摘要
目的 :观察α -黑色素细胞刺激素 (α -MSH)对脂多糖 (LPS)诱导小鼠腹腔巨噬细胞SOCS - 3mRNA表达及NO释放的影响 ,以探讨α -MSH拮抗LPS的作用机制。方法 :用半定量逆转录多聚酶链反应 (RT -PCR)的方法检测LPS诱导体外培养的小鼠腹腔巨噬细胞SOCS - 3mRNA表达水平和给予α -MSH后对SOCS - 3mRNA表达的影响 ;用Griess试剂检测单独给予LPS与同时给予α-MSH和LPS作用巨噬细胞后对NO生成量的影响。结果 :未受LPS刺激的小鼠腹腔巨噬细胞表达低水平的SOCS - 3。LPS组SOCS - 3的表达和NO的生成显著高于对照组 ,而同时给予α -MSH和LPS培养 ,巨噬细胞的SOCS - 3的表达明显低于LPS组 ,NO的生成则几乎完全阻断。结论 :LPS在启动炎症的过程中可能也激活了SOCS介导的负调节机制 ;但SOCS可能不参与α -MSH的抗LPS作用。
AIM: To explore the anti-LPS mechanisms of α-melanocyte-stimulating hormone (α-MSH), the effects of α-MSH on the expression of SOCS-3 mRNA and the production of NO in murine peritoneal macrophages induced by LPS were investigated. METHODS: BALB/c mouse peritoneal macrophages were cultured in vitro and induced by LPS, α-MSH and LPS with α-MSH, respectively. The expression of SOCS-3 mRNA was detected using reverse transcription polymerase chain reaction (RT-PCR). NO produced in macrophages was tested with Griess reagent. RESULTS: The level of NO and the expression of SOCS-3 mRNA were significantly increased in macrophages stimulated with LPS.α-MSH markedly decreased the expression of SOCS-3 mRNA and almost completely inhibited the production of NO induced by LPS. CONCLUSION: These results suggest that the negative regulative circuits operated by SOCS are activated during the inflammation induced by LPS, but SOCS might not be involved in the anti-LPS mechanism of α-MSH.
出处
《中国病理生理杂志》
CAS
CSCD
北大核心
2004年第5期729-732,共4页
Chinese Journal of Pathophysiology
基金
国家自然科学基金资助项目 (No .395 0 0 0 5 9)
关键词
α-促黑素
脂多糖类
巨噬细胞
腹膜
alpha-MSH
Lipopolysaccharides
Macrophages, peritoneal
