研究氧化应激(Oxidative stress, OS)在根尖周炎(apical periodontitis, AP)所致肝炎症中的作用。同时还研究了高脂血症下AP对根尖周、全身和肝脏的反应。16只雄性Sprague-Dawley大鼠分别饲喂高脂饮食(HD)和正常饮食(ND)。9周后，8只HD大鼠和8只ND大鼠的右上颌和下颌第一磨牙暴露，诱导AP (ND，ND+AP，HD和HD+AP组)。5周后，大鼠被安乐死，从心脏直接采集血液组织，测量炎症细胞因子的血清水平。利用苏木精伊红染色和马脱氧腺苷特异性碱性磷酸酶（Masson staining）对肝脏组织进行分析，并进行逆转录-聚合酶链反应（RT-PCR）以检测炎症细胞因子的mRNA表达。采用酶联免疫吸附试验（ELISA）测量血清、根尖周和肝脏氧化应激参数，包括总氧化状态（total oxidant status，TOS）、总抗氧化能力（total antioxidant capacity，TAOC）和氧化应激指数（oxidative stress index，OSI）。采用学生t检验对根尖周数据进行分析。采用一元方差分析和Kruskal-Wallis检验对其他数据进行分析。HD+AP组的上颌AP病变范围比ND+AP组大（P<0.05）。与ND组相比，ND+AP组显示出更高的血清白细胞介素（IL）-18、IL-1β、TOS、OSI水平，更低的血清TAOC水平，更高的肝脏肿瘤坏死因子（TNF）-α mRNA表达水平，和更高的肝脏TOS、OSI水平（P<0.05）。与HD组相比，HD+AP组血清IL-4水平更低、血清IL-1β水平更高、肝脏IL-6和转化生长因子（transforming growth factor，TGF）-β1 mRNA表达更高（P<0.05）。AP可通过促进血清IL-18、1L-1β、TOS、OSI表达而激活全身和肝脏炎症，增强肝脏TOS、OSI表达，并抑制血清TAOC表达。高脂血症下的AP会在上颌引起更加深刻的根尖周骨质破坏，通过提高血清IL-1β水平、降低血清IL-4水平和提高肝脏IL-6、TGF-β1表达导致系统和肝脏炎症反应。本文受版权保护。保留所有权利。

To explore the involvement of oxidative stress (OS) in the hepatic inflammation induced by apical periodontitis (AP). Periapical, systemic, and hepatic reaction to AP under hyperlipidemia was also investigated.16 male Sprague-Dawley rats were fed with a hyperlipidemic diet (HD) whereas another 16 rats with a normal diet (ND). After 9 weeks, the first molars of the right maxilla and mandible of 8 HD and 8 ND rats were exposed to induce AP (ND, ND+AP, HD, and HD+AP group). After five weeks, rats were euthanized and the haematological tissue was collected directly from the heart, and serum levels of inflammatory cytokines were measured. Liver tissue was analyzed by haematoxylin-eosin and Masson staining, and reverse transcription-polymerase chain reaction (RT-PCR) was performed to detect mRNA expression of inflammatory cytokines. Serum, periapical, and hepatic OS parameters including total oxidant status (TOS), total antioxidant capacity (TAOC), and oxidative stress index (OSI) were measured by enzyme-linked immunosorbent assay (ELISA). The area of AP lesion in the right maxilla or mandible was radiographically assessed. Student's t-test was performed on the periapical data. A one-way analysis of variance and the Kruskal-Wallis test were analyzed for others.The HD+AP group had a larger AP lesion in the maxilla, compared with the ND+AP group (P<0.05). The ND+AP group presented higher serum interleukin (IL)-18, IL-1β, TOS, OSI levels, lower serum TOAC levels, higher hepatic tumor necrosis factor (TNF)-α mRNA expression, and higher hepatic TOS, and OSI levels, compared with the ND group (P<0.05). The HD+AP group had lower serum IL-4 level, higher serum IL-1β level, and higher hepatic IL-6 and transforming growth factor (TGF) -β1 mRNA expression, compared with the HD group (P<0.05).AP could activate systemic and liver inflammation by promoting serum IL-18, 1L-1β, TOS, OSI expression, enhancing hepatic TOS, OSI expression, and inhibiting serum TOAC expression. AP under hyperlipidemia led to more profound periapical bone destruction in the maxilla and elicit systemic and liver inflammatory responses through elevating serum levels of IL-1β, descending serum IL-4 level, and improving hepatic IL-6, TGF-β1 expression.This article is protected by copyright. All rights reserved.