Hertzskaaning2716

These findings not only further support our previously-proposed redox mechanism for the protection against TCHQ-induced cytotoxicity by penicillamine, but also reveal a new mode of action for O2•- in the inhibition of haloquinoids-induced toxicity by thiol antioxidants.Cytochrome bc1, also known as mitochondrial complex III, is considered to be one of the important producers of reactive oxygen species (ROS) in living organisms. Under physiological conditions, a certain level of ROS produced by mitochondrial electron transport chain (ETC) might be beneficial and take part in cellular signaling. However, elevated levels of ROS might exhibit negative effects, resulting in cellular damage. It is well known that inhibiting the electron flow within mitochondrial complex III leads to high production of ROS. However, superoxide production by cytochrome bc1 in a non-inhibited system remained controversial. Here, we propose a novel method for ROS detection in ETC hybrid system in solution comprising bacterial cytochrome bc1 and mitochondrial complex IV. EGFR inhibitor We clearly show that non-inhibited cytochrome bc1 generates ROS and that adaptive and pathogenic mitochondrial mutations suppress and enhance ROS production, respectively. We also noted that cytochrome bc1 produces ROS in a rate-dependent manner and that the mechanism of ROS generation changes according to the rate of operation of the enzyme. This dependency has not yet been reported, but seems to be crucial when discussing ROS signaling originating from mitochondria.Inflammatory bowel diseases (IBDs) including colitis are intestinal disorders characterized by chronic inflammation, barrier dysfunction and dysbiosis. Specific forms of vitamin E have been shown to attenuate colitis, but the mechanisms are not fully understood. The objective of this study is to examine the impact of α-tocopherol (αT) and γ-tocopherol-rich tocopherols (γTmT) on gut inflammation, barrier integrity and microbiota in dextran sulfate sodium (DSS)-induced colitis in mice. We observe that αT and γTmT mitigated DSS-caused fecal bleeding, diarrhea and elevation of IL-6. These vitamin E forms inhibited colitis-induced loss of the tight junction protein occludin, and attenuated colitis-caused elevation of LPS-binding protein in the plasma, a surrogate marker of intestinal barrier dysfunction, suggesting protection of gut barrier integrity. Consistently, αT and γT mitigated TNF-α/IFN-γ-induced impairment of trans-epithelial electrical resistance in human intestinal epithelial Caco-2 cell monolayer. Using 16S rRNA gene sequencing of fecal DNA, we observe that DSS reduced gut microbial evenness and separated microbial composition from healthy controls. In colitis-induced mice, γTmT but not αT separated gut microbial composition from controls, and attenuated DSS-caused depletion of Roseburia, which contains butyrate producing bacteria and is decreased in IBD patients. Canonical correspondence analysis also supports that γTmT favorably altered gut microbial community. In contrast, neither αT nor γTmT affected gut microbes in healthy animals. These results provide evidence supporting protective effects of αT and γT on intestinal barrier function and that γTmT caused favorable changes of the gut microbiota in colitis-induced mice.Human gut microbiota consists of various microorganisms whose numbers are similar to those of human cells. Human gut microbes and the brain form bidirectional communications through the brain-gut-axis, and play a central role in normal physiological processes and in pathogenesis of many human diseases. Accumulating evidence has demonstrated the crucial effect of gut microbes in proper brain functions and under disease conditions. Here we first focus on revealing current knowledge of the role of gut microbes in neural development and functions. We then summarize mutual relationships between gut microbes and human diseases, in particular neurodegenerative disorders such as Alzheimer's disease, Parkinson's disease and Multiple sclerosis. Finally, we highlight ongoing studies in exploring gut microbes in treatments of human diseases. Applying gut microbes as a means in treatment of human diseases is becoming a promising research direction, and has a great potential in clinical practice.

To investigate the communities of fecal microbiota and the role of Toll-like receptors in patients with ulcerative colitis in the coastal area of northern China.

Stool samples from 31 patients with ulcerative colitis and 12 healthy individuals were collected. The total bacterial genomic DNA was extracted, and the V3+V4 hypervariable region in the bacterial 16S rRNA gene sequence was amplified by polymerase chain reaction (PCR). High-throughput sequencing analysis was performed on the Illumina Hiseq platform. The expression of TLR2, TLR4, Tollip, PPAR-γ, IL-6, and TNF-α in the colonic mucosa was measured by Western blots.

The diversity of the fecal microbiota in patients with ulcerative colitis was significantly less than that in healthy control individuals (p<0.05). The proportion of Bacteroidetes was significantly reduced (p<0.01), whereas Proteobacteria was prevalent (p<0.01) in patients with ulcerative colitis. At the genus level, the relative abundance of Streptococcus and Anaerostipes was microbiota and correlation with TLRs might play important roles in the pathogenesis and progression of ulcerative colitis.

There were significant changes in the diversity and composition of the fecal microbiota in patients with ulcerative colitis compared to healthy individuals. The dysbiosis of gut microbiota and correlation with TLRs might play important roles in the pathogenesis and progression of ulcerative colitis.The alternative antimicrobial strategies that mitigate the threat of antibiotic resistance is the quorum-sensing inhibition (QSI) mechanism, which targets autoinducer dependent virulence gene expression in bacterial pathogens. N-acyl homoserine lactone (AHL) acts as a key regulator in the production of virulence factors and biofilm formation in Pseudomonas aeruginosa PAO1 and violacein pigment production in Chromobacterium violaceum ATCC 12472. In the present study, the marine sponge Haliclona fibulata symbiont Brevibacterium casei strain Alu 1 showed potential QSI activity in a concentration-dependent manner (0.5-2% v/v) against the N-acyl homoserine lactone (AHL)-mediated violacein production in C. violaceum (75-95%), and biofilm formation (53-96%), protease (27-82%), pyocyanin (82-95%) and pyoverdin (29-38%) productions in P. aeruginosa. Further, the microscopic analyses validated the antibiofilm activity of the cell-free culture supernatant (CFCS) of B. casei against P. aeruginosa. Subsequently, the biofilm and pyoverdin inhibitory efficacy of the ethyl acetate extract of B.