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.

Protective effect of Lactobacillus fermentum CQPC04 on dextran sulfate sodium-induced colitis in mice is associated with modulation of the nuclear factor-κB signaling pathway.

Colitis severely affects the quality of life of patients, and lactic acid bacteria have been reported to be able to improve or treat colitis. In this study, we selected a strain of Lactobacillus fermentum (CQPC04) with good resistance in vitro to evaluate its effect on improvement in mice with dextran sulfate sodium (DSS)-induced colitis. We analyzed the effects of L. fermentum CQPC04 on mice with colitis macroscopically via colon length and histopathology. We also used conventional biochemical and ELISA kits, real-time quantitative PCR (RT-qPCR), and Western blotting to analyze microscopically the effects of L. fermentum CQPC04 on related oxidant indices and pro- and anti-inflammatory cytokines in serum and colon tissue of mice. The results indicated that L. fermentum CQPC04 notably increased colon length and ameliorated pathological damage of colon tissue in colitic mice. Serum indices showed that L. fermentum CQPC04 increased the enzyme activity of total superoxide dismutase (T-SOD) and catalase (CAT) and decreased the content of malondialdehyde (MDA) and the activity of myeloperoxidase (MPO). In addition, it inhibited the release of the pro-inflammatory cytokines tumor necrosis factor-α (TNF-α), IFN-γ, IL-1ß, IL-6, and IL-12, and increased the release of the anti-inflammatory cytokine IL-10 in serum. The RT-qPCR experiments confirmed that L. fermentum CQPC04 downregulated the expression of pro-inflammatory cytokine nuclear factor-κB-p65 (NF-κBp65), NF-κB inhibitor-α (IκB-α), TNF-α, IFN-γ, IL-1ß, IL-6, cyclooxygenase 2 (COX-2), and inducible nitric oxide synthase (iNOS), and upregulated the expression of IL-10 in colon tissue. Western blot analysis indicated that L. fermentum CQPC04 significantly reduced expression of NF-κBp65, TNF-α, IL-1ß, COX-2, and iNOS in mouse colon tissues, and increased expression of IκB-α and superoxide dismutase 2 (SOD2). Thus, L. fermentum CQPC04 could effectively alleviate the symptoms of DSS-induced colitis mice and is a potential probiotic for human experiments.

Preventive effect of Lactobacillus plantarum KSFY02 isolated from naturally fermented yogurt from Xinjiang, China, on d-galactose-induced oxidative aging in mice.

Yogurt from Xinjiang, China, is a traditional and naturally fermented food, and abundant microorganisms are produced during its fermentation process. In this study, we carried out in vivo animal experiments to explore the effect of a newly isolated lactic acid bacterial strain, Lactobacillus plantarum KSFY02 (LP-KSFY02), on oxidative aging. We used d-galactose to induce oxidative aging in mice and analyzed the serum and tissues of those mice using molecular biology detection methods. The results showed that LP-KSFY02 could inhibit the decreases in the thymic, cerebral, cardiac, liver, spleen, and kidney indices of mice caused by oxidative aging. The LP-KSFY02 strain increased activity of superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), and glutathione (GSH) and reduced levels of nitric oxide (NO) and malondialdehyde in the serum, liver, and spleen of the oxidative aging mice. Pathological observation demonstrated that LP-KSFY02 alleviated damage to the liver and spleen of oxidative aging mice. Quantitative PCR showed that LP-KSFY02 effectively upregulated mRNA expression of neuronal nitric oxide synthase (Nos1), endothelial nitric oxide synthase (Nos3), copper/zinc superoxide dismutase (Sod1), manganese superoxide dismutase (Sod2), catalase (Cat), heme oxygenase-1 (Hmox1), nuclear factor erythroid 2 related factor 2 (Nfe2l2), γ-glutamylcysteine synthetase (Gclm), and quinone oxidoreductase 1 (Nqo1) in mouse liver and spleen and downregulated expression of inducible nitric oxide synthase (Nos2). Western blot analysis revealed that LP-KSFY02 effectively upregulated protein expression of SOD1, SOD2, CAT, GSH1, and GSH2 in mouse liver and spleen tissues. Therefore, LP-KSFY02 can effectively prevent d-galactose-induced oxidative aging in mice. Its efficacy was superior to that of Lactobacillus delbrueckii ssp. bulgaricus (LDSB) and vitamin C, which are commonly used in the medical field as antioxidants. Thus, LP-KSFY02 is a high-quality strain with probiotic potential.

Hepatoprotective Effects of Lactobacillus on Carbon Tetrachloride-Induced Acute Liver Injury in Mice.

The aim of this study was to investigate and compare the effects of heat-killed and live Lactobacillus on carbon tetrachloride (CCl4)-induced acute liver injury mice. The indexes evaluated included liver pathological changes, the levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST), superoxide dismutase (SOD), glutathione (GSH), and malondialdehyde (MDA) in the serum, related gene expression (IL-1ß, TNF-α, Bcl-2, and Bax), and related proteins levels (Bax, Bcl-2, Caspase 3, and NF-κB p65). Compared with the model group, the results indicated that the levels of ALT, AST, and MDA in the serum, the expression levels of IL-1ß, TNF-α, and Bax, and the protein levels of Bax, Caspase 3, and NF-κB p65 significantly decreased, and the pathologic damage degree all significantly reduced after live Lactobacillus fermentum (L-LF) and live Lactobacillus plantarum (L-LP) treatment. Additionally, the levels of SOD and GSH in the serum, the gene expression of Bcl-2, and the protein level of Bcl-2 significantly increased after L-LF and L-LP treatment. Although HK-LF and HK-LP could also have obvious regulating effects on some of the evaluated indexes (ALT, AST, the expression levels of TNF-α and Bax, and the protein level of Bcl-2) and play an important role in weakening liver damage, the regulating effects of L-LF or L-LP on these indexes were all better compared with the corresponding heat-killed Lactobacillus fermentum (HK-LF) and heat-killed Lactobacillus plantarum (HK-LP). Therefore, these results suggested that LF and LP have an important role in liver disease.

Lactobacillus plantarum CQPC11 Isolated from Sichuan Pickled Cabbages Antagonizes d-galactose-Induced Oxidation and Aging in Mice.

Chinese pickled cabbage is a traditional fermented food that contains abundant microbes produced during the process of fermentation. In this work, an in vivo animal study was conducted to investigate the effects of a newly isolated lactic acid bacterium (Lactobacillus plantarum CQPC11, LP-CQPC11) on d-galactose-induced oxidation and aging in mice. Analysis of the serum and tissue samples of these mice using molecular biology approaches showed that LP-CQPC11 suppressed the decrease in thymus, brain, heart, liver, spleen, and kidney indices caused by oxidation and aging. Furthermore, LP-CQPC11 increased the levels of SOD (superoxide dismutase), GSH-Px (glutathione peroxidase), and GSH (glutathione), whereas it reduced the levels of NO (nitric oxide) and MDA (malondialdehyde) in the serum, liver, and spleen of oxidation and aging mouse models. Pathological observation indicated that LP-CQPC11 alleviated the damage caused by oxidation and aging on the liver and spleen of mice. qPCR analysis indicated that LP-CQPC11 effectively upregulated the expression of nNOS (neuronal nitric oxide synthase), eNOS (endothelial nitric oxide synthase), Cu/Zn-SOD (cuprozinc-superoxide dismutase), Mn-SOD (manganese superoxide dismutase), CAT (catalase), HO-1 (heme oxygenase-1), Nrf2 (nuclear factor-erythroid 2 related factor 2), γ-GCS (γ-glutamylcysteine synthetase), and NQO1 (NAD(P)H dehydrogenase [quinone] 1), but downregulated the expression of iNOS (inducible nitric oxide synthase) in the mouse liver and spleen. Western blot analysis showed that LP-CQPC11 effectively upregulated SOD1 (Cu/Zn-SOD), SOD2 (Mn-SOD), CAT, GSH1 (c-glutamylcysteine synthetase), and GSH2 (glutathione synthetase) protein expression in mouse liver and spleen tissues. These findings suggest that LP-CQPC11 can effectively prevent d-galactose-induced oxidation and aging in mice, and the effect is even better than that of the commonly used Lactobacillus delbruechii subsp. bulgaricus (LDSB) and vitamin C in the industry. Thus, LP-CQPC11 may be potentially employed as a probiotic strain.

Preventive Effect of Lactobacillus fermentum CQPC03 on Activated Carbon-Induced Constipation in ICR Mice.

Background and objectives: Paocai (pickled cabbage), which is fermented by lactic acid bacteria, is a traditional Chinese food. The microorganisms of Paocai were isolated and identified, and the constipation inhibition effect of one of the isolated Lactobacillus was investigated. Materials and Methods: The 16S rDNA technology was used for microbial identification. A mouse constipation model was established using activated carbon. After intragastric administration of Lactobacillus (108 CFU/mL), the mice were dissected to prepare pathological sections of the small intestine. Serum indicators were detected using kits, and the expression of small intestine-related mRNAs was detected by qPCR assay. Results: One strain of Lactobacillus was identified and named Lactobacillus fermentum CQPC03 (LF-CQPC03). Body weight and activated carbon propulsion rate were all higher in mice intragastrically administered with LF-CQPC03 compared with the control group, while the time to the first black stool in treated mice was lower than that in the control group. Serum assays showed that gastrin (Gas), endothelin (ET), and acetylcholinesterase (AchE) levels were significantly higher in the LF-CQPC03-treated mice than in the control group, while somatostatin (SS) levels were significantly lower than in the control mice. Mouse small intestine tissue showed that c-Kit, stem cell factor (SCF), and glial cell-derived neurotrophic factor (GDNF) mRNA expression levels were significantly higher in the LF-CQPC03 treated mice than in control mice, while transient receptor potential cation channel subfamily V member 1 (TRPV1) and inducible nitric oxide synthase (iNOS) expression levels were significantly lower in the LF-CQPC03 treated mice than in control mice. Conclusions: There is a better effect with high-dose LF-CQPC03, compared to the lower dose (LF-CQPC03-L), showing good probiotic potential, as well as development and application value.

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.

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.

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.

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 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.

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 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.

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.

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.

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.

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.

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 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.