An effective universal protocol for the extraction of fructooligosaccharide from the different agricultural byproducts.

Alternative bio-refinery technologies are required to promote the commercial utilization of plant biomass components. The fructooligosaccharide (FOS) obtained after hydrolysis of the hemicellulose fractions was mainly applied in the pharmaceutical and food industries. Agricultural bi-product is a rich constituent in dietary fibres, which have prebiotic effects on the intestinal microbiota and the host. Herein we explored the impact of FOS on microbiota modulation and the gut homeostasis effect. High fructooligosaccharide recovery was obtained using alkaline extraction techniques. The enzymatic method produced fructooligosaccharides with minor contamination from fructan and glucan components, although it had a low yield. But combining the alkaline and enzymatic process provides a higher yield ratio and purity of fructooligosaccharides. The structure of the fructooligosaccharide was confirmed, according to FTIR, 13C NMR, 1H NMR and 2D-NMR data. Our results could be applied to the development of efficient extraction of valuable products from agricultural materials using enzyme-mediated methods, which were found to be a cost-effective way to boost bio-refining value. Fructooligosaccharides with varying yields, purity, and structure can be obtained.

Dracocephalum moldavica Ethanol Extract Suppresses LPS-Induced Inflammatory Responses through Inhibition of the JNK/ERK/NF-κB Signaling Pathway and IL-6 Production in RAW 264.7 Macrophages and in Endotoxic-Treated Mice.

The excessive synthesis of interleukin-6 (IL-6) is related to cytokine storm in COVID-19 patients. Moreover, blocking IL-6 has been suggested as a treatment strategy for inflammatory diseases such as sepsis. Sepsis is a severe systemic inflammatory response syndrome with high mortality. In the present study, we investigated the anti-inflammatory and anti-septic effects and the underlying mechanisms of Dracocephalum moldavica ethanol extract (DMEE) on lipopolysaccharide (LPS)-induced inflammatory stimulation in RAW 264.7 macrophages along with septic mouse models. We found that DMEE suppressed the release of inflammatory mediators NO and PGE2 and inhibited both the mRNA and protein expression levels of iNOS and COX-2, respectively. In addition, DMEE reduced the release of proinflammatory cytokines, mainly IL-6 and IL-1ß, in RAW 264.7 cells by inhibiting the phosphorylation of JNK, ERK and p65. Furthermore, treatment with DMEE increased the survival rate and decreased the level of IL-6 in plasma in LPS-induced septic shock mice. Our findings suggest that DMEE elicits an anti-inflammatory effect in LPS-stimulated RAW 264.7 macrophages and an anti-septic effect on septic mouse model through the inhibition of the ERK/JNK/NF-κB signaling cascades and production of IL-6.

Mentha arvensis Essential Oil Exerts Anti-Inflammatory in LPS-Stimulated Inflammatory Responses via Inhibition of ERK/NF-κB Signaling Pathway and Anti-Atopic Dermatitis-like Effects in 2,4-Dinitrochlorobezene-Induced BALB/c Mice.

The mechanism of atopic dermatitis (AD) is modulated by the release of cytokines and chemokines through the mitogen-activated protein kinase (MAPK)/nuclear factor-kappa B (NF-κB) signaling pathway. Topical steroids are used to treat AD, but some people need safer anti-inflammatory drugs to avoid side effects. Mentha arvensis has been used as a herbal plant with medicinal properties, but its anti-inflammatory effects have not been elucidated in an AD model. In this study, we investigated the anti-inflammatory effects of M. arvensis essential oil (MAEO) and its underlying molecular mechanism in lipopolysaccharide (LPS)-stimulated RAW 264.7 macrophages and HaCaT cells (human epidermal keratinocyte). Additionally, we examined the ameliorating effects of the MAEO in a dinitrochlorobenzene (DNCB)-induced murine model of AD. We found, in both RAW 264.7 cells and HaCaT cells, MAEO inhibited LPS-stimulated inflammatory mediators such as nitric oxide (NO) and prostaglandin E2 and proinflammatory cytokines, including IL-1ß and IL-6, due to the suppression of COX-2 and iNOS expression. In LPS-stimulated macrophages, we also observed that MAEO inhibited the phosphorylation of ERK and P65. Furthermore, MAEO treatment attenuated AD symptoms, including the dermatitis score, ear thickness, epidermal thickness and infiltration of mast cells, in a DNCB-induced animal model of AD. Overall, our findings suggest that MAEO exerts anti-inflammatory and anti-atopic dermatitis effects via inhibition of the ERK/NF-κB signaling pathway.

Transcriptional regulation of NF-kappaB by ring type decoy oligodeoxynucleotide in an animal model of nephropathy.

Inflammation of the tubulointerstitial compartment, leading to fibrosis, is a major factor in the progressive loss of renal function in a wide variety of kidney diseases. In order to develop a therapeutic approach for nephropathy, we examined the simultaneous inhibition of transcription factor nuclear factor-kappaB (NF-kappaB), which is responsible for a wide range of cellular processes, especially inflammation, in a mouse model of unilateral ureteral obstruction. In this study, we employed a ring-type NF-kappaB (R-NF-kappaB) decoy oligodeoxynucleotide (ODN), containing consensus promoter sequences of NF-kappaB. This R-NF-kappaB decoy ODN is more highly resistant to degradation by nucleases than is the current phosphothiolated double stranded NF-kappaB decoy ODN. The inhibitory effect of R-NF-kappaB decoy ODN on nephropathy was confirmed by molecular and histological examinations. In addition, treatment with R-NF-kappaB decoy ODN reduced the activities of inflammatory cytokines, such as tumor necrosis factor-alpha and interleukin-1beta. Interestingly, the treatment with R-NF-kappaB decoy ODN also suppressed the gene expression of transforming growth factor-beta1 and fibronectin, resulting in the inhibition of fibrotic changes. These results suggest that the inhibition of NF-kappaB using R-NF-kappaB decoy ODN has potential therapeutic application in the prevention of renal fibrosis.