Chronic Administration of Lipopolysaccharide and Proteases Induces Periodontal Inflammation and Hepatic Steatosis in Rats

Tomofuji, Takaaki; Ekuni, Daisuke; Yamanaka, Reiko; Kusano, Hiroki; Azuma, Tetsuji; Sanbe, Toshihiro; Tamaki, Naofumi; Yamamoto, Tatsuo; Watanabe, Tatsuo; Miyauchi, Mutsumi; Takata, Takashi

doi:10.1902/jop.2007.070056

Cited by 88 publications

(137 citation statements)

References 36 publications

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“…Serum TNF-a concentration was determined with a rat TNF-a enzyme-linked immunosorbent assay (ELISA) kit (Biosource International, Camarillo, CA, USA). 37 Serum levels of C-reactive protein (CRP) were quantified by a highly sensitive ELISA kit (Life Diagnostics, West Chester, UK). 37 Serum levels of insulin were quantified by an ultrasensitive ELISA kit (Mercodia, Uppsala, Sweden).…”

Section: Measurement Of Reactive Oxygen Species Expression In Aortamentioning

confidence: 99%

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Effects of periodontitis on aortic insulin resistance in an obese rat model

Ekuni

Tomofuji

Irie

et al. 2010

Laboratory Investigation

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The combination of obesity and its associated risk factors, such as insulin resistance and inflammation, results in the development of atherosclerosis. However, the effects of periodontitis on atherosclerosis in an obese body remain unclear. The aim of the study was to investigate the effects of ligature-induced periodontitis in Zucker fatty rats on initiation of atherosclerosis by evaluating aortic insulin resistance. Zucker fatty rats (n ¼ 24) were divided into two groups. In the periodontitis group, periodontitis was ligature-induced for 4 weeks, whereas the control group was left unligated. After the 4-week experimental period, descending aorta was used for measuring the levels of lipid deposits, immunohistochemical analysis, and evaluation of gene expression. Levels of serum C-reactive protein (CRP), tumor necrosis factora (TNF-a), and insulin were also measured. Rats in the periodontitis group had significantly enhanced lipid deposits in the aorta, but not in the control group. Expression of suppressor of cytokine signaling 3, vascular cell adhesion molecule 1, reactive oxygen species, nitrotyrosine, and endothelin-1 in the periodontitis group was more intense than that in the control group. Significantly decreased levels of phosphatidylinositol 3-kinase (Pi3k) catalytic b-polypeptide (Pi3kcb), Pi3kp85, and insulin receptor substrate 1 and 2 were observed in the periodontitis group. Levels of serum CRP and TNF-a were significantly increased in the periodontitis group. Under insulin-stimulated conditions, aorta in the periodontitis group altered the Akt phosphorylation. Periodontitis in obesity induced the initial stage of atherosclerosis and disturbed aortic insulin signaling.

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Section: Measurement Of Reactive Oxygen Species Expression In Aortamentioning

confidence: 99%

“…37 Serum levels of C-reactive protein (CRP) were quantified by a highly sensitive ELISA kit (Life Diagnostics, West Chester, UK). 37 Serum levels of insulin were quantified by an ultrasensitive ELISA kit (Mercodia, Uppsala, Sweden). 38 The assays were performed in triplicate.…”

Section: Measurement Of Reactive Oxygen Species Expression In Aortamentioning

confidence: 99%

Effects of periodontitis on aortic insulin resistance in an obese rat model

Ekuni

Tomofuji

Irie

et al. 2010

Laboratory Investigation

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“…The mechanisms by which periodontitis affects these systemic diseases are still unclear. However, the prerequisite is believed to be the host inflammatory response to long-term exposure to bacterial pathogens, such as lipopolysaccharide (LPS) and proteases (27). In a periodontal lesion, polymorphonuclear leukocytes produce reactive oxygen species (ROS) as the initial host defense against bacterial pathogens (21).…”

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confidence: 99%

“…The level of serum HEL, a biomarker for early stage lipid peroxidation, was measured using an ELISA kit (Japan Institute for the Control of Aging, Shizuoka, Japan) (8). The concentration of serum LPS was determined using a kinetic Limulus Amebocyte Lysate test kit (Wako Pure Chemical Industries, Ltd., Osaka, Japan) (27). Serum levels of CRP were quantified by a highly sensitive ELISA (Life Diagnostics, Inc., West Chester, UK) (9).…”

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confidence: 99%

“…A single examiner (T. T.), blinded to the treatment assignment, performed the following histometric analyses using a microscope (Olympus Co., Tokyo, Japan). The distances between the cementoenamel junction and the alveolar bone crest (CEJ-ABC) and between the cemento-enamel junction and the most apical portion of the junctional epithelium (CEJ-JE) were measured with a microgrid at a magnification of ×200 (27). The polymorphonuclear leukocytes per unit area (0.05 mm × 0.05 mm) of the connective tissue subjacent to the junctional epithelium were counted at a magnification of ×400 (27).…”

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Relationships between periodontal inflammation, lipid peroxide and oxidative damage of multiple organs in rats

et al. 2011

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Gingival response to periodontal inflammation generates excessive lipid peroxide and such a condition may augment systemic health through increased circulating lipid peroxide. The purpose of the present study was to investigate whether the generation of lipid peroxide in periodontal inflammation could induce tissue injury in the liver, heart, kidney and brain using a rat model. Twelve Wistar rats (8 week-old male) were divided into 2 groups: the periodontal inflammation group, receiving topical application of lipopolysaccharide and proteases to the gingival sulcus for 4 weeks, and the control group using instead pyrogen-free water. After blood samples were collected, specimens from the brain, heart, liver and kidney were resected to determine the concentration of 8-hydroxydeoxyguanosine (an indicator of oxidative DNA damage). Gingival and serum levels for hexanoyl-lysine were measured to evaluate lipid peroxide. Administration of lipopolysaccharide and proteases induced periodontal inflammation, with increasing gingival and serum levels of hexanoyl-lysine. The level of 8-hydroxydeoxyguanosine increased 2.27, 2.01, 1.49 and 1.40 times in mitochondrial DNA from the liver, heart, kidney and brain of rats with periodontal inflammation, respectively. The results reveal that excessive production of lipid peroxide following periodontal inflammation is involved in oxidative DNA damage of the brain, heart, liver and kidney.

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Advances in Optical Imaging of Nonalcoholic Fatty Liver Disease

Shen

Zhou

et al. 2022

Chemistry An Asian Journal

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Nonalcoholic fatty liver disease (NAFLD), emerging as one of the most common chronic liver diseases including simple steatosis and non‐alcoholic steatohepatitis (NASH), is likely to progress to liver fibrosis and hepatic carcinoma if not treated in time. Therefore, early diagnosis and treatment of NAFLD are necessary. Currently, liver biopsy, as the gold standard for clinical diagnosis of NAFLD, is not widely accepted by patients due to its invasiveness. However, other non‐invasive methods that had been reported for NAFLD (such as magnetic resonance imaging, positron emission tomography, and ultrasound) still suffer from low resolution and sensitivity, which are available as a guide for liver biopsy sometimes. As a non‐invasive modality with high spatiotemporal resolution and superior sensitivity, optical imaging methods have been widely favored in recent years, mainly including fluorescence imaging, photoacoustic imaging, and bioluminescence imaging. With these optical imaging approaches, a series of optical probes based on optical and molecular‐specific design have been developed for the biomarker diagnosis and research of diseases. In this review, we summarize the existing non‐invasive optical imaging probes for the detection of biomarkers in NAFLD, including microenvironment (viscosity, polarity), ROS, RSS, ions, proteins, and nucleic acids. Design strategies for optical imaging probes and their applications in NAFLD bioimaging are discussed and focused on. We also highlight the potential challenges and prospects of designing new generations of optical imaging probes in NAFLD studies, which will further enhance the diversity, practicality, and clinical feasibility of NAFLD research.

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Chronic Administration of Lipopolysaccharide and Proteases Induces Periodontal Inflammation and Hepatic Steatosis in Rats

Abstract: Periodontal inflammation in a rat model induced fatty liver disease through increased serum LPS.

Cited by 88 publications

References 36 publications

Effects of periodontitis on aortic insulin resistance in an obese rat model

Effects of periodontitis on aortic insulin resistance in an obese rat model

Relationships between periodontal inflammation, lipid peroxide and oxidative damage of multiple organs in rats

Advances in Optical Imaging of Nonalcoholic Fatty Liver Disease

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