alpha (IκB-α) and downregulated the expression of inducible nitric oxide synthase (iNOS) and NF-κB p65. The Shoumei polyphenols had a preventive effect against CCl4-induced mouse liver injury equivalent to that of silymarin. The four polyphenols identified as the key substances responsible for this effect mediated the effect through their antioxidant capacity. These results suggest that Shoumei polyphenols are high-quality natural products with liver-protective effects.

Lactobacillus plantarum KSFY06 and geniposide counteract montmorillonite-induced constipation in Kunming mice.

Constipation is a common clinical manifestation of digestive system disorders and occurs worldwide. This study investigated the ability of Lactobacillus plantarum KSFY06 (LP-KSFY06) to promote the action of geniposide in preventing montmorillonite-induced constipation in Kunming mice, with the aim of providing a successful solution. The effects of LP-KSFY06 and geniposide on constipation were measured, and the results showed that the protective effect of geniposide on constipation was enhanced by LP-KSFY06 and that the combination resulted in increased weight, moisture content, and particle number of feces. The first black stool defecation time was decreased from 182 min to 87 min, which clearly indicates that defecating difficulty was alleviated in constipated mice. The synergic intervention of LP-KSFY06 and geniposide (LP + G) assisted in maintaining the body weight of constipated mice. The LP + G intervention significantly increased serum levels of motilin (MTL, 167.8 pg/ml), acetylcholinesterase (AChE, 45.3 pg/ml), substance P (SP, 61.0 pg/ml), vasoactive intestinal peptide (VIP, 70.5 pg/ml), endothelin-1 (ET-1, 16.1 pg/ml), and gastrin (73.0 pg/ml) and remarkably decreased somatostatin (SS, 35.2 pg/ml) when compared to those indexes in the LP-KSFY06 group and geniposide group. The LP + G treatment also significantly increased the mRNA expression of cluster of differentiation 117 (c-Kit), stem cell factor (SCF), glial cell-derived neurotrophic factor (GDNF), and remarkably downregulated the expression of inducible nitric oxide synthase (iNOS), transient receptor potential vanilloid-1 (TRPV1), and cyclooxygenase-2 (COX-2). The experimental results showed that the combination treatment has the strongest prevention effect against constipation, and LP-KSFY06 promotes the ability of geniposide to prevent constipation. Therefore, LP-KSFY06 is a potential probiotic strain with the capacity to prevent montmorillonite-induced constipation.

Preventive effect of insect tea primary leaf (Malus sieboldii (Regal) Rehd.) extract on D-galactose-induced oxidative damage in mice.

Insect tea is consumed as a health beverage in China. The insect tea primary leaf (ITPL) is rich in bioactive substances, which are also used as traditional Chinese medicine. This study investigated the role of ITPL in reducing the oxidative response induced by D-galactose in mice. Mice were intraperitoneally injected with D-galactose to induce oxidative damage. The effect of ITPL was tested by pathological observation, serum detection with kits, quantitative polymerase chain reaction, and Western blot. The experimental results show that ITPL increased the thymus, brain, heart, liver, spleen, and kidney indices of oxidized mice. ITPL increased superoxide dismutase, glutathione peroxidase, and glutathione levels and reduced nitric oxide and malondialdehyde levels in the serum, liver, and spleen in oxidative damaged mice. The pathological observations show that ITPL reduced the oxidative damage of the liver and spleen in mice induced with D-galactose. Simultaneously, ITPL upregulated mRNA expression of neuronal nitric oxide synthase, endothelial nitric oxide synthase, cuprozinc-superoxide dismutase, manganese superoxide dismutase, catalase, heme oxygenase-1, nuclear factor-erythroid 2 related factor 2, γ-glutamylcysteine synthetase, and NAD(P)H dehydrogenase [quinone] 1, and downregulated the expression of inducible nitric oxide synthase in the liver and spleen of oxidized mice. ITPL had beneficial preventive effects on the oxidative damage caused by D-galactose in mice and was more effective as an antioxidant than vitamin C. The component analysis test by high-performance liquid chromatography indicated that ITPL contained the following seven compounds: neochlorogenic acid, cryptochlorogenic acid, rutin, kaempferin, isochlorogenic acid B, isochlorogenic acid A, and hesperidin. ITPL is a plant with excellent antioxidant activities derived from its bioactive substances.

Lactobacillus fermentum CQPC06 in naturally fermented pickles prevents non-alcoholic fatty liver disease by stabilizing the gut-liver axis in mice.

Herein, we used a HFD/F to induce NAFLD in mice and intervened with CQPC06 to determine the preventive effect of CQPC06 on NAFLD and its potential regulatory mechanism. C57BL/6J mice were fed with LFD, HFD/F, HFD/F supplemented with CQPC06, and HFD/F supplemented with LDBS for 8 weeks to test the properties of the probiotic. Biochemical and molecular biology methods were used to determine the levels of related indexes in mouse serum, liver tissue, epididymal fat, small intestine tissue, and feces. The results showed that CQPC06 exhibited satisfactory probiotic properties, significantly inhibited mouse weight gain, and decreased the liver index and serum lipid levels, including ALT, AKP, AST, TC, TG, LDL-C, LPS, and HDL-C levels. The HOMA-IR index calculated based on the blood glucose levels and serum insulin levels showed that the HOMA-IR index of NAFLD mice treated with CQPC06 significantly decreased. From the molecular biology level, CQPC06 significantly increased the mRNA and protein expression of PPAR-α, CYP7A1, CPT1, and LPL in NAFLD mouse livers, and decreased the expression of PPAR-γ and C/EBP-α. Furthermore, CQPC06 enhanced the expression of ZO-1, occludin, and claudin-1 in the small intestine of NAFLD mice, and decreased the expression of CD36. CQPC06 decreased the level of Firmicutes and increased the levels of Bacteroides and Akkermansia in the feces of NAFLD mice, and the ratio of Firmicutes/Bacteroides was significantly decreased. CQPC06 is highly resistant in vitro and survived in the gastrointestinal tract and exerted its probiotic effect, altered the intestinal microecology of NAFLD mice, and played an important role in NAFLD prevention through the unique anatomical advantages of the gut-liver axis. There was a clear preventive effect with high concentrations of CQPC06 and it was stronger than that of l-carnitine.

Prophylactic Effect of Lactobacillus plantarum YS4 on Oxazolone-Induced Colitis in BALB/c Mice.

In the present research, the effects of Lactobacillus plantarum YS4 (LP-YS4) on colitis were tested in an oxazolone-induced mouse model. BALB/c mice were induced by oxazolone and then treated with LP-YS4. The serum levels of mice were analyzed using commercial kits and the protein and mRNA expression levels of mouse colon tissue were detected by Western blotting and qPCR assay, respectively. The results demonstrated that LP-YS4 significantly (P < 0.05) increased the colon length and ratio of colon weight/length in mice with colitis and attenuated the negative effects of colitis. The results also showed that treatment with LP-YS4 significantly reduced the serum concentrations of ET-1, SP, and IL-10 while significantly increasing those of SS, VIP, and IL-2 in colitis mice (P < 0.05). In addition, LP-YS4 significantly increased the activities of GSH and SOD while decreasing those of MPO and MDA in the colon tissue of colitis mice (P < 0.05). LP-YS4 also significantly upregulated the mRNA and protein expression of c-Kit, eNOS, nNOSe, and SCF in colitis mice while significantly downregulating the relative expression of iNOS. In summary, LP-YS4 could reduce the negative effects of colitis, and such effects were better than those of the common probiotic Lactobacillus bulgaricus.