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目的:LPS诱导体内外炎症模型,研究两头尖活性组分BU-6E的抗炎作用。方法:体外:脂多糖(LPS)诱导小鼠RAW264.7细胞构建炎症模型,MTT法检测BU-6E对RAW 264.7细胞增殖的影响,Griess法检测LPS诱导的细胞上清中一氧化氮(NO)含量,ELISA法检测炎症因子TNF-α、IL-6、IL-1β的分泌量;体内:BALB/c小鼠灌胃给药7天腹腔注射LPS构建炎症模型,ELISA法检测血清中TNF-α、IL-6、IL-1β的含量。结果:体外:BU-6E在25μg/ml、50μg/ml、100μg/ml能够显著的抑制LPS诱导的RAW 264.7细胞增殖水平,可以极显著的抑制LPS诱导的NO的释放,且无明显细胞毒性;BU-6E可减少炎症因子TNF-α、IL-6、IL-1β的分泌,且呈现剂量依赖关系;体内:与模型组相比,BU-6E组的TNF-α、IL-1β的分泌呈极显著性减少,IL-6的分泌呈显著性减少。结论:BU-6E可以抑制LPS诱导的NO释放以及炎症因子的分泌,在体外、体内均有一定的抗炎活性。
OBJECTIVE: To investigate the anti-inflammatory effects of LPS-induced inflammation in vivo and in vitro and to study the anti-inflammatory effects of BU-6E, a two-pronged active component. Methods: In vitro, lipopolysaccharide (LPS) was used to induce inflammation in RAW264.7 cells. The effect of BU-6E on the proliferation of RAW 264.7 cells was detected by MTT assay. Nitric oxide (NO) The levels of TNF-α, IL-6 and IL-1β were measured by enzyme-linked immunosorbent assay (ELISA). In vivo, BALB / c mice were intraperitoneally injected with LPS for 7 days to establish an inflammatory model. , IL-6, IL-1β content. Results: In vitro, BU-6E at 25μg / ml, 50μg / ml and 100μg / ml could significantly inhibit LPS-induced proliferation of RAW 264.7 cells and significantly inhibit the release of NO induced by LPS with no obvious cytotoxicity. BU-6E reduced the secretion of inflammatory cytokines TNF-α, IL-6 and IL-1β in a dose-dependent manner. In vivo, the secretion of TNF-αand IL-1β in BU- Significantly reduced, IL-6 secretion was significantly reduced. CONCLUSION: BU-6E can inhibit the release of NO induced by LPS and the secretion of inflammatory cytokines, and have certain anti-inflammatory activity both in vitro and in vivo.