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Effects of Intravenous Injection of Porphyromonas gingivalis on Rabbit Inflammatory Immune Response and Atherosclerosis

机译:牙龈卟啉单胞菌静脉注射对家兔炎性免疫反应和动脉粥样硬化的影响

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摘要

The effects of intravenous injection of Porphyromonas gingivalis (Pg) on rabbit inflammatory immune response and atherosclerosis were evaluated by establishing a microamount Pg bacteremia model combined with high-fat diet. Twenty-four New Zealand rabbits were randomly divided into Groups A-D (n = 6). After 14 weeks, levels of inflammatory factors (C-reactive protein (CRP), tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), and monocyte chemoattractant protein-1 (MCP-1)) in peripheral blood were detected by ELISA. The aorta was subjected to HE staining. Local aortic expressions of toll-like receptor-2 (TLR-2), TLR-4, TNF-α, CRP, IL-6, matrix metallopeptidase-9, and MCP-1 were detected by real-time PCR, and those of nuclear factor-κB (NF-κB) p65, phospho-p38 mitogen-activated protein kinase (MAPK), and phospho-c-Jun N-terminal kinase (JNK) proteins were detected by Western blot. Intravenous injection of Pg to the bloodstream alone induced atherosclerotic changes and significantly increased systemic and local aortic expressions of inflammatory factors, NF-κB p65, phospho-p38-MAPK, and JNK, especially in Group D. Injection of microamount Pg induced inflammatory immune response and accelerated atherosclerosis, in which the NF-κB p65, p38-MAPK, and JNK signaling pathways played important roles. Intravenous injection of Pg is not the same as Pg from human periodontitis entering the blood stream. Therefore, our results cannot be extrapolated to human periodontitis.
机译:通过建立微量的Pg菌血症模型和高脂饮食,评价静脉注射牙龈卟啉单胞菌(Pg)对家兔炎症免疫反应和动脉粥样硬化的影响。将24只新西兰兔随机分为A-D组(n = 6)。 14周后,炎症因子(C反应蛋白(CRP),肿瘤坏死因子-α(TNF-α),白介素6(IL-6)和单核细胞趋化蛋白1(MCP-1)的水平)通过ELISA检测外周血。对主动脉进行HE染色。实时荧光定量PCR检测toll样受体2(TLR-2),TLR-4,TNF-α,CRP,IL-6,基质金属肽酶9和MCP-1的局部主动脉表达,以及Western blot检测核因子-κB(NF-κB)p65,磷酸化-p38丝裂原活化蛋白激酶(MAPK)和磷酸化-c-Jun N端激酶(JNK)蛋白。仅静脉内注射Pg会引起动脉粥样硬化的变化,并显着增加炎症因子,NF-κBp65,磷酸化p38-MAPK和JNK的全身和局部主动脉表达,尤其是在D组中。并加速动脉粥样硬化,其中NF-κBp65,p38-MAPK和JNK信号通路发挥重要作用。静脉注射Pg与来自人牙周炎进入血流的Pg不同。因此,我们的结果不能外推至人类牙周炎。

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