Chronic administration of lipopolysaccharide and proteases induces periodontal inflammation and hepatic steatosis in rats
Chronic administration of lipopolysaccharide and proteases induces periodontal inflammation and hepatic steatosis in rats
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DOI：
10.1902/jop.2007.070056
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发表时间：
2007-10-01
影响因子：
4.3
通讯作者：
Takata, Takashi
中科院分区：
文献类型：
--
作者：
Tomofuji, Takaaki;Ekuni, Daisuke;Takata, Takashi
背景：流行病学研究表明牙周炎与肝病之间存在一定的关系。方法：14只雄性Wistar大鼠(8周龄)随机分为两组：牙周炎组用大肠杆菌脂多糖和灰色链霉菌蛋白酶进行牙周炎治疗8周，对照组用无热原水治疗。结果：慢性给予牙周组织和蛋白水解酶可引起牙周炎和肝脏损伤，表现为脂肪变性伴炎症和肝窦纤维化。牙周炎组大鼠牙周组织细胞凋亡，8-羟基脱氧鸟苷浓度升高，肝脏肿瘤坏死因子-α活性升高，牙周炎症、血清脂多糖和活性氧水平升高。结论：牙周炎大鼠模型通过血清脂多糖升高而诱发脂肪肝。
Background: Epidemiologic studies suggest a relationship between periodontitis and liver diseases. A rat periodontitis model was used to investigate whether a causal relationship exists between periodontitis and liver diseases.Methods: Fourteen male Wistar rats (8 weeks old) were divided into two groups: a periodontitis group in which Escherichia coli lipopolysaccharide (LPS) and Streptomyces griseus proteases were applied into the gingival sulcus for 8 weeks, and a control group using pyrogen-free water instead. After blood samples were collected, periodontal tissues and liver specimens were analyzed.Results: Chronic administration of LPS and proteases to the gingival sulcus induced periodontitis and liver injury, including steatosis with inflammation and sinusoidal fibrosis. Apoptosis, enhanced concentration of 8-hydroxydeoxyguanosine, and activated production of tumor necrosis factor-alpha in liver were observed in the periodontitis group, with increased gingival inflammation, serum LPS, and reactive oxygen species.Conclusion: Periodontal inflammation in a rat model induced fatty liver disease through increased serum LPS.