丁酸盐刺激组蛋白H3乙酰化作用,8-Isoprostane生产,RANKL的表达,调节Osteoprotegerin表达式/ mg - 63细胞成骨细胞的分泌。

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Chang MC,陈YJ,连YC, Chang,黄CC,黄西城,潘YH,刘正JH

丁酸盐刺激组蛋白H3乙酰化作用,8-Isoprostane生产,RANKL的表达,调节Osteoprotegerin表达式/ mg - 63细胞成骨细胞的分泌。

Int J摩尔Sci。2018年12月17日,19 (12)。pii: ijms19124071。doi: 10.3390 / ijms19124071。

PubMed ID

30562925 (在PubMed

]

文摘

丁酸作为组蛋白脱乙酰酶(HDAC抑制剂)是由牙周和根管微生物(如Porphyromonas、梭菌属等)。丁酸可能影响牙周/根尖周的细胞的生物活性如成骨细胞、牙周韧带细胞等,从而影响牙周/根尖周的组织破坏和愈合。本研究的目的是研究丁酸盐的毒性作用矩阵和mg - 63年矿化标志表达成骨细胞。细胞生存能力是由3 - 4,5-dimethylthiazol-2-yl) 2, 5-diphenyl溴化四唑试验(MTT)。细胞凋亡和坏死是由碘化propidium /膜联蛋白V流式细胞术分析。的蛋白质和mRNA表达osteoprotegerin(功能)和核因子kappa-B配体受体激活剂(RANKL)被免疫印迹分析和反向transcriptase-polymerase连锁反应(rt - pcr)。功能、可溶性RANKL (sRANKL)、8-isoprostane pro-collagen我,矩阵metalloproteinase-2 (MMP-2),骨粘连蛋白(SPARC)、骨钙素和骨桥蛋白(OPN)分泌到培养基被酶联immunosorbant试验测量。碱性磷酸酶(ALP)活性被高山染色检查。组蛋白H3乙酰化水平评估immunofluorescent染色(如果)和免疫印迹。我们发现丁酸激活mg - 63细胞的组蛋白H3乙酰化作用。 Exposure of MG-63 cells to butyrate partly decreased cell viability with no marked increase in apoptosis and necrosis. Twenty-four hours of exposure to butyrate stimulated RANKL protein expression, whereas it inhibited OPG protein expression. Butyrate also inhibited the secretion of OPG in MG-63 cells, whereas the sRANKL level was below the detection limit. However, 3 days of exposure to butyrate (1 to 8 mM) or other HDAC inhibitors such as phenylbutyrate, valproic acid and trichostatin stimulated OPG secretion. Butyrate stimulated 8-isoprostane, MMP-2 and OPN secretion, but not procollagen I, or osteocalcin in MG-63 cells. Exposure to butyrate (2(-)4 mM) for 3 days markedly stimulated osteonectin secretion and ALP activity. In conclusion, higher concentrations of butyric acid generated by periodontal and root canal microorganisms may potentially induce bone destruction and impair bone repair by the alteration of OPG/RANKL expression/secretion, 8-isoprostane, MMP-2 and OPN secretion, and affect cell viability. However, lower concentrations of butyrate (1(-)4 mM) may stimulate ALP, osteonectin and OPG. These effects are possibly related to increased histone acetylation. These events are important in the pathogenesis and repair of periodontal and periapical destruction.

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药物靶点

药物	目标	类	生物	药理作用	行动
Phenylbutyric酸	组蛋白脱乙酰酶(蛋白质组)	蛋白质组	人类	未知的	抑制剂	细节
丙戊酸	组蛋白脱乙酰酶(蛋白质组)	蛋白质组	人类	未知的	抑制剂	细节