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粉防己碱对雄黄所致小鼠免疫功能低下的影响

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摘要 目的:探讨雄黄中毒所致小鼠免疫功能低下后粉防己碱(Tet)的调节作用。方法:取小鼠随机分为正常对照组,模型对照组,粉防己碱(tetrandrine,Tet)高、中、低剂量组,二巯基丙磺酸钠(DMPS)组。正常对照组给予生理盐水,模型组灌胃给予70mg/kg雄黄混液,Tet高、中、低剂量组分别腹腔注射给予Tet98.0、49.0、24.5mg/kg,连续42d。采用重量法称量小鼠脾脏和胸腺质量,以其质量与体质量之比作为胸腺和脾脏指数。Giemsa染色计数腹腔巨噬细胞(PM圣)并计算吞噬百分率和吞噬指数。用比色法测定红细胞(RBC)裂解释放的空斑形成细胞(PFC)置。观察Giemsa染色后淋巴细胞个数并计算母细胞转化率。结果:Tet能增加小鼠脾脏和胸腺的重量,增强小鼠PMO的吞噬能力(P〈0.01),提高小鼠溶血值,增加PFC数(P〈0.01),能提高小鼠淋巴细胞转化率(P〈0.01),且有一定剂量差异。结论:对于雄黄所致的小鼠免疫功能低下,Tet的免疫增强作用可能是能使胸腺和脾脏重量增加,PM中的吞噬能力增强,淋巴细胞的转化率升高及抗体能力加强等作用有关。
出处 《长江大学学报(自然科学版)》 CAS 2012年第1期1-3,13,共4页 Journal of Yangtze University(Natural Science Edition)
基金 湖北省科技攻关项目(2006AA301C34)
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参考文献5

  • 1John Farmer, Green Shift. Towards a green sensibility in architecture. New York: USA Technology Future Inc, 1996
  • 2Pang L, Hoult J R. Cytotoxicity to macrophages of tetrandrine, an antisilicosis alkaloid, accompanied by on overproduction of prostaglandins [J]. BiochemPharmacol, 1997, 53 (6): 773-779.
  • 3Michael. J.Crosbie. Green Architecture-A guide to sustainable design. Massachusetts:Rockport publishers, 1994
  • 4Shen Y C, Chen C F, Wang S Y, et al. Impediment to calcium influx and reactive oxygen production accounts for the inhibition of neutrophil Mac-1 up-regulation and adhesion by tetrandrine [J] . Mol Pharmacol, 1999, 55 (1) : 186-191.
  • 5LAI Jenn-HaungRheumatology/Immunology and Allergy, Department of Medicine, Tri-Service General Hospital, National Defense Medical Center, Taipei, Taiwan, China.Immunomodulatory effects and mechanisms of plant alkaloid tetrandrine in autoimmune diseases[J].Acta Pharmacologica Sinica,2002,23(12):1093-1101. 被引量:18

二级参考文献83

  • 1Schirmer M, Vallejo AN, Weyand CM, Goronzy JJ. Resistance to apoptosis and elevated expression of Bcl-2 in clonally expanded CD4+CD28- T cells from rheumatoid arthritis patients. J Immunol 1998; 161: 1018-25.
  • 2Nishioka K, Hasunuma T, Kato T, Sumida T, Kobata T.Apoptosis in rheumatoid arthritis: a novel pathway in the regulation of synovial tissue. Arthritis Rheum 1998; 41: 1-9.
  • 3Eguchi K. Apoptosis in autoimmune diseases. Internal Med 2001; 40: 275-84.
  • 4Nagata S. Apoptosis by death factor. Cell 1997; 88: 355-65.
  • 5Jacobson MD, Weil M, Raft MC. Programmed cell death in animal development. Cell 1997; 88: 347-54.
  • 6Utz PJ, Hottelet M, Schur PH, Anderson P. Proteins phos-phorylated during stress-induced apoptosis are common targets for autoantibody production in patients with systemic lupus erythematosus. J Exp Med 1997, 185: 843-54.
  • 7Rosen A, Casciola-Rosen L. Autoantigens as substrates for apoptotic proteases: implications for the pathogenesis of systemic autoimmune disease. Cell Death Differ 1999; 6: 6-12.
  • 8Levine JS, Koh JS, Pender MP. The role of apoptosis in autoimmunity: immunogen, antigen, and accelerant: Genetically determined failure of activation-induced apoptosis of autoreactive T cells as a cause of multiple sclerosis. Semin Neohrol 1999; 19: 34-47.
  • 9Rovere P, Sabbadini MG, Fazzini F, Bondanza A,Zimmermann VS, Rugarli C, etaL Remnants of suicidal cells fostering systemic autoaggression. Apoptosis in the origin and maintenance of autoimmunity. Arthritis Rheum 2000,43: 1663-72.
  • 10Schirmer M, Vallejo AN, Weyand CM, Goronzy JJ. Resistance to apoptosis and elevated expression of Bcl-2 in clonally expanded CD4+CD28- T cells from rheumatoid arthritis patients. J Immunol 1998; 161: 1018-25.

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