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作 者:贡济宇[1] 安娜[1] 王莎莎[1] 云旭龙 李智萌[1] 蔡广知[1]
机构地区:[1]长春中医药大学,长春130117
出 处:《中药药理与临床》2017年第2期67-70,共4页Pharmacology and Clinics of Chinese Materia Medica
摘 要: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 study the anti-inflammatory effects of BU-6E extracted from Anemone raddeanae on inflammation model induced by LPS in vitro and in vivo. Methods: In vitro : This study applied LPS stimulating RAW 264.7 cell to set up inflammation model in vitro. MTT as-say was used to test the growth of RAW 264.7 cell. The culture supernatants of the above cells were examined for the determination of nitric oxide (NO) induced by LPS. Grless method was used. The concentrations of tumor neetosis factor-α(TNF-α) ,interleukin-1β (IL-β) and in- terleukin-6 (IL-6) were checked by enzyme linked immunosorbent assay (ELISA). In vivo: BU-6E was administered by intragastric gavage for 7 days. LPS was injected intraperitoneally into BALB/c mice to bulid inflammation model in vivo. The serum levels of TNF-α, IL-6 and IL-1βwere measured by ELISA immunoassay. Results: In vitro:BU-6E did not produce the response of the cell toxicity at the concentrations from 25 to 100μg/ml( P 〉 0.05 ) , significantly decreased the inflammation of RAW 264.7 cells ( P 〈 0.05 ) and secretions of NO ( P 〈 0. 01 ). BU-6E markedly inhibited secretion of TNF-α, IL-6 and IL-1 β in dose-dependent manner. In vivo: Compared with model group, BU-6E groups extremely significantly reduced the levels of TNF-α and IL-β( P 〈 0.01 ) , markedly lowered the concentrations of IL-6 (P 〈 0.05 ). : Conclusion BU-6E has anti- inflammatory effects in vitro and in vivo, and could significantly decrease release of NO and the secretion of in- flammatory factors activated by LPS.
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