學生姓名:
張祐誠
學期:
108下
摘 要:
Asthma is a chronic inflammatory, allergic disorder of the airways, which is characterized by inflammatory cells infiltration, airway inflammation, mucus hypersecretion and airway hyperresponsiveness (AHR). So far, it is estimated that 300 million individuals are affected by the disease worldwide. T helper 2 cell plays a pivotal role in the pathogenesis process of allergic asthma by producing the Th2 cytokines. These cytokines induce release of Immunoglobin E and the infiltration of eosinophils into the lungs, which lead to the development of allergic asthma. The nuclear factor κB (NF-κB) transcription factor drives the expression of target genes that regulate pro-inflammatory cytokines and chemokines. Asthmatic inflammation is linked to the persistent activation of NF-κB. Propofol is a widely used intravenous anesthetic and sedative agent with bronchodilatory effect. In this report, the effects of propofol on reducing the symptoms of allergic asthma by suppressing Th2 immune response and NF-κB signaling pathway will be investigated. Zhang et al. showed that propofol alleviated airway inflammation, attenuated histopathologic changes in the lung, and decreased the levels of IgE, Interleukin-4, IL-5 and IL-13 in asthmatic mice. Furthermore, propofol inhibited the activation of NF-κB in vitro and in vivo. Li et al. showed that propofol reduced the pro- inflammatory factors Tumor necrosis factor-α and IL-6, achieved protective effects by down-regulating the Toll-like receptor-4/Myeloid differentiation factor 88/NF-κB signal pathway. In conclusion, propofol can inhibit cytokine expression and NF-κB activation to ameliorates asthma-related symptoms.
專題討論_20200408_張祐誠_摘要.pdf