Some lactobacilli strains had beneficial effects on human beings due to their antioxidant activities. In this study lactobacilli strains stored in our laboratory were screened for potential antioxidant activities by investigating their 1,1-diphenyl-2-picrylhydrazyl free radical scavenging activity, oxygen radical absorbance capacity, resistance to H2O2, and hydroxyl free radical scavenging activity; then the antioxidant activities of the screened strains were evaluated by cellular antioxidant assay and protection for HT-29 cells against H2O2 injury assay. The results showed that Lactobacillus plantarum Y44 could scavenge oxygen free radicals, inhibit the production of intracellular reactive oxygen species without creating obvious cytotoxic effects, and protect HT-29 cells against H2O2 injury evidenced by the significant decrease of the Bcl-2-associated X protein (Bax)/B-cell lymphoma 2 (Bcl-2) ratio and heat shock protein 70 expression, increase of superoxide dismutase and glutathione peroxidase activities, and decrease of malondialdehyde level of HT-29 cells damaged by H2O2. It was speculated that L. plantarum Y44 protect HT-29 cells against oxygen radical injury through scavenging reactive oxygen species and activating intracellular antioxidant enzymes. A significant correlation was observed among the results of the hydroxyl radical scavenging assay, protection assay for HT-29 cells against H2O2 injury, and the cellular antioxidant assay. The findings indicated that L. plantarum Y44 could be a probiotic candidate with antioxidant properties and combining several chemical antioxidant methods and antioxidant cellular models could be an effective procedure to screen lactobacilli strains with antioxidant activity.

Some strains of lactobacilli can exert beneficial effects on a host when ingested in an adequate dose, such as immunoregulation and anti-inflammatory activities. In this study, the survival abilities under simulated gastrointestinal conditions, adhesion abilities on HT-29 cell monolayers, and hemolytic activities of four Lactobacillus plantarum strains were assessed. Among the four strains, L. plantarum-12 showed the higher survival rate under simulated gastrointestinal conditions and adhesion index on the HT-29 cell monolayers, exhibited γ-haemolytic activity and had no biological amine producing ability. L. plantarum-12 was administered to dextran sodium sulfate (DSS)-induced ulcerative colitis (UC) Balb/c mice by oral gavage for 10 days. It was observed that the UC Balb/c mice showed symptoms of colonic atrophy, intestinal histopathological change, gut microbial disturbance, and pro-inflammatory cytokine expression. L. plantarum-12 administration remarkably attenuated DSS-induced UC in mice. L. plantarum-12 administration could restore gut microbiota by increasing beneficial bacteria such as Lactobacillus and decreasing intestinal pathogenic bacteria like Proteobacteria. L. plantarum-12 administration could improve immunity via activating the janus kinase-signal transducer and the activator of the transcription (JAK-STAT) pathway and up-regulating adenosine deaminase (ADA) and interferon-induced protein with tetratricopeptide repeats 1 protein (IFIT1), and enforce the intestinal barrier function by up-regulating mucin 2 (MUC2) protein expression. In conclusion, L. plantarum-12 could attenuate DSS-induced UC in Balb/c mice by ameliorating intestinal inflammation, and restoring the disturbed gut microbiota. L. plantarum-12 could be used as promising probiotics to ameliorate colitis.

In our previous studies, Lactobacillus plantarum Y44 showed antioxidant activity and favorable gastric and intestinal transit tolerance. The purpose of this study is to determine whether L. plantarum Y44 could ameliorate intestinal inflammation and lipid metabolism disorder in obese mice fed with a high-fat diet. L. plantarum Y44 was administered by gavage to the mice fed with a high-fat diet for 12 weeks. The mice fed with a high fat diet only showed sustainably elevated body weight, liver lipid metabolism disorder, intestinal inflammation and a lower short chain fatty acid content in feces. Oral administration of L. plantarum Y44 regulated lipid metabolism disorder by inhibiting the expression of fatty acid synthase (FAS) and acetyl-CoA carboxylase (ACC) in the liver of obese mice, reducing the contents of total cholesterol (TC), triacylglycerols (TG), low density lipoprotein cholesterol (LDL-c), alanine aminotransferase (ALT), and aspartate transaminase (AST) and increasing the content of high-density lipoprotein cholesterol (HDL-c) in the serum of obese mice. Oral administration of L. plantarum Y44 up-regulated the expression of colon tight junction protein such as claudin-1 and occludin, down-regulated p38 and phospho-p38 levels and reduced serum interleukin-8 (IL-8) and tumor necrosis factor-α (TNF-α). Oral administration of L. plantarum Y44 increased Muribaculaceae, Rikenellaceae, and Lactobacillaceae levels, reduced the Firmicutes/Bacteroidetes ratio, and Desulfovibrionaceae and Proteobacteria levels in obese mice. Oral administration of L. plantarum Y44 also enhanced the contents of propionic acid, butyric acid, butanoicacid-3-methyl, pentanoic acid and acetic acid in the feces of the obese mice. Correlation analysis of Spearman revealed a significant correlation between changes in intestinal microflora and obesity-related symptoms. L. plantarum Y44 ameliorated intestinal inflammation and lipid metabolism disorders by modulating gut microbiota.

In our previous research, Lactiplantibacillus plantarum-12 alleviated inflammation in dextran sodium sulfate (DSS)-induced mice by regulating intestinal microbiota and preventing colon shortening (p < 0.05). The purpose of the present study was to evaluate whether L. plantarum-12 could ameliorate the colon cancer symptoms of azoxymethane (AOM)/DSS-treated C57BL/6 mice. The results showed that L. plantarum-12 alleviated colonic shortening (from 7.43 ± 0.15 to 8.23 ± 0.25) and weight loss (from 25.92 ± 0.21 to 27.75 ± 0.88) in AOM/DSS-treated mice. L. plantarum-12 oral administration down-regulated pro-inflammatory factors TNF-α (from 350.41 ± 15.80 to 247.72 ± 21.91), IL-8 (from 322.19 ± 11.83 to 226.08 ± 22.06), and IL-1β (111.43 ± 8.14 to 56.90 ± 2.70) levels and up-regulated anti-inflammatory factor IL-10 (from 126.08 ± 24.92 to 275.89 ± 21.87) level of AOM/DSS-treated mice. L. plantarum-12 oral administration restored the intestinal microbiota dysbiosis of the AOM/DSS treated mice by up-regulating beneficial Muribaculaceae, Lactobacillaceae, and Bifidobacteriaceae levels and down-regulating pathogenic Proteobacteria, Desulfovibrionaceae, and Erysipelotrichaceae levels. As a result, the fecal metabolites of the AOM/DSS-treated mice were altered, including xanthosine, uridine, 3,4-methylenesebacic acid, 3-hydroxytetradecanedioic acid, 4-hydroxyhexanoylglycine, beta-leucine, and glycitein, by L. plantarum-12 oral administration. Furthermore, L. plantarum-12 oral administration significantly ameliorated the colon injury of the AOM/DSS-treated mice by enhancing colonic tight junction protein level and promoting tumor cells death via down-regulating PCNA (proliferating cell nuclear antigen) and up-regulating pro-apoptotic Bax. (p < 0.05). Taken together, L. plantarum-12 oral administration could ameliorate the colon cancer burden and inflammation of AOM-DSS-treated C57BL/6 mice through regulating the intestinal microbiota, manipulating fecal metabolites, enhancing colon barrier function, and inhibiting NF-κB signaling. These results suggest that L. plantarum-12 might be an excellent probiotic candidate for the prevention of colon cancer.

Exopolysaccharide produced by Lactiplantibacillus plantarum-12 (LPEPS) exhibited the anti-proliferating effect on human colon cancer cell line HT-29 in vitro. The purpose of the study was to determine the alleviating effects of LPEPS on colon cancer development of the C57BL/6 mice treated by azoxymethane/dextran sulfate sodium salt (AOM/DSS). The C57BL/6 mice treated by AOM/DSS were orally administered LPEPS daily for 85 days. The results showed that LPEPS oral administration enhanced colon tight-junction protein expression and ameliorated colon shortening and tumor burden of the AOM/DSS treated mice. Furthermore, LPEPS oral administration significantly reduced pro-inflammatory factors TNF-α, IL-8, and IL-1β levels and increased anti-inflammatory factor IL-10 level in the serum of the AOM/DSS-treated mice. LPEPS oral administration reversed the alterations of gut flora in AOM/DSS-treated mice, as evidenced by the increasing of the abundance of Bacteroidetes, Bacteroidetes/Firmicutes ratio, Muribaculaceae, Burkholderiaceae, and norank_o__Rhodospirillales and the decreasing of the abundance of Firmicutes, Desulfovibrionaceae, Erysipelotrichaceae, and Helicobacteraceae. The fecal metabolites of the AOM/DSS-treated mice were altered by LPEPS oral administration, involving lipid metabolism and amino acid metabolism. Together, these results suggested that LPEPS oral administration alleviated AOM/DSS-induced colon cancer symptoms of the C57BL/6 mice by modulating gut microbiota and metabolites, enhancing intestine barrier, inhibiting NF-κB pathway, and activating caspase cascade.