蛋白酶体抑制剂乳胞素(LAC)对LPS诱导的人关节软骨细胞炎症反应的抑制作用

Proteasome Inhibitor Lactacystin Inhibited the Inflammation in Human Chondrocytes Induced by Lipopolysaccharide

目的:探讨蛋白酶体抑制剂乳胞素(LAC)对LPS诱导的人关节软骨细胞炎症反应的抑制作用。方法:体外培养原代人关节软骨细胞,分为四组,即对照组、LPS组(100 ng/mL LPS处理6小时)、LAC组(5μM LAC处理1小时)和LAC+LPS组(5μMLAC预处理1小时后,给予LPS处理6小时),分别用ELISA和western blot检测和比较各组细胞内20s蛋白酶体,NF-κB,TNF-α和iNOS的含量。结果:LPS处理后的人关节软骨细胞内20s蛋白酶体,NF-κB,TNF-α和iNOS的表达均较对照组显著升高(P<0.05),LAC+LPS组以上指标较LPS组均显著降低(P<0.05),而LAC组和LAC+LPS组以上指标与对照组比较均无显著性差异(P>0.05)。结论:LAC可显著抑制LPS诱导的人关节软骨细胞炎症反应。

Objective： To explore the effects of lactacystin on LPS-induced inflammation in human chondrocytes.Methods： Primary human chondrocytes were cultured in vitro and divided into four groups： control group,LPS group（100 ng/mL LPS for 6h）,LAC group（5 μM LAC for 1h）,LAC＋LPS group（5 μM LAC for 1h followed by 100 ng/mL LPS for 6h）.20s Proteasome,NF-κB,TNF-α and iNOS were measured by ELISA and western blot,respectively.Results： Compared with the control group,the expression of 20s Proteasome,NF-κB,TNF-α and iNOS in chondrocytes were significantly up-regulated in response to LPS stimulation（P0.05）,which were all also significantly higher than those in LAC＋LPS group（P0.05）.However,there was no significant difference between LAC group and LAC＋LPS group（P0.05）.Conclusion： LAC could significantly inhibit LPS-induced inflammatory response in human chondrocytes.