丹参酮ⅡA磺酸钠注射液改善脂多糖-高糖腹膜透析液诱导的人腹膜间皮细胞损伤的实验研究
Sulfotanshinone ⅡA Sodium Ameliorates Lipopolysaccharide-Peritoneal Dialysis Solution-Elicited Human Peritoneal Mesothelial Cells Injury
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摘要: 目的 评估丹参酮ⅡA磺酸钠注射液（STS）减轻脂多糖-高糖腹膜透析液（LPS-PDS）诱导的人腹膜间皮细胞（HPMCs）损伤以及抑制腹膜纤维化的作用。方法 HPMCs来自腹腔外科手术患者腹膜细胞的原代培养。以LPS-PDS诱导的HPMCs损伤为模型，通过观察STS对HPMCs增殖活性、转化生长因子-β（TGF-β1）分泌、基质金属蛋白酶-9（MMP-9）、组织基质金属蛋白酶抑制因子-1（TIMP1）等的影响，阐明STS对HPMCs的保护作用及抗腹膜纤维化的机理。结果 LPS-PDS可造成HPMCs损伤，表现为活性下降，STS可明显减轻LPS-PDS对HPMCs的毒性，改善其造成的细胞活性下降，减轻LPS-PDS诱导的TGF-β1、TIMP1 mRNA上调和MMP-9 mRNA表达下降。结论 STS可以减轻LPS-PDS诱导的HPMCs损伤，可能是通过调节TGF-β1、TIMP1、MMP-9等蛋白的表达，发挥保护腹膜细胞和拮抗腹膜纤维化的作用。Abstract: OBJECTIVE To study the effect and mechanism of sulfotanshinone ⅡA sodium (STS) in human peritoneal mesothelial cells (HPMCs) injury and peritoneal fibrosis caused by lipopolysaccharide-peritoneal dialysis solution (LPS-PDS). METHODS HPMCs was primary cultured from patients undergoing peritoneal surgery. The cells were incubated with LPS-PDS to mimic the peritoneal dialysis conditions in vitro. After treatment of cells with STS， cellular viability was tested and mRNA were collected and subjected to RT-PCR to evaluated the level of TGF-β1， TIMP-1 and MMP-9. RESULTS Incubation HPMCs with LPS-PDS elicited cell injury. STS attenuated LPS-PDS-induced cell injury by improvement of cellular viability. Furthermore， STS inhibited HPMCs fibrosis as evidenced by suppression of TGF-β1 and TIMP1 induced by LPS-PDS and increasing MMP-9 mRNA level. CONCLUSION STS protects HPMCs against LPS-PDS-induced cell injury. Moreover， STS retards HPMCs fibrosis by decreasing TGF-β1 and TIMP1 mRNA level and increasing MMP-9 mRNA.
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