To investigate the effects of carvacrol on helper T cell subtypes and 2 asthma-related symptoms

學生姓名: 張祐誠
指導教授: 吳彰哲
學期: 109上
摘　　要: Asthma is a chronic inflammatory disorder of the airways with chronic airway inflammation and airway remodeling. Progression of asthma is accompanied by activation of T helper cells which are considered the key driver of the inflammatory response in asthma. Naïve T cells will differentiate into Th1 (Helper T cell type 1), Th2, and Treg cells according to the purpose. CD4+ 17 T cells play an important role in lunginflammation in asthma by releasing cytokines and start a cascade of inflammatory mediators to initiate and perpetuate the inflammatory response. In addition, it was found that the expression of reactive oxygen species (ROS) and reactive nitrogen (RNS) increased in asthma patients. These substances induce oxidative stress and inflammatory processes contributing to allergic asthma. Carvacrol has antioxidative, anti-inflammatory, antimicrobial, antitussive, anti-tumor, neuroprotective and smooth muscle relaxant pharmacological effects. In this report, the effects of carvacrol on improving the balance
of Th cells in asthmatic mouse models and its anti-inflammatory properties on asthma26 related symptoms will be investigated. Kianmehr et al. showed that carvacrol potentiated Th1 and Treg cells but reduced Th2 and Th17 cells leading to improvement of Th1/Th2 imbalance. Furthermore, carvacrol reduced the activities of proinflammatory cytokines as well as relevant cell subtypes, finally alleviating asthma-related symptoms. Ezz-Eldin et al. showed that carvacrol attenuated histopathologic changes and inflammatory cell infiltration in the lung, and decreased the levels of Th2 cytokines in asthmatic mice. In addition, carvacrol reduced the inflammatory response by reducing the oxidative stress produced by ROS and RNS. In conclusion, carvacrol can inhibit pro-inflammatory cytokines and oxidative stress to ameliorates asthma-related symptoms. In conclusion, carvacrol ameliorates asthma-related symptoms by regulating helper T cell subtypes and inhibiting pro-inflammatory cytokines and oxidative stress.