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Tingting Jia, Ya-nan Wang, Dongjiao Zhang and Xin Xu

Diabetes-induced advanced glycation end products (AGEs) overproduction would result in compromised osseointegration of titanium implant and high rate of implantation failure. 1α,25-dihydroxyvitamin D3 (1,25VD3) plays a vital role in osteogenesis, whereas its effects on the osseointegration and the underlying mechanism are unclear. The purpose of this study was to investigate that 1,25VD3 might promote the defensive ability of osseointegration through suppressing AGEs/RAGE in type 2 diabetes mellitus. In animal study, streptozotocin-induced diabetic rats accepted implant surgery, with or without 1,25VD3 intervention for 12 weeks. After killing, the serum AGEs level, bone microarchitecture and biomechanical index of rats were measured systematically. In vitro study, osteoblasts differentiation capacity was analyzed by alizarin red staining, alkaline phosphatase assay and Western blotting, after treatment with BSA, AGEs, AGEs with RAGE inhibitor and AGEs with 1,25VD3. And the expression of RAGE protein was detected to explore the mechanism. Results showed that 1,25VD3 could reverse the impaired osseointegration and mechanical strength, which possibly resulted from the increased AGEs. Moreover, 1,25VD3 could ameliorate AGEs-induced damage of cell osteogenic differentiation, as well as downregulating the RAGE expression. These data may provide a theoretical basis that 1,25VD3 could work as an adjuvant treatment against poor osseointegration in patients with type 2 diabetes mellitus.

Open access

Xuan Luo, Tingting Zheng, Chaoming Mao, Xin Dong, Xiao Mou, Chengcheng Xu, Qingyan Lu, Baocui Liu, Shengjun Wang and Yichuan Xiao

Myeloid-related protein 14 (MRP14) is responsible for inflammatory reactions. However, the correlation between MRP14 and Hashimoto’s thyroiditis (HT) is still not clear. In this study, we examined the status of MRP14 in thyroid tissues and sera of HT patients and explored the mechanism of IL-1β-mediated regulation of MRP14 expression, as well as the effects of MRP14 on pro-inflammatory chemokine secretion in thyroid follicular cells (TFCs), to elucidate the role of MRP14 in HT development. Our results showed dramatically increased MRP14 expression in thyroid tissues and sera from HT patients. In addition, IL-1β significantly promoted the expression of MRP14 in TFCs, which was mediated by activation of the MAPK/NF-κB signalling pathway. More importantly, IL-1β induced the secretion of the chemokines GRO-2, CXCL9 and CCL22, which was dependent on the regulation of MRP14 in TFCs. Therefore, these findings suggested that under pro-inflammatory conditions, TFCs secreted chemokines with the help of MRP14 regulation, which might suggest a potential pathological mechanism of lymphocyte infiltration into the thyroid gland in HT.