1. Academic Validation
  2. Ligature induced periodontitis in rats causes gut dysbiosis leading to hepatic injury through SCD1/AMPK signalling pathway

Ligature induced periodontitis in rats causes gut dysbiosis leading to hepatic injury through SCD1/AMPK signalling pathway

  • Life Sci. 2022 Jan 1;288:120162. doi: 10.1016/j.lfs.2021.120162.
Tian Xing 1 Yajing Liu 2 Huixin Cheng 1 Miaomiao Bai 1 Jingning Chen 3 Huafeng Ji 3 Maozhang He 4 Keyang Chen 5
Affiliations

Affiliations

  • 1 College & Hospital of Stomatology, Anhui Medical University, Key Lab. of Oral Diseases Research of Anhui Province, Hefei 230032, China.
  • 2 Department of Public Health Inspection and Quarantine, Anhui Medical University School of Public Health, Hefei, Anhui 230032, China.
  • 3 The Key Laboratory of Microbiology and Parasitology of Anhui Province, The Provincial Key Laboratory of Zoonoses of High Institutions in Anhui, Hefei 230032, China.
  • 4 Department of Microbiology, The Key Laboratory of Microbiology and Parasitology of Anhui Province, The Key Laboratory of Zoonoses of High Institutions in Anhui, School of Basic Medical Sciences, Anhui Medical University, No. 81 Meishan Road, Hefei 230022, China. Electronic address: hmz91@ahmu.edu.cn.
  • 5 Department of Public Health Inspection and Quarantine, Anhui Medical University School of Public Health, Hefei, Anhui 230032, China. Electronic address: chenkeyang@ahmu.edu.cn.
Abstract

Aims: Previous studies have demonstrated that chronic periodontitis (CP) is closely associated with the occurrence and development of a variety of systemic diseases. In this study, we successfully constructed a rat CP model through dental silk ligation, and the corresponding inflammatory reactions and fatty lesions were observed in the liver.

Main methods: Sprague-Dawley rats (n = 6) underwent tooth ligation at the bilateral first molars with silk thread to induce CP and were sacrificed 8 weeks later and compared to non-ligated rats (n = 6). RNA Sequencing and 16S rRNA analysis were performed to determine the molecular mechanisms of CP involved in inducing liver disease. Alveolar bone loss, liver Enzymes, mandible and liver histopathology, and inflammatory responses were compared between groups.

Key findings: RNA Sequencing of liver tissue showed that the expression of SCD1 increased significantly in CP rats compared to controls. KEGG enrichment analysis showed that the AMPK signalling pathway may be involved in liver steatosis. The intestinal flora of faecal samples of rats were analysed by 16S rRNA Sequencing, and the results indicated that the intestinal flora of the CP group was evidently imbalanced. The expression levels of tight junction proteins (ZO-1, occludin, and claudin-1) were significantly reduced in CP rats. Meanwhile, increases in serum IL-1β and lipopolysaccharide in CP rats reflected a systemic inflammatory response.

Significance: CP may be involved in the occurrence and development of hepatic injury and liver steatosis, and its mechanism may be related to the oral-gut-liver axis and SCD1/AMPK signal activation in the liver.

Keywords

Intestinal flora; Liver steatosis; Periodontitis; SCD-1/AMPK signalling pathway.

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