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The present study aimed to increase the content of minor ginsenosides and enhance the anti-colorectal cancer activity of ginsenosides via biotransformation by Lactiplantibacillus plantarum MB11 screened from fermented foods. A subcutaneous transplantation tumor model of murine colorectal cancer CT26 cells was established in mice to study the anticarcinogenic activities and mechanism of fermented total ginsenosides (FTGs). The results showed that L. plantarum MB11 fermentation increased the content of minor ginsenosides and decreased that of major ginsenosides. FTGs reduced the tumor weight and size compared with the model group. Immunofluorescence and TdT-mediated dUTP nick end labeling (TUNEL) analysis showed that FTGs significantly increase the number of caspase-3 cells in tumor tissue and induce cell apoptosis. Mechanically, FTGs activate AMPK/mTOR autophagy pathway and regulate JAK2/STAT3 and Bax/Bcl-2/caspase-3 apoptosis pathway. Overall, fermentation with L. plantarum MB11 enhanced minor ginsenosides in total ginsenosides, and FTGs induced subcutaneous transplantation tumor autophagy and apoptosis in mice.

Probiotic intervention has beneficial effects on host brain function and behavior via regulating microbiota-gut-brain axis; however, the underlying mechanism is not yet understood. Herein, we investigated that the effects of Lactobacillus plantarum DP189 (DP189) administration in preventing cognitive dysfunction and pathology of Alzheimer's disease (AD) in D-galactose (D-gal) and AlCl 3 -induced AD model mice. After L. plantarum DP189 intervention for 10 weeks, we assessed cognitive behavior, neurotransmitter expression, histological changes, microbial communities, and the mechanisms underlying the disease in AD model mice. The results showed that L. plantarum DP189 intervention prevented cognitive dysfunction by behavioral test. Increased levels of serotonin, dopamine, and gamma-aminobutyric acid positively affected the pathological processes by ameliorating neuronal damage, beta-amyloid deposition, and tau pathology. L. plantarum DP189 intervention simultaneously modulated the gut microbial communities to alleviate gut dysbiosis. Moreover, L . plantarum DP189 inhibited tau hyperphosphorylation by regulating the PI3 K/Akt/GSK-3β pathway. These findings indicated that L. plantarum DP189 intervention is a promising therapeutic strategy to prevent the onset and development of AD.

Probiotics are considered to play an crucial role in the treatment of high-fat diet (HFD)-induced lipid metabolic diseases, including metabolic syndrome (MS). This study aimed to investigate the effects of Lactobacillus plantarum S9 on MS in HFD-fed rats, and to explore the underlying role of probiotics in the treatment of MS. Sprague-Dawley rats were fed with HFD for 8 weeks, followed by the treatment of L. plantarum S9 for 6 weeks, and The body weight and blood glucose level of rats were detected on time. The results showed that L. plantarum S9 significantly decreased the body weight gain, Lee's index, and liver index. Additionally, L. plantarum S9 reduced the levels of serum lipids and insulin resistance. L. plantarum S9 also decreased the levels of alanine aminotransferase (ALT) and aspartate transaminase (AST) in liver. Moreover, the serum levels of MS-related inflammatory signaling molecules, including lipopolysaccharide (LPS) and tumor necrosis factor-α (TNF-α), were significantly elevated. Western blot analysis showed that L. plantarum S9 inhibited the activation of nuclear factor-κB (NF-κB) pathway, decreased the expression level of Toll-like receptor 4 (TLR4), suppressed the activation of inflammatory signaling pathways, and reduced the expression levels of inflammatory factors in HFD-fed rats. Moreover, it further decreased the ratios of p-IκBα/IκBα, p-p65/NF-κB p65, and p-p38/p38. In summary, L. plantarum S9, as a potential functional strain, prevents or can prevent onset of MS., (© 2022. The Author(s).)

This study aimed to evaluate the attenuating effect of Lactobacillus plantarum DP189 on α-synuclein (α-SYN) aggregates in the substantia nigra (SN) of Parkinson's disease (PD) mice via 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced. Our results indicated that L. plantarum DP189 increased the levels of superoxide dismutase (SOD), glutathione peroxide (GSH-Px), and interleukin-10 (IL-10) and decreased the levels of malondialdehyde (MDA), reactive oxygen species (ROS), tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), and interleukin-1β (IL-1β). Moreover, L. plantarum DP189 reduced the α-SYN accumulation in SN. Mechanistically, L. plantarum DP189 activated the expression of nuclear factor erythroid 2-related factor (Nrf2)/ARE and PGC-1α pathways and suppressed the NLRP3 inflammasome. Furthermore, fecal analysis showed that L. plantarum DP189 reshaped the gut microbiota in PD mice by reducing the number of pathogenic bacteria ( Proteobacteria and Actinobacteria ) and increased the abundance of probiotics ( Lactobacillus and Prevotella ). Our results suggested that L. plantarum DP189 could delay the neurodegeneration caused by the accumulation of α-SYN in the SN of PD mice via suppressing oxidative stress, repressing proinflammatory response, and modulating gut microbiota.

Probiotic antidepressant effects demonstrated previously in clinical studies and animal models act via unknown mechanisms. Here we used a corticosterone injection-induced Sprague-Dawley rat chronic stress exposure model to investigate antidepressant-like effects of potential probiotic Lactobacillus plantarum DP189 (DP189) isolated from Chinese traditional fermented sauerkraut. After administration of DP189 (1.0 × 10 9 CFU/d) suspension by gavage for 21 days, behavioral, histopathological and biochemical changes were assessed, including hippocampal neuronal apoptosis assessments via TUNEL staining and Western blot analysis. Behaviorally, DP189 treatment improved memory and spatial learning and reduced anhedonia, as measured using Morris water maze and sucrose preference tests, respectively. Histopathologically, DP189 treatment ameliorated hippocampal pathological changes and dramatically reduced TUNEL-positive cell numbers. Biochemically, DP189 decreased serum IL-1β and TNF-α levels, decreased hippocampal mitogen-activated protein kinase kinase 7 and c-Jun N-terminal kinase 2 levels, down-regulated pro-apoptosis protein Bax immunocontent and up-regulated anti-apoptosis protein Bcl-2 immunocontent. Collectively, these results suggest that DP189 treatment may prevent and/or alleviate depression-like behaviors and hippocampal neural injury induced by CORT., (Copyright © 2020 Elsevier B.V. All rights reserved.)

Gut microbiota dysbiosis, associated with insulin resistance, weak intestinal barrier integrity, and inflammation, may also play a role in the development of dietary-induced nonalcoholic fatty liver disease (NAFLD). This study investigates the effects of dietary Lactobacillus plantarum NA136 administration on gut microbiota composition in an insulin-resistant C57BL/6J mouse NAFLD model. Comparison of mice with and without L. plantarum NA136 treatment revealed that L. plantarum NA136 treatment not only relieved insulin resistance but also significantly increased relative proportions of Desulfovibrio, Alistipes, Prevotella, and Enterorhabdus in gut microbiota of NAFLD mice. Meanwhile, L. plantarum NA136 administration also inhibited pathogenic bacterial growth, while promoting growth of probiotics such as Allobaculum, Lactobacillus, and, most markedly, Bifidobacterium. Moreover, L. plantarum NA136 treatment of NAFLD mice improved intestinal barrier integrity and attenuated high-fat and fructose diet (HFD/F)-induced inflammation. These results implicate gut-liver-axis-dependent microbiota modulation as the underlying mechanism for L. plantarum NA136-induced amelioration of NAFLD.Key points• L. plantarum NA136 corrects gut microbiota disorders caused by a high-fat and fructose diet. • L. plantarum NA136 strengthens the intestinal barrier and reduces inflammation in the liver. • L. plantarum NA136 relieves NAFLD by improving the gut-liver axis.

Microbial enzymes within adjunct cultures are important for cheese ripening. Here, survival and proteolytic function of adjunct cultures of Lactobacillus plantarum strains MU12 and S6-4 on Cheddar cheese ripening were studied. Cheeses were ripened at 4°C, and samples were collected for analysis after 1, 30, 60, and 90 days. Lactococci numbers decreased by 2 to 3 log versus control, except in a few samples exhibiting significantly elevated numbers. Lactobacilli mainly originated from adjunct cultures, with lactobacilli numbers in adjunct-treated cheese significantly exceeding control numbers after day 30. Postripening, no significant differences were observed in composition (fat, protein, and moisture) and texture among cheeses, although observed significant differences in small nitrogen-containing compound levels (water-soluble nitrogen, trichloroacetic acid-soluble nitrogen, and phosphotungstic acid-soluble nitrogen) reflected proteolytic differences during ripening. Hydrolyzed protein, free amino acids, and volatile levels were consistently higher in adjunct-treated versus control cheeses and affected flavor. Cheddar cheeses may serve to effectively deliver beneficial organisms possessing proteolytic function.

Background: Probiotics play an important role in the human and animal defense against liver damage. However, the protective mechanism of Lactobacillus plantarum C88 on chronic liver injury induced by mycotoxin remains unclear., Results: In this study, the addition of L. plantarum C88 obviously ameliorated the increased contents of alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase (ALP), total cholesterol and triglyceride, the diminish contents of total protein and albumin in serum of mice challenged with AFB 1 . Simultaneously, L. plantarum C88 attenuated the inflammatory response via significantly reducing the levels of pro-inflammatory factors, including interleukin-1β (IL-1β), IL-6, IL-8, interferon-γ (IFN-γ) and tumor necrosis factor-α (TNF-α) in serum. Furthermore, L. plantarum C88 remarkably down-regulated the nuclear factor kappa B (NF-κB) signaling pathways by weakening the expression of toll-like receptor 2 (TLR2) and TLR4, and inhibited NF-κB nuclear translocation through enhancing the expression of NF-κB inhibitor (IκB). Neutralization experiments confirmed that L. plantarum C88 decreased the levels of some pro-inflammatory factors due to the suppression of the NF-κB signaling pathways. Besides, L. plantarum C88 decreased the levels of Bax and Caspase-3, elevated the level of Bcl-2, and reduced mRNA expressions of Fatty acid synthetase receptor (Fas), FAS-associated death domain (FADD), TNF receptor associated death domain (TRADD) and Caspase-8 in the liver., Conclusions: Probiotic L. plantarum C88 prevented AFB 1 -induced secretion of pro-inflammatory cytokines by modulating TLR2/NF-κB and TLR4/NF-κB pathways. The molecular mechanisms of L. plantarum C88 in ameliorating AFB 1 -induced excessive apoptosis included regulating the mitochondrial pathway and cell death receptor pathways.

Hepatic lipid metabolic disorders and oxidative stress are involved in the development of non-alcoholic fatty liver disease (NAFLD). This study is to determine the protective effects of Lactobacillus plantarum NA136 on high-fat diet and fructose (HFD/F)-induced NAFLD and to elucidate its underlying molecular mechanisms. Male C57BL/6J mice had been fed with normal diet (ND), HFD/F, or HFD/F supplemented with L. plantarum NA136 for 16 weeks. Treatment with L. plantarum NA136 significantly lowered the body weight gain and decreased the mass of fat tissues, lipids, AST, and ALT levels of HFD/F-treated mice. Our results showed that L. plantarum NA136 activated AMPK pathway to phosphorylate ACC and to suppress the SREBP-1/FAS signaling to inhibit the de novo lipogenesis and increase the fatty acid oxidation. Furthermore, with treatment of L. plantarum NA136, the nuclear translocation of NF-E2-related factor 2 (Nrf2) was also increased which could activate antioxidant pathway. These findings suggested that L. plantarum NA136 improved NAFLD by regulating the fatty acid metabolism and defending against oxidative stress through AMPK and Nrf2 pathways, respectively.

Probiotic intervention has beneficial effects on host brain function and behavior via regulating microbiota-gut-brain axis; however, the underlying mechanism is not yet understood. Herein, we investigated that the effects of Lactobacillus plantarum DP189 (DP189) administration in preventing cognitive dysfunction and pathology of Alzheimer's disease (AD) in D-galactose (D-gal) and AlCl3-induced AD model mice. After L. plantarum DP189 intervention for 10 weeks, we assessed cognitive behavior, neurotransmitter expression, histological changes, microbial communities, and the mechanisms underlying the disease in AD model mice. The results showed that L. plantarum DP189 intervention prevented cognitive dysfunction by behavioral test. Increased levels of serotonin, dopamine, and gamma-aminobutyric acid positively affected the pathological processes by ameliorating neuronal damage, beta-amyloid deposition, and tau pathology. L. plantarum DP189 intervention simultaneously modulated the gut microbial communities to alleviate gut dysbiosis. Moreover, L. plantarum DP189 inhibited tau hyperphosphorylation by regulating the PI3 K/Akt/GSK-3β pathway. These findings indicated that L. plantarum DP189 intervention is a promising therapeutic strategy to prevent the onset and development of AD. [ABSTRACT FROM AUTHOR]

Acute liver failure (ALF) is a life-threatening clinical condition resulting from massive apoptosis of hepatocytes. This study aims to examine the protective effects of Lactobacillus plantarum C88 on LPS/D-GalN-induced ALF and elucidate its underlying molecular mechanisms in mice. The results showed that L. plantarum C88 pretreatment significantly reduced the levels of plasma ALT and AST in mice with LPS/D-GalN–induced liver injury. L. plantarum C88 pretreatment decreased the secretion of inflammatory cytokines. In addition, L. plantarum C88 remarkably increased the expression levels and nuclear translocations of Nrf2 mRNA in liver tissues, but inhibited NF-κB nuclear translocations and P65, P38 phosphorylation levels. Moreover, L. plantarum C88 enhanced the intestinal mucosal barrier by upregulating the expressions of tight junction proteins as well as HIF-1α. These results suggest that L. plantarum C88 protects against ALF associated with Nrf2 and the MAPK/NF-κB signaling pathways. [ABSTRACT FROM AUTHOR]

[Display omitted] • DP189 has a neuroprotective effect in PD mice by MPTP-induced. • DP189 improves the spatial learning and memory ability in PD mice. • DP189 improves the pathological changes of substantia nigra in PD mice. • DP189 prevents the apoptosis of dopaminergic neurons by AKT/mTOR and Bcl-2 pathway. Probiotic has significant potential as a therapeutic target for Parkinson's disease (PD), but how it contributes to disease processes and symptoms remains uncertain. This study aimed to evaluate the protective effect of Lactobacillus plantarum DP189 on the apoptosis of dopaminergic neurons in the substantia nigra (SN) of PD model mice. Male C57BL/6 mice were subjected to a PD model and treated by oral administration of L. plantarum DP189 for 14 days. The results indicated that L. plantarum DP189 improved behavioral ability and increased the levels of 5-hydroxytryptamine and dopamine of PD mice. L. plantarum DP189 significantly increased the positive rate of tyrosine hydroxylase cells. L. plantarum DP189 activated the ERK2 and AKT/mTOR pathways, promoted the expression of Bcl-2, and inhibited the activities of Bax and Caspase 3. The results indicated that L. plantarum DP189 had a significant protective effect on the SN dopaminergic neurons in PD mice. [ABSTRACT FROM AUTHOR]

Background: Probiotics play an important role in the human and animal defense against liver damage. However, the protective mechanism of Lactobacillus plantarum C88 on chronic liver injury induced by mycotoxin remains unclear. Results: In this study, the addition of L. plantarum C88 obviously ameliorated the increased contents of alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase (ALP), total cholesterol and triglyceride, the diminish contents of total protein and albumin in serum of mice challenged with AFB1. Simultaneously, L. plantarum C88 attenuated the inflammatory response via significantly reducing the levels of pro-inflammatory factors, including interleukin-1β (IL-1β), IL-6, IL-8, interferon-γ (IFN-γ) and tumor necrosis factor-α (TNF-α) in serum. Furthermore, L. plantarum C88 remarkably down-regulated the nuclear factor kappa B (NF-κB) signaling pathways by weakening the expression of toll-like receptor 2 (TLR2) and TLR4, and inhibited NF-κB nuclear translocation through enhancing the expression of NF-κB inhibitor (IκB). Neutralization experiments confirmed that L. plantarum C88 decreased the levels of some pro-inflammatory factors due to the suppression of the NF-κB signaling pathways. Besides, L. plantarum C88 decreased the levels of Bax and Caspase-3, elevated the level of Bcl-2, and reduced mRNA expressions of Fatty acid synthetase receptor (Fas), FAS-associated death domain (FADD), TNF receptor associated death domain (TRADD) and Caspase-8 in the liver. Conclusions: Probiotic L. plantarum C88 prevented AFB1-induced secretion of pro-inflammatory cytokines by modulating TLR2/NF-κB and TLR4/NF-κB pathways. The molecular mechanisms of L. plantarum C88 in ameliorating AFB1-induced excessive apoptosis included regulating the mitochondrial pathway and cell death receptor pathways. [ABSTRACT FROM AUTHOR]