Streptococcus mutans is a recognized cariogenic bacterium and a major producer of biofilm matrix. The presence of Candida albicans in dental plaque with S. mutans enhances the virulence leading to the onset of rampant caries which is similar to early childhood caries (ECC). The purpose of this study was to explore the effect of Lactobacillus plantarum CCFM8724 (CCFM8724) on the treatment and prevention of dental caries induced by S. mutans and C. albicans in vivo. Rats were divided into 6 groups: the control group and model group, 2 treatment groups, and 2 prevention groups (0.02% chlorhexidine or CCFM8724). The fluctuation of microbial colonization and the change of bacteria flora in rat oral cavity after sowing of L. plantarum CCFM8724 were investigated by colony-forming units (CFU) and microflora analysis. The caries of rats were assessed by microcomputed tomography (micro-CT) and Keyes scoring method. The results showed that L. plantarum CCFM8724 in both the treatment and prevention groups could significantly decrease the population of S. mutans and C. albicans in the rats’ oral cavity ( p < 0.001 ), the mineral loss of enamel ( p < 0.05 ), and the scores of caries ( p < 0.05 ). Besides, L. plantarum CCFM8724 exhibited better effects than chlorhexidine. Hence, L. plantarum CCFM8724 was proved to be a potential oral probiotic on caries treatment and prevention in vivo and it may have the prospect of application in dental caries (especially ECC) prevention products.
Colitis has become a major health concern worldwide. The objective of the present study was to determine the probiotic influence of different strains of B. pseudolongum (Bp7 and Bp8) on alleviating colitis and to explore its possible potential mechanisms. Our results displayed that Bp7 and Bp8 intervention effectively reduced dextran sodium sulfate (DSS)-caused body weight loss and the release of several pro-inflammatory factors (interleukin (IL)-6, IL-1β, and tumor necrosis factor-α (TNF-α)) and increased the activities of antioxidant enzymes (T-AOC, SOD, and GSH) and the concentrations of tight junction proteins (occludin, claudin-1, and ZO-1). Moreover, Bp7 and Bp8 intervention drastically down-regulated the expression of colonic MyD88, NF-κB, iNOS and COX2 and drastically elevated the expression of colonic STAT3, Nrf2, and PPARγ. Gas chromatography-mass spectrometry results revealed that the cecal levels of isobutyric, butyric, and isovaleric acids were drastically increased in colitis mice intervened with Bp7 and Bp8. Moreover, 16S rRNA sequencing revealed that Bp7 and Bp8 intervention modulated the intestinal microbiota structure, particularly by enhancing the proportion of Eubacterium coprostanoligenes group, Marvinbryantia, Enterorhabdus, Faecalibaculum, Coriobacteriaceae UCG 002, Alistipes, and Bifidobacterium, which are relevant to the levels of cecal isobutyric acid, butyric acid, isovaleric acid, and inflammatory cytokines. Collectively, these findings suggest that Bp7 and Bp8 intervention alleviates the intestinal barrier function, possibly by blocking the secretion of proinflammatory cytokines, maintaining the intestinal physical barrier integrity, activating the PPARγ/STAT3 pathway, and modulating intestinal microbiota composition. Our study also suggested that B. pseudolongum is a promising probiotic for colitis treatment.
Capsaicin (CAP) is an ingredient of peppers that has biological activities at low doses but causes gastrointestinal (GI) discomfort at high doses. However, the GI effects of high doses of CAP and the evaluation criteria to determine this remain unknown. To elucidate the dose-related effects of CAP on GI health, CAP was administered to mice at 40, 60, and 80 mg/kg doses. The results showed that 40 mg/kg CAP did not negatively affect GI tissues, while 60 and 80 mg/kg CAP damaged GI tissues and caused significant inflammation in the jejunum, ileum, and colon. The levels of serum substance P (SP) and calcitonin gene-related peptide (CGRP) were CAP-dose-dependent, and short-chain fatty acids (SCFAs) content significantly increased in the 80 mg/kg group. Correlation analysis revealed that the underlying mechanisms might be related to the regulation of gut microbiota, especially Bifidobacterium, Lactobacillus, Faecalibacterium, and Butyricimonas. These results suggest that oral administration of 60 and 80 mg/kg CAP in mice causes intestinal inflammation and high levels of serum neuropeptides and cecal SCFAs, which may be related to alterations in gut microbiota.
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