Mg-based alloys have great potential for development into fixation implants because of their highly biocompatible and biodegradable metallic properties. In this study, we sought to determine the biocompatibility of Mg60Zn35Ca5 bulk metallic glass composite (BMGC) with fabricated implants in a rabbit tendon–bone interference fixation model. We investigated the cellular cytotoxicity of Mg60Zn35Ca5 BMGC toward rabbit osteoblasts and compared it with conventional titanium alloy (Ti6Al4V) and polylactic acid (PLA). The results show that Mg60Zn35Ca5 BMGC may be classed as slightly toxic on the basis of the standard ISO 10993-5. We further characterized the osteogenic effect of the Mg60Zn35Ca5 BMGC extraction medium on rabbit osteoblasts by quantifying extracellular calcium and mineral deposition, as well as cellular alkaline phosphatase activity. The results of these tests were found to be promising. The chemotactic effect of the Mg60Zn35Ca5 BMGC extraction medium on rabbit osteoblasts was demonstrated through a transwell migration assay. For the in vivo section of this study, a rabbit tendon–bone interference fixation model was established to determine the biocompatibility and osteogenic potential of Mg60Zn35Ca5 BMGC in a created bony tunnel for a period of up to 24 weeks. The results show that Mg60Zn35Ca5 BMGC induced considerable new bone formation at the implant site in comparison with conventional titanium alloy after 24 weeks of implantation. In conclusion, this study revealed that Mg60Zn35Ca5 BMGC demonstrated adequate biocompatibility and exhibited significant osteogenic potential both in vitro and in vivo. These advantages may be clinically beneficial to the development of Mg60Zn35Ca5 BMGC implants for future applications.
Insulin and (-)-epigallocatechin gallate (EGCG) are reported to regulate obesity and fat accumulation, respectively. This study investigated the pathways involved in EGCG modulation of insulin-stimulated glucose uptake in 3T3-L1 and C3H10T1/2 adipocytes. EGCG inhibited insulin stimulation of adipocyte glucose uptake in a dose- and time-dependent manner. The concentration of EGCG that decreased insulin-stimulated glucose uptake by 50-60% was approximately 5-10 µM for a period of 2 h. At 10 µM, EGCG and gallic acid were more effective than (-)-epicatechin, (-)-epigallocatechin, and (-)-epicatechin 3-gallate. We identified the EGCG receptor [also known as the 67-kDa laminin receptor (67LR)] in fat cells and extended the findings for this study to clarify whether EGCG-induced changes in insulin-stimulated glucose uptake in adipocytes could be mediated through the 67LR. Pretreatment of adipocytes with a 67LR antibody, but not normal rabbit immunoglobulin, prevented the effects of EGCG on insulin-increased glucose uptake. This suggests that the 67LR mediates the effect of EGCG on insulin-stimulated glucose uptake in adipocytes. Moreover, pretreatment with an AMP-activated protein kinase (AMPK) inhibitor, such as compound C, but not with a glutathione (GSH) activator, such as N-acetyl-L-cysteine (NAC), blocked the antiinsulin effect of EGCG on adipocyte glucose uptake. These data suggest that EGCG exerts its anti-insulin action on adipocyte glucose uptake via the AMPK, but not the GSH, pathway. The results of this study possibly support that EGCG mediates fat content.
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