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Updated: Mar 22, 2026
Induction of Periodontitis via a Combination of Ligature and Lipopolysaccharide Injection in a Rat Model
Published on: February 17, 2023
Effect of Ligustrazine on rat peritoneal mesothelial cells treated with lipopolysaccharide
Hui Zhang1, Dongxia Li2, Zhiyong Li3
1a College of Pharmacy , Xinxiang Medical University , Xingxiang , China ;
Abstract:
The apoptosis of peritoneal mesothelial cells (PMCs) and peritoneal fibrosis may induce failure of peritoneal membrane function. The study explored the changes of apoptosis and fibrosis in PMCs under lipopolysaccharides (LPS) culture and investigated whether Ligustrazine can affect LPS-induced apoptosis and fibrosis. We found that exposure of rat PMCs to 5 mg·L(-1) LPS for 24 h resulted in a significant induction of apoptosis and increased levels in Reactive oxygen species, and caspase-3 activity. Fibronectin, Collagen I, p-p38, and matrix metalloprotein-9 (MMP-9) levels were also significantly increased by LPS. But superoxide dismutase levels were remarkably decreased. Ligustrazine can restore the changes induced by LPS. The protective effect of Ligustrazine on LPS-induced apoptosis and fibrosis may act through inhibition of oxidative stress and p38/MAPKS, ROS/MMP-9 activation in PMCs.
Insights
Lipopolysaccharides (LPS) induce peritoneal mesothelial cell apoptosis and fibrosis. Ligustrazine protects against LPS effects by inhibiting oxidative stress and related pathways, preserving peritoneal membrane function.
Area of Science:
- Cell Biology
- Biochemistry
- Physiology
Background:
- Peritoneal mesothelial cell (PMC) apoptosis and fibrosis can impair peritoneal membrane function.
- Lipopolysaccharides (LPS) are implicated in these pathological processes.
Purpose of the Study:
- To investigate LPS-induced apoptosis and fibrosis in PMCs.
- To determine if Ligustrazine mitigates LPS-induced damage to PMCs.
Main Methods:
- Rat PMCs were cultured with LPS (5 mg·L⁻¹ for 24 h).
- Apoptosis, reactive oxygen species (ROS), caspase-3, fibronectin, Collagen I, p-p38, matrix metalloprotein-9 (MMP-9), and superoxide dismutase levels were assessed.
- The effects of Ligustrazine on these parameters were evaluated.
Main Results:
- LPS significantly increased PMC apoptosis, ROS, caspase-3 activity, fibronectin, Collagen I, p-p38, and MMP-9 levels.
- LPS significantly decreased superoxide dismutase levels.
- Ligustrazine treatment reversed the LPS-induced changes, restoring normal levels.
Conclusions:
- LPS induces apoptosis and fibrosis in PMCs, potentially via oxidative stress and p38/MAPK, ROS/MMP-9 pathways.
- Ligustrazine exhibits protective effects against LPS-induced PMC damage by inhibiting these pathways.
