Pei Chen1, Xiao Chen1, Hongxing Chu1, Wei Xia1, Xiaoyan Zou1, Dan Wang2, Mingdeng Rong1. 1. Department of Periodontology and Implantology, Stomatological Hospital, Southern Medical University Guangzhou 510280, Guangdong, China. 2. Haizhu Square Branch of Stomatological Hospital, Southern Medical University Guangzhou 510120, Guangdong, China.
Abstract
OBJECTIVE: To determine the impact of periodontitis on renal impairment induced by obesity. METHODS: Periodontitis and obesity models were induced using silk ligatures with bacteria and high-fat diet, respectively. Indicators of renal function were compared. Renal tubular epithelial cells (RTECs) were treated with lipopolysaccharides from periodontal pathogens in a high-fat environment to induce cell models of periodontitis and obesity. The transforming growth factor-β/mothers against decapentaplegic homolog (Smad) (TGF-β/Smad) pathway was evaluated both in vivo and in vitro. The indicators of renal function, renal pathological changes, and serum inflammatory cytokines were measured. The viability/apoptosis of RTECs and the expression of inflammatory cytokines were determined. RESULTS: Periodontitis resulted in an increase in TGF-β/Smad activity in the kidney of obese mice. Moreover, the activity of RTECs was also increased in vitro. Downregulation of TGF-β led to reduced TGF-β, p-Smad2, p-Smad3, and Smad7 levels in kidney tissue and RTECs, ameliorated renal function indicators and renal pathological changes, increased viability and apoptosis of RTECs, and decreased levels of inflammatory cytokines. CONCLUSION: Periodontitis regulates renal impairment via the TGF-β/Smad pathway in obese mice. AJTR
OBJECTIVE: To determine the impact of periodontitis on renal impairment induced by obesity. METHODS: Periodontitis and obesity models were induced using silk ligatures with bacteria and high-fat diet, respectively. Indicators of renal function were compared. Renal tubular epithelial cells (RTECs) were treated with lipopolysaccharides from periodontal pathogens in a high-fat environment to induce cell models of periodontitis and obesity. The transforming growth factor-β/mothers against decapentaplegic homolog (Smad) (TGF-β/Smad) pathway was evaluated both in vivo and in vitro. The indicators of renal function, renal pathological changes, and serum inflammatory cytokines were measured. The viability/apoptosis of RTECs and the expression of inflammatory cytokines were determined. RESULTS: Periodontitis resulted in an increase in TGF-β/Smad activity in the kidney of obese mice. Moreover, the activity of RTECs was also increased in vitro. Downregulation of TGF-β led to reduced TGF-β, p-Smad2, p-Smad3, and Smad7 levels in kidney tissue and RTECs, ameliorated renal function indicators and renal pathological changes, increased viability and apoptosis of RTECs, and decreased levels of inflammatory cytokines. CONCLUSION: Periodontitis regulates renal impairment via the TGF-β/Smad pathway in obese mice. AJTR
Authors: Li Jie; Qiu Pengcheng; He Qiaoyan; Bi Linlin; Zhang Meng; Wang Fang; Jia Min; Yan Li; Zhang Ya; Yang Qian; Wang Siwang Journal: Eur J Pharmacol Date: 2017-06-17 Impact factor: 4.432
Authors: Shahrukh Khan; Silvana Bettiol; Katherine Kent; Marco A Peres; Tony Barnett; Leonard A Crocombe; Murthy Mittinty Journal: J Periodontol Date: 2020-09-29 Impact factor: 6.993