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升清降浊丸对免疫性肝损伤模型小鼠细胞因子TNF-α、IL-4、IL-6、IFN-γ的影响 被引量:7

Lab Study of Shengqingjiangzhuo Pill on Cell Factor of TNF-α,IL-4,IL-6,IFN-γ in Immunity Hepatic Injury Mice
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摘要 目的:观察升清降浊丸对免疫性肝损伤模型小鼠细胞因子的作用机理。方法:将90只昆明小鼠随机分为6组,正常对照组,BCG+LPS模型组,香菇多糖片阳性药+BCG+LPS对照组,中药小剂量+BCG+LPS组,中药中剂量+BCG+LPS组,中药大剂量+BCG+LPS组,各组分别给予相应药物。观察升清降浊丸对免疫性肝损伤模型小鼠细胞因子TNF-α、IL-4、IL-6、IFN-γ的影响。结果:实验中升清降浊丸能明显抑制肝损伤小鼠血清丙氨酸氨基转移酶(ALT)和门冬氨酸氨基转移酶(AST)活性;抑制细胞因子肿瘤坏死因子,白介素6(TNF-α,IL-6)的水平;降低脾细胞产生Thl型细胞因子干扰素-γ(IFN-γ)的能力;降低Th2型细胞因子白介素4(IL-4)的含量。结论:升清降浊丸对细胞免疫和体液免疫均有一定的调节作用。 Objective, To probe the mechnanism of Shengqingjiangzhuo Pill on cell factor TNF-α, IL-4, IL-6, IFN-γ in the immunity Hepatic injury mice . Method: 90 mice were divided into control group, model group, positive group, high dose group , middle dose group and high dose group randomly. The content of ALT , AST, TNF-α, IL-4, IL-6 and IFN-γwere determined. Results: The content of ALT ,AST TNF-α, IL-6 and IL-4 were decreased; the ptoducing of IFN-γ in Thl type cell of spleen cell was inhibited. Conclusion: Shengqingjiangzhuo Pill has effects on cell immunity and humoral immunity.
作者 王菲 张书文
出处 《世界中西医结合杂志》 2007年第4期210-212,共3页 World Journal of Integrated Traditional and Western Medicine
基金 河南省科技厅基金资助项目
关键词 乙型病毒性肝炎 升清降浊丸 实验研究 免疫性肝损伤 B type virus hepatitis Shengqijiangzhuo pill lab study immunity Hepatic injury
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  • 1胡大荣,谢青.几种治疗重型肝炎药物对急性肝损害动物存活率的影响[J].中华传染病杂志,1993,11(2):104-105. 被引量:4
  • 2戴俐明,高本波,徐叔云.丹皮总甙肝保护作用的研究[J].中国药理学通报,1994,10(1):58-60. 被引量:19
  • 3唐世刚,董克礼.肿瘤坏死因子在重型肝炎发病机制中的作用[J].中华传染病杂志,1994,12(4):229-230. 被引量:7
  • 4范开.细菌脂多糖对小鼠巨噬细胞生长的调节作用[J].中华肝脏病杂志,1996,4(2):94-96. 被引量:3
  • 5Moncada S, Marina R, Diane E et al. Hepatic nitric oxide production following acute endotoxemia in rats in mediated by increased inducible nitric oxide synthas geneexpression. Hepatology, 1995,22(1) :223.
  • 6Kerr J, Wyllie A, Currie A. Apoptosis:a basic biological phenomenom with wideranging implication in tissue kinetics.Br J Cancer, 1992,26: 239.
  • 7Lwao K, Soichiro M, Hajime H et al. Increased intric oxide synthase activity as a cause of mitochondrial dysfunction in rat hepatocytes. Hepatology, 1996,24: 1185.
  • 8Tsuji H, Harada A, Mukaida N et al. Tumor necrosis factor receptor P55 is essential for intrahepatic granloma formation and hepatocelluar apoptosis in a murine model of bacterium-induced fulminant hepatitis. Infet-Tmmun, 1997,65(5): 1892 ~ 1898.
  • 9Harbrecht B G, Billiar T R, Stadler J et al. Inhibition of nitric oxide synthesis during endotoxemia promotes intrahepatic thrombosis and an oxygen radicalmediated hepatic injury. J Leuk Biol, 1992,52:390.
  • 10Hespeling U, Jungermann K, Puschel G P. Feedbackinhibition of glucagon-stimulated glycogenolysis in heptocyte/ kupffer cell cocultures by glucagon-elicited prostaglandin production in kupffer cells. Hepatology. 1995, 22:1577.

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