Search

Additional file 4: Supplementary table 3. Meta-regression results.

Additional file 1: Supplementary Figure 1. Funnel plot in themeta-analysis on the association of waist circumference between prematureovarian insufficiency and control group. Supplementary Figure 2. Funnel plot in the meta-analysis on the association of systolic blood pressure betweenpremature ovarian insufficiency and control group. Supplementary Figure 3. Funnel plot in the meta-analysis on the association of diastolic blood pressurebetween premature ovarian insufficiency and control group. Supplementary Figure 4. Funnel plot in the meta-analysis on the association of fasting glucose betweenpremature ovarian insufficiency and control group. Supplementary Figure 5. Funnel plot in the meta-analysis on the association of insulin betweenpremature ovarian insufficiency and control group. Supplementary Figure 6.Funnel plot in the meta-analysis on the association of total cholesterol betweenpremature ovarian insufficiency and control group. Supplementary Figure 7. Funnel plot in the meta-analysis on the association of high-density lipoproteinbetween premature ovarian insufficiency and control group. Supplementary Figure 8. Funnel plot in the meta-analysis on the association of low-density lipoprotein betweenpremature ovarian insufficiency and control group. Supplementary Figure 9. Funnel plot in the meta-analysis on the association of triglycerides betweenpremature ovarian insufficiency and control group.

Additional file 2: Supplementary table 1. PRISMA 2022 checklist.

Additional file 3: Supplementary table 2. Search strategy.

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.

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 × 109CFU/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.

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.

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.

The protective effects of L. plantarum C88 against chronic alcohol-induced liver injury in mice were investigated. The pretreatment with L. plantarum C88 significantly decreased the levels of alanine transaminase and aspartate aminotransferase in chronic alcohol-challenged mice. L. plantarum C88 was also found to suppress the content of malondialdehyde (MDA) and enhance the activity of superoxide dismutase (SOD) in the liver, which are well-correlated with the downregulation of hepatic cytochrome P450 2E1 and upregulation of nuclear factor erythroid 2-related factor 2 (Nrf2). Moreover, L. plantarum C88 significantly abrogated the increased serum levels of TNF-α, IL-6, and IFN-γ induced by ethanol. L. plantarum C88 ameliorated gut leakiness by upregulating the expressions of tight junction proteins and suppressed the endotoxin-mediated inflammation by decreasing P38 phosphorylation and down-regulating NF-κB. These results demonstrate that L. plantarum C88 efficiently protects against alcoholic chronic liver injury.

Genome shuffling is an important method for rapid improvement in microbial strains for desired phenotypes. In this study, ultraviolet irradiation and nitrosoguanidine were used as mutagens to enhance the adhesion of the wild-type Lactobacillus plantarum C88. Four strains with better property were screened after mutagenesis to develop a library of parent strains for three rounds of genome shuffling. Fusants F3-1, F3-2, F3-3, and F3-4 were screened as the improved strains. The in vivo and in vitro tests results indicated that the population after three rounds of genome shuffling exhibited improved adhesive property. Random Amplified Polymorphic DNA results showed significant differences between the parent strain and recombinant strains at DNA level. These results suggest that the adhesive property of L. plantarum C88 can be significantly improved by genome shuffling. Improvement in the adhesive property of bacterial cells by genome shuffling enhances the colonization of probiotic strains which further benefits to exist probiotic 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 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. Electronic supplementary material The online version of this article (10.1186/s12866-019-1525-4) contains supplementary material, which is available to authorized users.

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.

Pathophysiologic mechanisms underlying atherosclerosis (AS) development are linked to dyslipidemia and inflammation. Pediococcus acidilactici AS185, a probiotic, was isolated from traditional farmers’ soybean paste (Yanji, China). This study aimed to assess P. acidilactici AS185 anti-atherosclerotic effects and elucidate molecular mechanisms of action using an early AS model of SD rats fed a high-fat diet with intraperitoneal vitamin D3 (VD3) injections. For 8 weeks, model rats received P. acidilactici AS185 via gavage once/day. Post-treatment serum levels of inflammatory mediators, lipids, adhesion molecules, aortic histopathological characteristics and AS-related aortic protein expression levels were assessed. P. acidilactici AS185 administration markedly increased serum HDL-C and IL-10 levels, while reducing serum TG, LDL-C, TC, Ox-LDL, ICAM-1, VCAM-1, TNF-α, IFN-γ, IL-1β, and IL-6 levels. Notably, P. acidilactici AS185 inhibited p-p38 and ERK1/2 MAPK pathways and decreased Ox-LDL and CD36 expression to attenuate early AS by altering lipid profiles and MAPK-signaling-based inflammation.

In this study, we investigated the potential of Lactobacillus plantarum isolated from Chinese traditional fermented foods to reduce the toxicity of aflatoxin B1 (AFB1), and its subsequent detoxification mechanism. Among all the investigated L. plantarum strains, L. plantarum C88 showed the strongest AFB1 binding capacity in vitro, and was orally administered to mice with liver oxidative damage induced by AFB1. In the therapy groups, the mice that received L. plantarum C88, especially heat-killed L. plantarum C88, after a single dose of AFB1 exposure, showed an increase in unabsorbed AFB1 in the feces. Moreover, the effects of L. plantarum C88 on the enzymes and non-enzymes antioxidant abilities in serum and liver, histological alterations of liver were assayed. The results indicated that compared to the control group, L. plantarum C88 alone administration induced significant increase of antioxidant capacity, but did not induce any significant changes in the histological picture. Compared to the mice that received AFB1 only, L. plantarum C88 treatment could weaken oxidative stress by enhancing the activity of antioxidant enzymes and elevating the expression of Glutathione S-transferase (GST) A3 through Nuclear factor erythroid (derived factor 2) related factor 2 (Nrf2) pathway. Furthermore, cytochrome P450 (CYP 450) 1A2 and CYP 3A4 expression was inhibited by L. plantarum C88, and urinary aflatoxin B1-N7-guanine (AFB-N7-guanine), a AFB1 metabolite formed by CYP 1A2 and CYP 3A4, was significantly reduced by the presence of viable L. plantarum C88. Meanwhile, the significant improvements were showed in histological pictures of the liver tissues in mice orally administered with viable L. plantarum C88. Collectively, L. plantarum C88 may alleviate AFB1 toxicity by increasing fecal AFB1 excretion, reversing deficits in antioxidant defense systems and regulating the metabolism of AFB1.