摘要
为探讨腹膜硬化的发生机制,采用腹膜间皮细胞培养、纤维蛋白平板方法和Northern杂交技术观察了不同浓度葡萄糖和抗生素庆大霉素与头孢唑啉钠对大鼠腹膜间皮细胞纤溶酶原激活物抑制物(PAI)产生和转化生长因子-β(TGF-β)mRNA表达的影响。结果表明腹膜间皮细胞可表达PAI-1mRNA和产生活性PAI;培养12小时,11.2mmol/L的高渗葡萄糖、庆大霉素和头孢唑啉钠可增强腹膜间皮细胞PAI-1mRNA的表达和增加活性PAI的分泌;培养至24小时,11.2mmol/L的高渗葡萄糖继续诱导腹膜间皮细胞产生活性PAI增加,庆大霉素既可以继续引起PAI-1mRNA表达增加,而且还可以使腹膜间皮细胞活性PAI产生增加。同时在培养24小时,11.2mmol/L的高渗葡萄糖和庆大霉素与头孢唑啉钠均可引起腹膜间皮细胞TGF-βmRNA表达增加。结果提示:11.2mmol/L的高渗葡萄糖和庆大霉素与头孢唑啉钠可以导致间皮细胞表达PAI和TGF-β上调,在腹膜硬化发生机制中起着重要作用。
To investigate the mechanism of fibrosis in peritoneal dialysis, we observed the effects of the hyperosmotic glucose and antibiotics such as gentamicin and cefazolin on rat peritoneal mesothelial cells with cell culture, fibrin plate lyzing and Northern blotting analysis method. The peritoneal mesothelial cells may express PAI 1 mRNA. The expressions of PAI 1 mRNA in peritoneal mesothelial cells and acti vities of PAI in the supernatants were enhanced by 11.2 mmol/L glucose, gentamicin and cefazolin at 12hr. By 24hr, the activity of PAI 1 also increased in the supernatants with 11.2 mmol/L glucose. The expressions of PAI 1 mRNA and production of PAI activities by the peritoneal mesothelial cells were increased by gentamicin, and the TGF β mRNA increased in the peritoneal mesothelial cells was induced by 11.2 mmol/L glucose, gentamicin and cefazolin. The results suggested that 11.2 mmol/L glucose, gentamicin and cefazolin may increase the expressions or productions of PAI and TGF β in peritoneal mesothelial cells. So by perosmotic glucose, cefazolin and gentamicin promote the peritoneal fibrosis in patients with CAPD.
出处
《中华内科杂志》
CAS
CSCD
北大核心
1997年第10期689-692,共4页
Chinese Journal of Internal Medicine
关键词
葡萄糖
抗生素类
PAI
腹膜间皮细胞
Glucose Antibiotics Type 1 plasminogen activator inhibitor