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阿司匹林对脂多糖和猪肺泡巨噬细胞PKC和PTP活性变化的影响 被引量:2

Effects of aspirin on PKC and PTP activities induced by LPS in porcine alveolar macrophages in vitro
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摘要 目的 探讨脂多糖 (LPS)刺激后猪肺泡巨噬细胞蛋白激酶C(PKC)、蛋白酪氨酸磷酸酶 (PTP)活性变化及阿司匹林的干预效果。方法 LPS刺激猪肺泡巨噬细胞 (AM) ,并单独或联用阿司匹林、CalphostinC以及过氧钒酸盐进行干预 ,分别测定其胞质PKC和PTP活性。结果 LPS(1 μg/ml)刺激后 ,AMPKC活性在 5min即显著升高 ,并于 1 0min达到峰值 ;AM胞质内PTP相对活性水平则逐渐减低 ,低谷出现在LPS刺激后 1 5min。治疗剂量阿司匹林可抑制LPS引起的AMPKC活性增加 ,并明显抑制LPS引起的AMPTP活性降低。PTP抑制剂POV可相对增强LPS刺激后AMPKC活性 ,阿司匹林能减低该效应 ;PKC非特异性抑制剂CalphostinC可使LPS引起的AMPTP活性降低有轻微回升 ,阿司匹林与之具协同效应。结论 阿司匹林对可通过影响AM蛋白激酶 磷酸酶系统平衡 。 Objective To study the effects of aspirin on the changes of protein kinase C (PKC) and protein tyrosine phosphatase (PTP) activities induced by lipopolysaccharide (LPS) in cultured porcine alveolar macrophages (AM). Methods LPS was used to stimulate the AM with or without the intervention of aspirin, calphostin C and peroxovandium (POV), then the PKC and PTP activity was assayed respectively. Results The PKC activity in AM was increased markedly 5 min after being stimulated with LPS, and reached to the peak value at 10 min. On the contrary, the PTP activity reduced gradually, and to the bottom about 15 min after the stimulation with LPS. Aspirin inhibited the increase of PKC activity and the decrease of PTP markedly in AM induced with LPS. PTP inhibitor POV increased the PKC activity indirectly in AM, and aspirin weakened this effect. But the unspecific PKC inhibitor calphostin C increased the PTP activity gently, and aspirin had synergistic effects on it. Conclusion Aspirin can adjust the alteration of PKC and PTP activities in AM induced with LPS, suggesting that aspirin can exert its anti inflammation effect by interfering the signal protein phosphorylation through its effect on the balance of protein kinase protein phosphatase.
出处 《第三军医大学学报》 CAS CSCD 北大核心 2002年第7期786-789,共4页 Journal of Third Military Medical University
基金 国家自然科学基金资助项目 ( 3 980 0 0 64)
关键词 肺泡巨噬细胞 磷酸酶 蛋白激酶 阿司匹林 脂多糖 phosphatase protein kinases aspirin lipopolysaccharide
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  • 1Bone RC, Balk RA, Cerra FB et al. Definitions for sepsis and organ failure and guidelines for the use of innovative therapies in sepsis. The ACCP/SCCM Consensus Conference Committee. American College of Chest Physicians Isociety of Critical Care Medicine. Chest, 1992, 101 (6) : 1644.
  • 2Bone RC. Sepsis, sepsis syndrome and the systemic inflammatory syndrome (SIRS). JAMA, 1995,273(2): 155.
  • 3Way LW ed. Current Surgical Diagnosis and Treatment. 10ed. Norwalk:App leton, 1994,94-128.
  • 4Pinsky MR, Dhainaut JA. Pathophysiologic Fondations of Critical Care. 1 ed. Baltimore: Williams, 1993,170-187.
  • 5Byan KM, Ernst MK, Rice NR et al. Role of NF-κB in p53-midiated programmed cell death. Nature, 2000, 404 (20) :892.
  • 6Schwartz MD, Moore EE, Moore FAet al. Nuclear factor - kappa B is activated in alveolar macrophages from patients with acute respiratory distress syndrome. Crit Care IVied, 1996,24(8) : 1285.
  • 7Tritos N,Kitraki E, Philippidis H et al. Neurotransmitter modulation of glucocorticoid receptor mRNA levels in the rat hippocampus. J Neuroendocrindogy, 1999,69(5) : 324.
  • 8Blackwell TS, Blackwell TR, HokdenN EP et al. In vivo antioxidant treatment suppresses NF-κB activation and neutrophilic lung inflammation. J Immunol, 1996,157 (4) : 1630.
  • 9Yumi Y, Richard BG. Therapeutic potential of inhibition of the NF-κB pathway in the treatment of inflammation and cancer. J Clin Invest,2001,107(2) :135.
  • 10Nemeth ZH, Deitch EA , Szabo C et al. Pyrrolidine dithiocarbamate inhibits NF-kappa B activation and IL-8 production in intestinal epithelial cells. Immunol Lett, 2003,85(1) :41.

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