Effect of Ligustrazine on rat peritoneal mesothelial cells treated with lipopolysaccharide

被引:16
作者
Zhang, Hui [1 ]
Li, Dongxia [2 ]
Li, Zhiyong [3 ]
Song, Yu [1 ]
机构
[1] Xinxiang Med Univ, Coll Pharm, Xingxiang 453003, Henan Province, Peoples R China
[2] Xinxiang Med Univ, Coll Basic Med, Xingxiang, Peoples R China
[3] Third Peoples Hosp Anyang City, Dept Cerebral Surg, Anyang, Peoples R China
关键词
Ligustrazine; MMP-9; oxidative stress; p38; MAPKS; RPMCs; EPITHELIAL-MESENCHYMAL TRANSITION; OXIDATIVE STRESS; ENDOTHELIAL-CELLS; MATRIX METALLOPROTEINASES; INDUCED APOPTOSIS; IN-VITRO; DIALYSIS; DEATH; MEMBRANE; GLUCOSE;
D O I
10.3109/0886022X.2016.1165053
中图分类号
R5 [内科学]; R69 [泌尿科学(泌尿生殖系疾病)];
学科分类号
100201 [内科学]; 100221 [泌尿外科学];
摘要
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 5mgL(-1) LPS for 24h 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.
引用
收藏
页码:961 / 969
页数:9
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