Gadus morhua Eggs Sialoglycoprotein Prevent Estrogen Deficiency-Induced High Bone Turnover by Controlling OPG/RANKL/TRAF6 Pathway and Serum Metabolism.

In recent years, the development of safe and effective anti-osteoporosis factors has attracted extensive attention. In this study, an estrogen-deficient osteoporosis rat model was employed to study the improving mechanism of sialoglycoprotein isolated from Gadus morhua eggs (Gds) against osteoporosis. The results showed that compared with OVX, Gds ameliorated the trabecular microstructure, especially the increased trabecular thickness, decreased trabecular separation, and enhanced the trabecular number. The analysis of qRT-PCR and western blotting found that Gds reduced bone resorption by inhibiting RANKL-induced osteoclastogenesis. The LC-MS/MS was used to investigate serum metabolism, and the enrichment metabolites were analyzed by the KEGG pathway. The results revealed that the Gds significantly altered the fat anabolism pathway, which includes ovarian steroidogenesis pathway and arachidonic acid metabolism pathway. Altogether, Gds could improve osteoporosis by suppressing high bone turnover via controlling OPG/RANKL/TRAF6 pathway, which is implicated with ovarian steroidogenesis pathway and arachidonic acid metabolism pathway. These findings indicated that Gds could be a candidate factor for anti-osteoporosis.

Tilapia head glycolipids protect mice against dextran sulfate sodium-induced colitis by ameliorating the gut barrier and suppressing NF-kappa B signaling pathway.

The purpose of this study was to evaluate the relieving effect of tilapia head glycolipids (TH-GLs) on dextran sulfate sodium (DSS)-induced colitis in mice and to further explore its mechanism. Mice were orally administered 3% (w/v) DSS to establish a model of ulcerative colitis (UC), and subsequently treated with TH-GLs or sulfasalazine. In addition, the expression of key targets in the intestinal mucosal barrier and the inflammatory signal pathway were studied by combining immunochemical analysis techniques. The results showed that varying doses of TH-GLs can significantly improve colon lesions caused by DSS, reduce histological scores, increase mucus secretion, extend colon length, increase weight, and inhibit the occurrence of inflammatory cytokines such as tumor necrosis factor-α (TNF-α), interferon-γ (IFN-γ), Interleukin-1ß (IL-1ß), and Interleukin- 6 (IL-6). Further, studies have shown that TH-GLs increase the secretion of MUC2 and up-regulate the expression of tight junction related proteins, such as ZO-1 and Occludin. In addition, TH-GLs significantly down-regulated the protein expression levels of TNF-α, IKK-ß, and nuclear factor-κB (NF-κB). Here, we have elucidated the potential mechanism of TH-GLs in protecting mice with colitis. In general, this study shows that TH-GLs could improve the symptoms of UC by improving the gut barrier and inhibiting inflammatory signals, which provides a scientific basis for future clinical applications.

Arecanut (Areca catechu L.) Seed Polyphenol-Ameliorated Osteoporosis by Altering Gut Microbiome via LYZ and the Immune System in Estrogen-Deficient Rats.

Polyphenol can improve osteoporosis and is closely associated with gut microbiota, while the mechanism and the relationship among polyphenol, osteoporosis, and gut microbiota colonization remain unclear. Here, an osteoporosis rat model established by ovariectomy was employed to investigate the improving mechanism of arecanut (Areca catechu L.) seed polyphenol (ACP) on osteoporosis by regulating gut microbiota. We analyzed the bone microstructure, Paneth cells, regulating microbial protein (lysozyme (LYZ)), proinflammatory cytokines, macrophage infiltration levels, and gut microbial communities in a rat. ACP improved the trabecular microstructure compared to OVX, including the increased trabecular number (Tb.N) (P < 0.01) and trabecular thickness (Tb.Th) (P < 0.001) and decreased trabecular separation (Tb.Sp) (P < 0.01). At the phylum level, Bacteroidetes was increased after ovariectomy (P < 0.001) and Firmicutes and Proteobacteria were increased in ACP (P < 0.001). Antiosteoporosis groups with lower LYZ and Paneth cells (P < 0.001) showed that the microbiota Alistipes, which have a negative effect on bone metabolism were decreased in ACP (P < 0.001). Altogether, these studies showed that the estrogen deficiency could induce the shedding of Paneth cells, which leads to the decrease of LYZ, while ACP could increase the LYZ expression by maintaining the population of Paneth cells in an estrogen-deficient host, which were implicated in gut microbiota regulation and improved osteoporosis by controlling the inflammatory reaction.

Tilapia nilotica Head Lipids Improved Bone Loss by Regulating Inflammation and Serum Metabolism Through Gut Microbiota in Ovariectomized Rats.

Osteoporosis is a global health problem, and it is of great significance to replace the drugs with natural functional factors. In this study, we investigated the antiosteoporotic activity of lipids prepared from Tilapia nilotica fish head lipids (THLs) in the ovariectomized osteoporosis rats. THLs are composed of neutral lipids (NL, 77.84%), phospholipids (PL, 11.86%), and glycolipids (GL, 6.47%). There were apparent differences in the fatty acid composition of disparate components, and PL contains the most abundant Ω-3 polyunsaturated fatty acids. The results proved that THLs could improve bone microstructure, increase bone mineral density, and decrease bone resorption. To illustrate the antiosteoporotic mechanism, we analyzed the changes in gut microbial communities, proinflammation factors, serum metabolites, and metabolic pathways. Further study on gut microbiota showed that THLs significantly decreased the content of Alistipes in the gut and dramatically increased the beneficial bacteria such as Oscillospira, Roseburia, and Dubosiella. Meanwhile, proinflammation factors of serum in OVX rats decreased significantly, and metabolites were changed. Therefore, we speculated that THLs improved bone loss through reducing inflammation and changing the metabolites and metabolic pathways such as arachidonic acid metabolism and primary bile acid metabolism, etc., by altering gut microbiota. The results indicated that THLs could be a functional factor with antiosteoporotic activity.

Collagen Peptides Isolated from Salmo salar and Tilapia nilotica Skin Accelerate Wound Healing by Altering Cutaneous Microbiome Colonization via Upregulated NOD2 and BD14.

Collagen peptides can promote wound healing and are closely related to microbiome colonization. We investigated the relationship among collagen peptides, wound healing, and wound microflora colonization by administering the murine wound model with Salmo salar skin collagen peptides (Ss-SCPs) and Tilapia nilotica skin collagen peptides (Tn-SCPs). We analyzed the vascular endothelial growth factor (VEGF), fibroblast growth factors (ß-FGF), pattern recognition receptor (NOD2), antimicrobial peptides (ß-defence14, BD14), proinflammatory (TNF-α, IL-6, and IL-8) and anti-inflammatory (IL-10) cytokines, macrophages, neutrophil infiltration levels, and microbial communities in the rat wound. The healing rates of the Ss-SCP- and Tn-SCP-treated groups were significantly accelerated, associated with decreased TNF-α, IL-6, and IL-8 and upregulated BD14, NOD2, IL-10, VEGF, and ß-FGF. Accelerated healing in the collagen peptide group shows that the wound microflora such as Leuconostoc, Enterococcus, and Bacillus have a positive effect on wound healing (P < 0.01). Other microbiome species such as Stenotrophomonas, Bradyrhizobium, Sphingomonas, and Phyllobacterium had a negative influence and decreased colonization (P < 0.01). Altogether, these studies show that collagen peptide could upregulate wound NOD2 and BD14, which were implicated in microflora colonization regulation in the wound tissue and promoted wound healing by controlling the inflammatory reaction and increasing wound angiogenesis and collagen deposition.