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It is also not clear in these patients whether the lung production of H2S was altered. In any rate, this clinical study was mirrored by a later animal study. Chen et al. (2009a) found that serum H2S level in ovalbumin-treated asthma rats decreased by 81% and H2S production from the lungs in these rats decreased by 80%. The CSE expression level and CSE activity were decreased significantly in lung tissues from ovalbumin-treated mice, which may explain the decreased endogenous levels of H2S in lung tissues and serum in these animals. Chen et al. (2009a) also found that the peak expiratory flow was 55.4% lower in ovalbumin-treated rats than that of control rats, and the proportions of eosinophils, lymphocytes and neutrophils in bronchoalveolar lavage fluid were significantly increased. Administration of exogenous H2S (NaHS) Cobimetinib datasheet improved peak expiratory PD-1/PD-L1 inhibitor 2 flow and alleviated airway inflammation and airway remodelling in this rat model. Mitochondrial dysfunction and oxidative stress are associated with the development and progression of asthma (Reddy, 2011). Activated inflammatory cells generate more reactive oxygen species. In contrast, antioxidants decreased mitochondrial dysfunction and oxidative stress in asthmatic mice (Mabalirajan et al. 2009). Antioxidants have been used to prevent and treat mitochondrial abnormality in asthma patients (Gvozdj��kov��et al. 2005). Macromolecule antioxidants, such as vitamins E and C, cannot enter mitochondria to scavenge reactive oxygen species. In contrast, the gasotransmitter H2S can freely cross the plasma membrane and the mitochondrial membrane. Once inside mitochondria, H2S acts as a reducing agent, which can help to decrease oxidative stress and enhance endogenous antioxidant defenses, leading to the preservation of both mitochondrial structure and function (Elrod et al. 2007). Hu et al. (2009) ALG1 reported that H2S prevented rotenone-induced mitochondrial membrane depolarization, cytochrome c release and a decrease in Bcl-2:Bax ratio in a human-derived dopaminergic neuroblastoma cell line. These protective effects of H2S may be mediated by mitochondrial ATP-sensitive potassium (KATP) channels. To date, whether H2S can attenuate airway inflammation and hyper-responsiveness in asthma by affecting the mitochondrial/oxidative stress pathway is not clear. Hydrogen sulfide induces smooth muscle relaxation via its actions on two different types of ion channels. One is the KATP channel located on vascular SMCs and the other is the small to medium conductance KCa channel located on vascular endothelial cells. The opening of these two channels by H2S leads to membrane hyperpolarization and smooth muscle relaxation. Therefore, H2S can be characterized as an endothelium-derived relaxing factor (Wang, 2011).