Matrine suppresses lipopolysaccharide-induced fibrosis in human peritoneal mesothelial cells by inhibiting the epithelial-mesenchymal transition.
10.1097/CM9.0000000000000127
- Author:
Yi-Zheng LI
1
;
Xi PENG
2
;
Yun-Hua MA
3
;
Fu-Ji LI
4
;
Yun-Hua LIAO
4
Author Information
1. Scientific Research Department, The First Affiliated Hospital of Guangxi Medical University, Nanning, Guangxi 530021, China.
2. Guangxi Medical College, Nanning, Guangxi 530021, China.
3. Department of Nephrology, The First People's Hospital of Nanning, Nanning, Guangxi 530021, China.
4. Renal Division, Department of Medicine, The First Affiliated Hospital of Guangxi Medical University, Nanning, Guangxi 530021, China.
- Publication Type:Journal Article
- MeSH:
Actins;
metabolism;
Alkaloids;
therapeutic use;
Cadherins;
metabolism;
Cells, Cultured;
Epithelial-Mesenchymal Transition;
drug effects;
Epithelium;
drug effects;
Fibrosis;
chemically induced;
genetics;
metabolism;
Humans;
Lipopolysaccharides;
toxicity;
MicroRNAs;
metabolism;
Peritoneal Fibrosis;
drug therapy;
Quinolizines;
therapeutic use
- From:
Chinese Medical Journal
2019;132(6):664-670
- CountryChina
- Language:English
-
Abstract:
BACKGROUND:Peritoneal fibrosis is the primary reason that patients with end-stage renal disease (ESRD) have to cease peritoneal dialysis. Peritonitis caused by Gram-negative bacteria such as Escherichia coli (E. coli) were on the rise. We had previously shown that matrine inhibited the formation of biofilm by E. coli. However, the role of matrine on the epithelial-mesenchymal transition (EMT) in peritoneal mesothelial cells under chronic inflammatory conditions is still unknown.
METHODS:We cultured human peritoneal mesothelial cells (HPMCs) with lipopolysaccharide (LPS) to induce an environment that mimicked peritonitis and investigated whether matrine could inhibit LPS-induced EMT in these cells. In addition, we investigated the change in expression levels of the miR-29b and miR-129-5p.
RESULTS:We found that 10 μg/ml of LPS induced EMT in HPMCs. Matrine inhibited LPS-induced EMT in HPMCs in a dose-dependent manner. We observed that treatment with matrine increased the expression of E-cadherin (F = 50.993, P < 0.01), and decreased the expression of alpha-smooth muscle actin (F = 32.913, P < 0.01). Furthermore, we found that LPS reduced the expression levels of miR-29b and miR-129-5P in HPMCs, while matrine promoted the expression levels of miR-29b and miR-129-5P.
CONCLUSIONS:Matrine could inhibit LPS-induced EMT in HPMCs and reverse LPS inhibited expressions of miR-29 b and miR-129-5P in HPMCs, ultimately reduce peritoneal fibrosis. These findings provide a potential theoretical basis for using matrine in the prevention and treatment of peritoneal fibrosis.
