The hedgehog (HH) signaling pathway is central to the regulation of bone development and homeostasis. HH signaling is not only involved in osteoblast differentiation from bone marrow mesenchymal stem cells (BM-MSCs), but also acts upstream within osteoblasts via the OPG/RANK/RANKL axis to control the expression of RANKL. HH signaling has been found to up-regulate parathyroid hormone related protein (PTHrP) expression in osteoblasts, which in turn activates its downstream targets nuclear factor of activated T cells (NFAT) and cAMP responsive element binding protein (CREB), and as a result CREB and NFAT cooperatively increase RANKL expression and osteoclastogenesis. Osteoblasts must remain in balance with osteoclasts in order to avoid excessive bone formation or resorption, thereby maintaining bone homeostasis. This review systemically summarizes the mechanisms whereby HH signaling induces osteoblast development and controls RANKL expression through PTHrP in osteoblasts. Proper targeting of HH signaling may offer a therapeutic option for treating bone homeostasis disorders.

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Problem The Staphylococcus aureus has been found to be associated with clinical endometritis of cow. The result of oral antibiotic remains poor. Therefore, this study investigates the role of nisin in endometritis. Method of study The effect of nisin on the growth and cell wall of S aureus were determined in vitro. Besides the blank control group, animals with established post‐partum were inoculated with 0.1 mL S aureus intravaginally. Two days post‐inoculation, the animals were administered nisin (25 mg/kg), kanamycin (30 mg/kg), and water (model group) for 7 days. On the seventh day, serum and uterine organs were obtained for pro‐ and anti‐inflammatory analysis. The uterine tissue samples were weighed, and histopathological analysis was performed. Results The results showed that nisin had an inhibitory effect on the growth and cell wall formation of S aureus. Nisin and kanamycin treatment prevented a S aureus‐induced decrease in pro‐inflammatory cytokines and promoted an increase in the level of serum anti‐inflammatory cytokines in the endometrium of these animals. Nisin and kanamycin, significantly decreased (P < 0.05) the endometritis‐induced increases in uterine weight, restored endometrial architecture and significantly (P < 0.05) normalized uterine neutrophils to control levels. Additionally, improved levels of B7‐2, IFN‐γ, IL‐2, and IL‐8 were observed when treated with nisin. Conclusion Our findings suggest that nisin compared favorably with kanamycin in endometritis prevention, suggesting that nisin can be used in S aureus‐induced endometritis by protecting the uterus from S aureus infection.

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Background The effects of Arula-7 powder (ASP) on diarrhea and intestinal barrier function associated with its regulation of intestinal microflora in calves infected with pathogenic Escherichia coli O1 (E. coli O1) were studied. Method Twenty Holstein calves were randomly divided into four treatment groups: normal control (NC), model control (MC), 0.5 mg/kg ciprofloxacin (CIP) and 2.50 g/kg ASP groups. Results ASP inhibited the relative abundance of Proteobacteria, Selenomonadales, and Enterobacteriales, and increased the relative abundance of Lactobacillus, Faecalibacterium, and Alloprevotella. Moreover, we demonstrated for the first time that the ASP and CIP promoted weight gain, reduced the diarrhea rate (P < 0.05), and enhanced antioxidant capacity (P < 0.05) due to the increase in average daily gain (ADG), total protein (TP), and albumin (ALB). In addition, ASP and CIP increased the expression of Zunola occludens-1 (ZO-1), Occludin, and Claudin-1 in the ileum (P < 0.05), and improved immunity due to increase levels of interleukin-2 (IL-2), interleukin-4 (IL-4), interferon-γ (IFN-γ), immunoglobulin A (IgA), and immunoglobulin G (IgG) in the serum, strengthened CD4+T levels in the ileal mucosa and reducing CD8+T and CD11c+T (P < 0.05). Conclusion Hence, The intestinal microbiota environment formed by early intervention of ASP powder has a protective effect on the intestinal mucosal function of calves infected with pathogenic E. coli.