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引用本文:伏建峰,赵华,史清海,周郁,刘正祥,冉继华,葛迪,李晓玲,何雁,张红明,余元伦.栀子苷拮抗内毒素的实验研究[J].中国现代应用药学,2013,30(4):352-356.
FU Jianfeng,ZHAO Hua,SHI Qinghai,ZHOU Yu,LIU Zhengxiang,RAN Jihua,GE Di,LI Xiaoling,HE Yan,ZHANG Hongming,YU Yuanlun.Anti-lipopolysaccharide Activity Study of Jasminoidin[J].Chin J Mod Appl Pharm(中国现代应用药学),2013,30(4):352-356.
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栀子苷拮抗内毒素的实验研究
伏建峰1, 赵华2, 史清海1, 周郁1, 刘正祥1, 冉继华1, 葛迪1, 李晓玲1, 何雁1, 张红明1, 余元伦1
1.兰州军区乌鲁木齐总医院,全军临床检验诊断中心,乌鲁木齐 830000;2.兰州军区乌鲁木齐总医院,耳鼻咽喉头颈外科,乌鲁木齐 830000
摘要:
目的 研究栀子苷的抗内毒素生物学活性。方法 应用生物传感器技术检测栀子苷与内毒素(LPS)活性中心Lipid A的结合活性、动态比浊法鲎试验检测栀子苷(0,2.5,5.0,10.0 mg·L-1)对LPS(0.1 μg·L-1)的中和活性、ELISA法检测栀子苷(0,25,50,100 mg·L-1)对LPS(100 μg·L-1)刺激RAW264.7细胞释放细胞因子的影响,进而观察栀子苷(10,20,40 mg·kg-1)对致死剂量LPS攻击模型小鼠的保护作用。结果 栀子苷与Lipid A具有结合活性,量效关系明显;栀子苷(2.5,5.0,10.0 mg·L-1)在体外对LPS(0.1 μg·L-1)具有显著的直接中和作用(P<0.01);栀子苷在50~100 mg·L-1能够显著抑制LPS(100 μg·L-1)刺激RAW264.7细胞释放TNF-α(P<0.01);40 mg·kg-1的栀子苷对脓毒症模型小鼠具有显著的保护作用(P<0.01)。结论 栀子苷可能通过与Lipid A结合中和LPS的活性,抑制LPS介导的细胞活化,减少细胞因子释放,进而保护脓毒症模型小鼠。
关键词:  栀子苷  内毒素  脓毒症
DOI:
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基金项目:国家自然科学基金面上项目(81071535)
Anti-lipopolysaccharide Activity Study of Jasminoidin
FU Jianfeng1, ZHAO Hua2, SHI Qinghai1, ZHOU Yu1, LIU Zhengxiang1, RAN Jihua1, GE Di1, LI Xiaoling1, HE Yan1, ZHANG Hongming1, YU Yuanlun1
1.Urumqi General Hospital, Lanzhou Military, Clinical Laboratory Diagnostic Center, Urumqi 830000, China;2.Urumqi General Hospital, Lanzhou Military, Department of Otolaryngology, Urumqi 830000, China
Abstract:
OBJECTIVE To investigate the anti-lipopolysaccharide(LPS) activity of jasminoidin in vitro and in vivo. METHODS The binding activity of jasminodin to Lipid A and the neutralization on LPS were detected by the biosensor technology and kinetic turbidimetric limulus test. Meanwhile, ELISA was used to measure the release of cytokine from RAW264.7 cells exposure to LPS with or without pretreatment of jasminoidin. Furthermore, the protective effect on mice subjected to lethal dose of LPS challenge with or without treatment of jasminoidin was observed. RESULTS Jasminoidin had binding activity to Lipid A and significantly neutralized LPS(0.1 μg·L-1) in dose of 2.5, 5.0, 10.0 mg·L-1(P<0.01). Subsequently, the release of TNF-α from RAW264.7 cells exposure to LPS(100 μg·L-1) was significant attenuated by pretreatment with jasminoidin in the dose of 50, 100 mg·L-1(P<0.01). In vivo experiment, jasminoidin could significant protect mice against a lethal challenge with LPS at the dose of 40 mg·kg-1(P<0.01). CONCLUSION Jasminoidin can neutralize LPS and suppress the activating of RAW264.7 cells induced by LPS. In vivo, jasminoidin can significantly protect mice against a lethal challenge with LPS. Jasminoidin has anti-lipopolysaccharide activity.
Key words:  jasminoidin  lipopolysaccharide  sepsis
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