Oral malodorous compound activates mitochondrial pathway inducing apoptosis in human gingival fibroblasts
Oral malodorous compound activates mitochondrial pathway inducing apoptosis in human gingival fibroblasts
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DOI：
10.1007/s00784-009-0301-5
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发表时间：
2010-08-01
影响因子：
3.4
通讯作者：
Izumi, Yuichi
中科院分区：
文献类型：
--
作者：
Fujimura, Maiko;Calenic, Bogdan;Izumi, Yuichi
硫化氢（H2S）是引起生理性口臭的主要原因。H2S可诱导牙龈细胞凋亡，这可能在牙周病理学中起重要作用。近年来，有研究表明硫化氢可通过增加活性氧水平诱导牙龈成纤维细胞（HGF）凋亡和DNA损伤。然而，H2S诱导的细胞凋亡的机制尚未阐明。本研究的目的是确定H2S在HGF中激活的凋亡途径。HGF暴露于50 ng/mL H2S，导致培养基中的浓度为18 ng/mL，低于牙周袋中的浓度。培养24和48 h后凋亡细胞数显著高于对照组（p < 0.05）。线粒体膜去极化和细胞色素c、caspase-3和caspase-9的释放在孵育24和48 h后也显著增加（p < 0.05），而caspase-8（受体配体介导的导致凋亡的途径中的关键酶）未被激活。目前的研究表明，H2S触发线粒体途径导致细胞凋亡的HGF，但没有激活受体配体介导的途径。
Hydrogen sulfide (H2S) is a main cause of physiologic halitosis. H2S induces apoptosis in human gingival cells, which may play an important role in periodontal pathology. Recently, it has been reported that H2S induced apoptosis and DNA damage in human gingival fibroblasts (HGFs) by increasing the levels of reactive oxygen species. However, the mechanisms of H2S-induced apoptosis have not been clarified in HGFs. The objective of this study was to determine the apoptotic pathway activated by H2S in HGFs. The HGFs were exposed to 50 ng/mL H2S, resulting in 18 ng/mL in the culture medium, which is lower than the concentration in periodontal pockets. The number of apoptotic cells after 24 and 48 h incubation was significantly higher than that in the control cultures (p < 0.05). Mitochondrial membrane depolarization and the release of cytochrome c, and caspase-3, and caspase-9 were also significantly increased after both 24- and 48-h incubation (p < 0.05), whereas caspase-8, a key enzyme in the receptor ligand-mediated pathway causing apoptosis, was not activated. The present study shows that H2S triggered the mitochondrial pathway causing apoptosis in HGFs but did not activate the receptor ligand-mediated pathway.