Methylglyoxal (MG) is a reactive dicarbonyl compound produced by glycolytic processing, which has been identified as a precursor of advanced glycation end products. Elevated MG levels in patients with diabetes are believed to contribute to diabetic complications, including bone defects. The objective of this study was to evaluate the effect of MG on RANKL-induced osteoclast differentiation in RAW264.7 cells, a murine macrophage cell line. RAW264.7 cells were cultured in medium containing 50 ng/mL RANKL and different concentrations of MG. Tartrate-resistant acid phosphatase (TRAP) activity and osteoclast bone resorbing activity were assessed and changes in intracellular calcium concentration, mitochondrial mass, mitochondrial membrane potential, and glyoxalase I level were examined. In addition, real-time RT-PCR assay was used to analyse osteoclast-associated genes. MG markedly inhibited RANKL-induced TRAP activity. MG treatment resulted in a significant decrease in intracellular calcium concentration, mitochondrial mass, mitochondrial membrane potential, and glyoxalase I level during osteoclastogenesis. In addition, MG increased the formation of mitochondrial superoxide. Quantitative reverse transcriptase-polymerase chain reaction revealed increased expression of the TRAF6, GAB2, ERK1, c-Fos, NFATc1, CLCN7, and OSTM1 genes, decreased expression of TCIRG and carbonic anhydrase II, and unchanged expression of cathepsin K and MMP-9 upon MG treatment. MG had no effect on the bone resorbing activity of osteoclasts. Our findings indicate that MG inhibits TRAP and glyoxalase I activity and impairs mitochondrial function in osteoclasts. Further validation of the underlying pathway is necessary.

甲基乙二醛（MG）是一种通过糖酵解工艺生产的反应性二羰基化合物，已被确定为高级糖基化终产物的前体。糖尿病患者的MG水平升高被认为会导致糖尿病并发症，包括骨缺损。这项研究的目的是评估MG对RANKL诱导的小鼠巨噬细胞系RAW264.7细胞中破骨细胞分化的影响。RAW264.7细胞在含有50 ng / mL RANKL和不同浓度MG的培养基中培养。评估了抗酒石酸酸性磷酸酶（TRAP）的活性和破骨细胞的骨吸收活性，并检测了细胞内钙浓度，线粒体质量，线粒体膜电位和乙二醛酶I水平的变化。此外，实时RT-PCR测定法用于分析破骨细胞相关基因。MG明显抑制RANKL诱导的TRAP活性。MG治疗导致破骨细胞生成过程中细胞内钙浓度，线粒体质量，线粒体膜电位和乙二醛酶I水平显着降低。另外，MG增加了线粒体超氧化物的形成。定量逆转录聚合酶链反应显示TRAF6，GAB2，ERK1，c-Fos，NFATc1，CLCN7和OSTM1基因的表达增加，TCIRG和碳酸酐酶II的表达减少，组织蛋白酶K和MMP-9的表达不变。 MG治疗。MG对破骨细胞的骨吸收活性没有影响。我们的发现表明，MG抑制破骨细胞的TRAP和乙二醛酶I活性并损害线粒体功能。