Abstract Vitamin D is necessary for maintaining the bone function, and its deficiency is linked with the development of obesity. Moreover, bone health is correlated with obesity through many mechanisms by modulating bone marrow mesenchymal stem cells to differentiate as adipose cells, inflammatory response, glucose metabolism, oxidative homeostasis, energy metabolism and gut microbiota. Based on previous studies, vitamin D, obesity, and bone health are linked with each other at multiple levels. However, our knowledge of the associations of vitamin D with coexisting abnormalities, such as bone health-related issues and obesity, is still in its infancy. The complex relationships still need to be investigated and elucidated further. Therefore, in this review, the relationships between vitamin D, obesity and bone health have been discussed. This review identified that evidence proving the capacity to reduce or prevent obesity-related disorders by targeting vitamin D intakes is mainly unknown. However, the inverse relationships of vitamin D levels with obesity and bone health-related issues are apparent.

This research aimed to explore the molecular mechanism of microRNA (miR)-106b in cell apoptosis of atherosclerosis (AS). Human aortic endothelial cells (HAECs) were divided into control group, oxidized-low-density lipoproteins (ox-LDL) group, miR-106b NC+ox-LDL group, miR-106b mimics+ox-LDL group, miR-106b mimics+PTEN+ox-LDL group, and miR-106b mimics+empty+ox-LDL group. Real-time fluorescence quantitative polymerase chain reaction, cholecystokinin, TdT-mediated biotinylated nick end-labeling assay, luciferase reporter gene assay, and flow cytometry analysis were performed to determine the morphology, proliferation, and apoptosis in HSECs. Moreover, the levels of phosphatase and tensin homolog deleted on chromosome 10 (PTEN), Bcl-2, p-P13K, and p-AKT in HAECs were detected by western blot. MiR-106b was down-regulated in ox-LDL-induced HAECs. PTEN was the target gene of miR-106b-5p. Overexpression of PTEN inhibited the anti-apoptotic effect of miR-106b. Compared with the control group, the proportion and number of HAECs apoptosis and Bax, caspase-3, and caspase-9 expression in ox-LDL and miR-106b mimics+PTEN+ox-LDL groups were significantly increased (all P<0.05). Moreover, the activity of HAECs and Bcl-2 were decreased significantly (all P<0.05). Overexpression of miR-106b in ox-LDL-induced AS inhibited endothelial cell apoptosis. Furthermore, miR-106b might activate the PI3K/AKT pathway by down-regulating the expression of PTEN in ox-LDL-induced HAECs.

Abstract Purpose Changrui enema, a traditional Chinese medicine prescription, is used as a supplementary treatment for acute radiation proctitis (ARP). Herein we explored the inhibition effects of Changrui enema on NF-κB and VEGF in ARP mice. Methods A total of 120 C57BL/6 mice were divided randomly into normal mice group, ARP mice group, western medicine enema group (dexamethasone combined with gentamicin), and Changrui enema group. ARP mice were established by pelvic local irradiation. The expression of IL-1β, NF-κB, VEGF, AQP1, AQP3, p-ERK1/2 and p-JNK was determined by immunohistochemistry or western blot. Results The study firstly found that Changrui enema alleviated ARP mice. The expression of IL-1β, NF-κB, VEGF, AQP1 and p-ERK1/2 was increased in ARP mice, and was reserved by Changrui enema. However, the expression of AQP3 and p-JNK was decreased in ARP mice, and was up-regulated by Changrui enema. Conclusions Changrui enema is an effective treatment with fewer side effects for ARP. The mechanism of Changrui enema may be related to the inhibition of inflammation-induced angiogenesis. Changrui enema inhibits IL-1β and NF-κB expression as well as VEGF expression. Interestingly, AQP1 promotes angiogenesis, while AQP3 inhibits inflammation. Changrui enema probably inhibits AQP1 expression by down-regulating p-ERK1/2, and improves AQP3 expression by up-regulating p-JNK.

Abstract Pre-harvest sprouting (PHS) is a major abiotic factor affecting grain weight and quality, and is caused by an early break in seed dormancy. Association mapping (AM) is used to detect correlations between phenotypes and genotypes based on linkage disequilibrium (LD) in wheat breeding programs. We evaluated seed dormancy in 80 Chinese wheat founder parents in five environments and performed a genome-wide association study using 6,057 markers, including 93 simple sequence repeat (SSR), 1,472 diversity array technology (DArT), and 4,492 single nucleotide polymorphism (SNP) markers. The general linear model (GLM) and the mixed linear model (MLM) were used in this study, and two significant markers (tPt-7980 and wPt-6457) were identified. Both markers were located on Chromosome 1B, with wPt-6457 having been identified in a previously reported chromosomal position. The significantly associated loci contain essential information for cloning genes related to resistance to PHS and can be used in wheat breeding programs.