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ABSTRACT

Kefir is a fermented product from yeast and lactic acid bacteria, and has been associated with various health benefits including relieving inflammatory bowel disease. Recently, it has been shown that gram-positive bacteria produce extracellular vesicles (EV). The EV could be appearing as potentially important mediators of cell to cell interaction. In this study, we explored the role of kefir grain Lactobacillus-derived EV in modulating inflammation responses via alleviating the production of inflammatory cytokines in tumor necrosis factor-alpha (TNF-alpha)-induced inflammation in Caco-2 cells and the 2,4,6-trinitrobenzene sulfonic acid-induced inflammatory bowel disease mouse model. Kefir-derived Lactobacillus EV were isolated by ultracentrifugation of the culture medium of 3 different kefir-derived strains (i.e., Lactobacillus kefir, Lactobacillus kefiranofaciens, and Lactobacillus kefirgranum). Nanoparticle tracking analysis showed that the size of isolated kefir-derived Lactobacillus EV was within 80 to 400 nm, and kefir-derived Lactobacillus EV uptake into recipient Caco-2 cells was confirmed by fluorescence labeling. Treatment of each kefir-derived Lactobacillus EV onto TNF-alpha-stimulated Caco-2 cells significantly reduced the level of both mRNA expression and secretion of IL-8, and Western blot analysis revealed that such an effect was related to inhibition of TNF-alpha signaling mediated by reducing the phosphorylation of p65, a subunit of NF-kB. Subsequent administration of kefir-derived Lactobacillus EV into inflammatory bowel disease-induced mice significantly alleviated the body weight loss and rectal bleeding, and enhanced stool consistency. Histological examination showed that kefir-derived Lactobacillus EV substantially reduced the infiltration of transmural leukocytes and loss of goblet cells within the colon, and the serum level of myeloperoxidase was significantly lower in the EV-treated group than control group. Our study demonstrates that kefir-derived Lactobacillus EV can be potentially used for developing innovative strategies for alleviating inflammatory bowel disease.

Abstract

Current anticonvulsant therapies are principally aimed at suppressing neuronal hyperexcitability to prevent or control the incidence of seizures. However, the role of oxidative stress processes in seizures led to the proposition that antioxidant compounds may be considered as promising candidates for limiting the progression of epilepsy. Accordingly, the aim of this study is to determine if coenzyme Q10 (CoQ10) and alpha-tocopherol (alpha-Toc) have a neuroprotective effect in rats against the observed oxidative stress and inflammation during seizures induced by pentylenetetrazole (PTZ) in rats, and to study their interactions with the conventional antiseizure drug phenytoin (PHT), either alone or in combination. Overall, the data revealed that alpha-Toc and CoQ10 supplementation can ameliorate PTZ-induced seizures and recommended that nuclear factor erythroid 2–related factor 2 (NRF2) and silencing information regulator 1 (Sirt1) signaling pathways may exemplify strategic molecular targets for seizure therapies. The results of the present study provide novel mechanistic insights regarding the protective effects of antioxidants and suggest an efficient therapeutic strategy to attenuate seizures. Additionally, concurrent supplementation of CoQ10 and alpha-Toc may be more effective than either antioxidant alone in decreasing inflammation and oxidative stress in both cortical and hippocampal tissues. Also, CoQ10 and alpha-Toc effectively reverse the PHT-mediated alterations in the brain antioxidant status when compared to PHT only.

Graphical abstract

A schematic illustration of the role of phenytoin (PHT) and/or antioxidants supplementation like alpha-tocopherol (alpha-Toc) and coenzyme Q10 (CoQ10) in status (SE) epilepticus induced by pentylenetetrazole (PTZ).


Abstract

Aldrin, dieldrin, and DDT are chlorinated insecticides that are unintentionally widespread in the environment. It was previously shown that all of the aforementioned compounds increased secretion of ovarian oxytocin (OT), which is a potent uterotonic agent. However, only DDT and its metabolite (DDE) promoted, while aldrin and dieldrin inhibited basal and OT-stimulated myometrial contractions in cows. Therefore, the aim of this study was to determine the effect of these treatments on the reception and further transmission of the OT-signal for myometrial contractions and on the levels of contractile-associated integral proteins (caveolin; CAV) and gap junction proteins (GAPs). Moreover, their effect on reception of signal for the relaxation of myometrium was also studied. Myometrial strips or cells from non-pregnant (8–12 days of oestrous cycle) or late pregnant (5–8 months) cows were incubated with the studied compounds at environmentally relevant dose (10?ng/ml), which was chosen according to the previous studies. DDT and DDE increased the CAV protein level, while dieldrin decreased the GAPs level. None of the studied compounds affected mRNA expression of the OT receptor and expression of the second messengers (DAG, IP3, PKC, MLCK). Oppositely, DDE and dieldrin decreased mRNA expression of the relaxin (RLX) receptor. Changes in the amount of contractile-associated integral proteins may be involved in the molecular mechanism underlying the adverse effects of the studied insecticides on myometrial motility. Admittedly, none of the studied compounds impaired the reception or further intracellular transmission of the OT signal to promote contractions during the oestrous cycle, while they showed potential to impair the transmission the signal between cells as well as to diminish the effects of one of the primary inhibitor (RLX) of myometrial contractions during gestation.

Abstract

Use of huge amounts of antibiotics in farm animal production has promoted the prevalence of antibiotic-resistant bacteria, which poses a serious threat to public health. Therefore, alternative approaches are needed to reduce or replace antibiotic usage in the food animal industry. PR-39 is a pig-derived proline-rich antimicrobial peptide that has a broad spectrum of antibacterial activity and a low propensity for development of resistance by microorganisms. To test whether ubiquitous expression of PR-39 in transgenic (TG) mice can increase resistance against bacterial infection, we generated TG mice that ubiquitously express a pig-derived antimicrobial peptide PR-39 and analyzed their growth and resistance to infection of the highly pathogenic Actinobacillus pleuropneumoniae (APP) isolated from swine. The growth performance was significantly increased in TG mice compared with their wild-type (WT) littermates. After the APP challenge, TG mice exhibited a significantly higher survival rate and significantly lower tissue bacterial load than WT littermates. Furthermore, the tissue lesion severity that resulted from APP infection was milder in TG mice than that in their WT littermates. This study provides a good foundation for the development of PR-39-expressing TG animals, which could reduce the use of antibiotics in the farm animal industry.

Keywords

Antimicrobial peptides PR-39 Transgenic animals Actinobacillus pleuropneumoniae infection Growth

Abstract

Background

Angiopoietin-like protein 8(ANGPTL8) and apolipoprotein CIII (apoCIII) were found to inhibit the activity of lipoprotein lipase (LPL) and disrupt the clearance of triglyceride-rich lipoproteins (TRLs), leading to hypertriglyceridemia. Whether any relationship exists between these two important modulators of triglyceride metabolism has not been reported. Besides, whether ANGPTL8 concentration is altered in the patients with coronary artery disease (CAD) is still unclear.

Methods

A hospital-based case-control study was conducted. Sixty-eight CAD subjects and fifty-two nonCAD controls were recruited. Plasma apoCIII, ANGPTL8 was measured.

Results

ANGPTL8 and apoCIII concentration exhibited no significant difference between CAD group and nonCAD group. Both ANGPTL8 and apoCIII were significantly correlated with triglyceride level(r = − 0.243, P = 0.008; r = 0.335, P < 0.001, respectively). Regression analysis revealed that apoCIII was an independent contributor to triglyceride level independent of ANGPTL8 concentration (standardized beta= 0.230, P < 0.01).

Conclusion

ApoCIII may mediate the effects of ANGPTL8 on triglyceride metabolism.

Keywords

ANGPTL8 apoCIII Triglyceride Coronary artery disease

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