牙周炎通过TGF-β/Smad信号通路调节肥胖小鼠的肾功能损害。
Periodontitis regulates renal impairment in obese mice via TGF-β/Smad pathway.
作者信息
Chen Pei, Chen Xiao, Chu Hongxing, Xia Wei, Zou Xiaoyan, Wang Dan, Rong Mingdeng
机构信息
Department of Periodontology and Implantology, Stomatological Hospital, Southern Medical University Guangzhou 510280, Guangdong, China.
Haizhu Square Branch of Stomatological Hospital, Southern Medical University Guangzhou 510120, Guangdong, China.
出版信息
Am J Transl Res. 2021 Nov 15;13(11):12523-12535. eCollection 2021.
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 and . 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 . 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.
目的
确定牙周炎对肥胖所致肾功能损害的影响。
方法
分别使用带有细菌的丝线结扎和高脂饮食诱导牙周炎和肥胖模型。比较肾功能指标。在高脂环境下，用牙周病原体的脂多糖处理肾小管上皮细胞（RTECs），以诱导牙周炎和肥胖的细胞模型。评估转化生长因子-β/抗五聚体蛋白同源物（Smad）（TGF-β/Smad）信号通路。检测肾功能指标、肾脏病理变化和血清炎性细胞因子。测定RTECs的活力/凋亡情况以及炎性细胞因子的表达。
结果
牙周炎导致肥胖小鼠肾脏中TGF-β/Smad活性增加。此外，RTECs的活性也增加。TGF-β的下调导致肾组织和RTECs中TGF-β、p-Smad2、p-Smad3和Smad7水平降低，改善了肾功能指标和肾脏病理变化，增加了RTECs的活力和凋亡，并降低了炎性细胞因子水平。
结论
在肥胖小鼠中，牙周炎通过TGF-β/Smad信号通路调节肾功能损害。
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