首页> 中文期刊> 《中国药物与临床》 >左旋多巴对脂多糖诱导小胶质细胞产生致炎因子的影响及黄芪保护作用

左旋多巴对脂多糖诱导小胶质细胞产生致炎因子的影响及黄芪保护作用

         

摘要

目的 探讨左旋多巴(L-DOPA)对脂多糖(LPS)诱导小胶质细胞产生致炎因子的影响及黄芪多糖(ASP)的保护作用.方法 不同浓度LPS(1、5、10 ng/ml)和(或)L-DOPA(50、100、500 μmol/L)及ASP (20 μg/ml)+LPS(10 ng/ml)+L-DOPA(50 μmol/L)处理小胶质细胞培养液,于0、4、24、48 h动态观察一氧化氮(NO)的含量、肿瘤坏死因子-α(TNF-α)的水平及黄芪多糖对上述指标的影响.结果 LPS处理小胶质细胞培养液,当LPS浓度5 ng/ml 48 h、10 ng/ml 24 h、L-DOPA浓度为100 μmol/L 72 h、500 μmol/L 24 h以后、LPS+L-DOPA组各个时间点NO的含量均高于对照组(P<0.05),LPS+L-DOPA组显著高于单独用LPS或L-DOPA处理组(P<0.05).LPS 5 ng/ml 24 h、10 ng/ml 4 h、L-DOPA500 μmol/L 72 h、LPS+L-DOPA组各时间点TNF-α的含量均高于对照组(P<0.05),LPS+L-DOPA组显著高于单独用LPS或L-DOPA处理组(P<0.05),黄芪多糖处理组明显降低NO的含量和TNF-α的水平(P<0.05).结论 LPS致炎作用有时间剂量依赖性,小剂量L-DOPA无致炎作用,但L-DOPA增强LPS的致炎作用,黄芪多糖通过抑制NO、TNF-α的释放发挥抗炎保护作用.%Objective To explore effect of L-DOPA on inflammatory factors releasing induced by LPS and the protective effect of Asragulus Polysacharin (ASP). Methods Cultured microgliawere treated with LPS(1,5 and 10 ng/ ml) or/and L-DOPA(50,100,500 μmol/L), ASP 20 μg/ml and LPS(10 ng/ml)+L-DOPA(50 μmol/L). Changes of NO level and TNF-α level were dynamic observed at 0, 4, 24, 48 h, as well as the protective effect of ASP. Results When treated with LPS of 5 ng/ml after 48 h, of 10 ng/ml after 24 h, L-DOPA of 100 αmol/L after 72 h or 500 αmol/ L after 24 h, NO level was significantly higher than that of control(P<0.05); Treated with LPS+L-DOPA of 50 μmol/L, NO level was significantly higher than that of control; NO level of LPS+L-DOPA was significantly higher than group treated with LPS or L-DOPA alone (P<0.05). Of LPS 5 ng/ml 24 h, 10 ng/ml 4 h, L-DOPA 500 μl 72 h, LPS+L-DOPA group, TNF-α level was significantly higher than that of control (P<0.05 )in any hour; TNF-a level were significantly higher than group treated with LPS or L-DOPA (P<0.05). APS could significantly decrease NO and TNF-α level(P<0.05). Conclusions Inflammation effect induced by LPS was time- and dose-dependent. Low-dose L-DOPA may not be pro-inflammatory but can enhance the inflammatory effect induced by LPS. APS could inhibit NO and TNF-α releasing.

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