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目的研究藁本内酯(Lig)对细菌脂多糖(LPS)诱导的神经炎症的抑制作用。方法用1、2.5、5、10、20μmol·L~(-1)Lig作用于小鼠RAW264.7巨噬细胞,加1μg·m L~(-1)LPS刺激构建细胞炎症反应模型,采用MTT法检测细胞毒性,一步法检测NO的释放量,ELISA法检测TNF-α、IL-6的释放量,免疫细胞化学法检测i NOS的水平;将LPS注入小鼠侧脑室构建体内神经炎症模型,术前30 min及术后6 h于腹腔注射30 mg·kg~(-1)Lig,造模后24 h取大脑,用免疫组织化学法检测GFAP、TNF-α的蛋白表达。结果经Lig处理后,细胞存活率无明显变化,细胞分泌NO显著减少(P<0.05或P<0.01),且呈剂量依赖性,TNF-α、IL-6、i NOS的表达均明显下调(P<0.05);Lig能显著降低小鼠海马区GFAP、TNF-α的表达(P<0.01)。结论Lig能够抑制LPS诱导的小鼠体内外的炎症反应,提示Lig对神经炎症相关的多种疾病可能具有潜在的治疗作用。
Objective To investigate the inhibitory effect of ligustilide (Lig) on neuroinflammation induced by bacterial lipopolysaccharide (LPS). Methods Mouse RAW264.7 macrophages were treated with 1, 2.5, 5, 10, 20 μmol·L -1 Lig, and stimulated with 1 μg · m L -1 of LPS to establish the model of inflammatory reaction. MTT The levels of TNF-α and IL-6 were measured by ELISA, and the level of iNOS was detected by immunocytochemistry. The model of neuroinflammation was established by injecting LPS into the lateral ventricle of mice, The rats were injected intraperitoneally with 30 mg · kg -1 Lig 30 min before operation and 6 h after operation. The brains were harvested at 24 h after operation. The protein expressions of GFAP and TNF-α were detected by immunohistochemistry. Results After Lig treatment, there was no significant change in cell viability and NO secretion (P <0.05 or P <0.01) in a dose-dependent manner. The expression of TNF-α, IL-6 and iNOS were significantly down- P <0.05). Lig significantly reduced the expression of GFAP and TNF-α in hippocampus of mice (P <0.01). Conclusion Lig can inhibit LPS-induced inflammation in vivo and in vitro in mice, suggesting that Lig may have a potential therapeutic effect on various diseases associated with neuroinflammation.