Pretreatment with Bifidobacterium longum BAA2573 ameliorates dextran sulfate sodium (DSS)-induced colitis by modulating gut microbiota.

Objectives: Inflammatory bowel disease (IBD) is a chronic lifelong inflammatory disease. Probiotics such as Bifidobacterium longum are considered to be beneficial to the recovery of intestinal inflammation by interaction with gut microbiota. Our goals were to define the effect of the exclusive use of BAA2573 on dextran sulfate sodium (DSS)-induced colitis, including improvement of symptoms, alleviation of histopathological damage, and modulation of gut microbiota. Methods: In the present study, we pretreated C57BL/6J mice with Bifidobacterium longum BAA2573, one of the main components in an over-the-counter (OTC) probiotic mixture BIFOTO capsule, before modeling with DSS. 16S rDNA sequencing and liquid chromatography-tandem mass spectrometry (LC-MS/MS)-based non-targeted metabolomic profiling were performed with the collected feces. Results: We found that pretreatment of Bifidobacterium longum BAA2573 given by gavage significantly improved symptoms and histopathological damage in DSS-induced colitis mice. After the BAA2573 intervention, 57 genera and 39 metabolites were significantly altered. Pathway enrichment analysis demonstrated that starch and sucrose metabolism, vitamin B6 metabolism, and sphingolipid metabolism may contribute to ameliorating colitis. Moreover, we revealed that the gut microbiome and metabolites were interrelated in the BAA2573 intervention group, while Alistipes was the core genus. Conclusion: Our study demonstrates the impact of BAA2573 on the gut microbiota and reveals a possible novel adjuvant therapy for IBD patients.

Bioactive effects of nonthermal argon-oxygen plasma on inorganic bovine bone surface.

As a commonly used bone substitute material in the clinic, inorganic bovine bone has the characteristics of osteoconduction but not osteoinduction. This study aimed to treat inorganic bovine bone using nonthermal argon-oxygen plasma (NTAOP) to obtain greater bioreactivity for enhancing adhesion, proliferation and differentiation of mouse preosteoblast MC3T3-E1 cells. In this study, inorganic bovine bone was activated by NTAOP, and the surface characteristics were analyzed. MC3T3-E1 cells were then seeded onto the surface of inorganic bovine bone. Cell morphology, proliferation and osteogenic differentiation were examined. There was no obvious change in the surface morphology of specimens between the two groups. Regarding the elemental composition of the material, the amount of surface carbon was reduced, whereas oxygen, phosphorus and calcium levels were increased in the NTAOP group. Further studies showed that the NTAOP groups performed better than their untreated counterparts in terms of supporting cell proliferation and differentiation. Inorganic bovine bone treated with NTAOP can promote preosteoblast adhesion, proliferation and differentiation.

Flavonoids from persimmon (Diospyros kaki L.) leaves inhibit proliferation and induce apoptosis in PC-3 cells by activation of oxidative stress and mitochondrial apoptosis.

Persimmon (Diospyros kaki L.) leaves are extensively used in Chinese medicine and are also excellent source of dietary polyphenols. Here we investigated the antiproliferative and pro-apoptotic activity of the total flavonoids extracted from persimmon leaves (FPL) in PC-3 cells. After treating cells with different concentration of FPL, Quercetin or Rutin for 24 h, MTT and flow cytometry were used to measure the cytotoxicity, apoptotic rate and cell cycle arrest. Compared with Quercetin and Rutin, FPL showed higher cytotoxicity at 12.5 and 25 µg/ml concentrations and also presented lower IC50 in PC-3 cells. In addition, FPL induced PC-3 cells apoptosis by activation of oxidative stress, as detected by ROS, MDA, nitrite and iNOS activity, and increased mitochondrial membrane permeability. Morphological changes, inactivation of Bcl-2, upregulation of BAX, release of cytochrome c and activation of downstream apoptotic signaling in FPL-treated PC-3 cells also suggested apoptotic death. Meanwhile, FPL significantly inhibited migration of PC-3 cells. Therefore, FPL inhibited proliferation, migration and induced apoptosis of PC-3 cells by activation of oxidative stress and mitochondrial-related apoptosis.