本文研究了竹节参总提物对脂多糖（lipopolysaccharide, LPS）刺激所致的BV2小胶质细胞炎症反应的保护作用及其机制。MTT筛选不同浓度竹节参总提取对小胶质细胞增殖影响；一氧化氮试剂盒检测NO表达水平；PCR检测IL-1β、TNF-α和iNOS的mRNA表达；免疫荧光检测NF-κB表达及定位。竹节参总提物在3.125~50 mg/L对正常状态及LPS 1 μg/mL诱导的炎症状态下小胶质细胞生长均无明显影响；与正常组比较，模型组NO释放量是其11.82倍，TNF-α、IL-1β和iNOS的mRNA表达量分别是正常组的1.35、1.78和2.50倍，并且NF-κB核移位明显；与模型组比较，竹节参总提物在3.125~50 mg/L均能不同程度抑制NO释放量，并减少IL-1β、TNF-α和iNOS的mRNA表达水平；25、50 mg/L竹节参总提物有效抑制了小胶质细胞中NF-κB的核移位。竹节参总提物可减轻LPS诱导的BV2小胶质细胞炎症反应，其主要机制为抑制NF-κB的核移位，进而降低了炎症因子的分泌。

To investigate the protective effects of total extract of Panacis japonici Rhizoma on lipopolysaccharide-induced inflammation in BV2 cells and its underlying mechanisms. The viability of BV2 cells was detected by MTT. Nitric oxide (NO) levels were measured by Griess. The mRNA expression of TNF-α, IL-1β and iNOS were evaluated by PCR. Immunofluorescence was performed to detect the expression and location of NF-κB. MTT results showed that different concentrations of total extract of Panacis japonici Rhizoma (3.125~50 mg/L) have no effect on the growth of microglia, regardless of normal state or LPS(1 μg/L)-induced inflammatory condition. Compared with the normal group, the release of NO in the model group was 11.82 times, and the mRNA expressions of TNF-α, IL-1β and iNOS in the model group were 1.35 times, 1.78 times and 2.50 times, respectively. There was an obvious nuclear shift of NF-κB after LPS induction. After administration of total extract of Panacis japonici Rhizoma (3.125~50 mg/L), over-expression of IL-1β, TNF-α, iNOS and NO induced by LPS were effectively reversed. Moreover, total extract of Panacis japonici Rhizoma (25, 50 mg/L) can effectively inhibit nuclear translocation of NF-κB. Total extract of Panacis japonici Rhizoma can effectively improve LPS-induced inflammatory response in BV2 microglia. The underlying mechanism is mainly to inhibit nuclear translocation of NF-κB and thereby reducing the secretion of inflammatory factors.

国家自然科学基金项目（81673778）