Intermittent local periodontal inflammation causes endothelial dysfunction of the systemic artery via increased levels of hydrogen peroxide concomitantly with overexpression of superoxide dismutase.
Intermittent local periodontal inflammation causes endothelial dysfunction of the systemic artery via increased levels of hydrogen peroxide concomitantly with overexpression of superoxide dismutase.
复制标题
间歇性局部牙周炎症通过过氧化氢水平升高以及超氧化物歧化酶过度表达导致全身动脉内皮功能障碍。
DOI：
10.1016/j.ijcard.2016.08.099
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发表时间：
2016
期刊：
影响因子：
--
通讯作者：
Kinoshita H.
中科院分区：
文献类型：
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作者：
Yamamoto Y;Saito T;Feng GG;Li J;Yasuda Y;Kazaoka Y;Fujiwara Y;Kinoshita H.
背景本研究旨在探讨间歇性局部牙周炎是否会引起氧化应激引起的体动脉内皮功能障碍，以及过氧化氢水平的升高与超氧化物歧化酶（SOD）和NADPH氧化酶的过度表达是否参与了氧化应激。实验组于8 ~ 11周龄时，每隔一周于双侧下颌牙龈注射LPS 1500 μg。离体下颌骨或牙周组织进行评估的组织病理学变化，等长力记录，活性氧使用2′，7 ′-二氯荧光素二乙酸酯（10 - 5 mol/L）和NADPH氧化酶亚基和SOD的蛋白表达，分别。乙酰胆碱（10 - 9 ~ 10 - 5 mol/L）诱导的舒张作用仅在LPS组的大鼠腹主动脉中减弱。Gp 91 ds-tat和PEG-过氧化氢酶恢复LPS组受损的动脉扩张。LPS组大鼠肺组织中活性氧水平升高，而gp 91-ds-tat或PEG-过氧化氢酶处理则抑制了活性氧水平的升高。NADPH氧化酶亚基p47 phox和CuZn-SOD的表达增加在LPS group.ConclusionsThe间歇性局部牙周炎症诱导系统性内皮功能障碍引起的过度生产的活性氧在大鼠的体动脉和过度表达的CuZn-SOD以及NADPH氧化酶胞浆亚基有助于增加过氧化氢水平在血管中的动物模型。
BackgroundThe present study was designed to examine whether the intermittent local periodontal inflammation induces endothelial dysfunction of the systemic artery caused by oxidative stress and if increased levels of hydrogen peroxide coexisted with overexpression of superoxide dismutase (SOD) as well as NADPH oxidase contribute to the oxidative stress.MethodsThe rats in lipopolysaccharides (LPS) group received 1500 μg LPS injection to bilateral gingiva of the lower jaw a week interval from eight- to eleven-week-old. Isolated mandibles or aortas were subjected to the evaluation of histopathological changes, isometric force recordings, reactive oxygen species using 2′,7′-dichlorofluorescin diacetate (10− 5mol/L) and protein expression of NADPH oxidase subunits and SOD, respectively.ResultsMandible sections demonstrated the periodontal inflammation only in the LPS group at three days, but not seven days, after the LSP injection. Acetylcholine (10− 9to 10− 5mol/L)-induced relaxation was reduced only in aortas from the LPS group. Gp91ds-tat and PEG-catalase restored the impaired dilation in arteries from the LPS group. Levels of reactive oxygen species were enhanced in aortas from the LPS group, whereas the increment was abolished by the treatment with gp91-ds-tat or PEG-catalase. Expression of a NADPH oxidase subunit p47phox and CuZn-SOD increased in the LPS group.ConclusionsThe intermittent local periodontal inflammation induces systemic endothelial dysfunction caused by overproduction of reactive oxygen species in the systemic artery of rats and that overexpression of CuZn-SOD as well as a NADPH oxidase cytosolic subunit contributes to increased levels of hydrogen peroxide in blood vessels of this animal model.