Abstract
Hydroxysafflor yellow A (HSYA) is a chemical component isolated from the Chinese medicine Carthamus tinctorius L. HSYA has numerous pharmacological effects, including protecting against and mitigating some respiratory diseases such as acute lung injury and chronic obstructive pulmonary disease; however, its effect on asthma remains unclear. We previously found that HSYA attenuated ovalbumin-induced allergic asthma in guinea pigs. Platelet activating factor (PAF) is a phospholipid mediator of inflammation and an important factor in the pathological process of asthma. In this study, we investigated the anti-inflammatory effects of HSYA and its underlying mechanisms in PAF-induced human small airway epithelial cells (HSAECs). PAF-activated cells were pretreated with HSYA and/or the PAF receptor inhibitor, ginkgolide B, and we observed changes in the expression of interleukin (IL)-1β, IL-6, and tumor necrosis factor alpha, monolayer permeability of HSAECs, and inflammatory signaling pathways. HSYA attenuated the PAF-induced increase in expression of inflammatory factors and destruction of cell-barrier function, and inhibited the expression of protein kinase C, mitogen-activated protein kinases, activator protein-1, and nuclear factor-κB activation induced by PAF. These findings suggest that HSYA may represent a potential new drug for the treatment of asthma.
Highlights
Bronchial asthma is a chronic inflammatory airway disease characterized by allergic airway inflammation, airway remodeling, and airway hyperresponsiveness (AHR) (Liu et al, 2017)
We measured the effects of Hydroxysafflor yellow A (HSYA) on IL-6, IL-1β, and TNF-α mRNA expression levels in platelet activating factor (PAF)-stimulated human small airway epithelial cells (HSAECs) by Real-Time Polymerase Chain Reaction (RT-PCR)
Expression levels were reduced by pretreatment with various concentrations of HSYA (9, 27, and 81 μmol/L) compared with the PAF group, in a concentration-dependent manner. mRNA levels of these cytokines were reduced almost to control levels in cells treated with PAF + ginkgolide B (GB) and PAF + GB + HSYA
Summary
Bronchial asthma (asthma) is a chronic inflammatory airway disease characterized by allergic airway inflammation, airway remodeling, and airway hyperresponsiveness (AHR) (Liu et al, 2017). Inhibiting the inflammatory response is an important means of relieving symptoms in patients with asthmatic diseases (Chung, 1986; Locksley, 2010; Kim et al, 2013). The occurrence and development of asthma inflammation involve a large number of inflammatory mediators, including platelet activating factor (PAF), which plays an important role in the pathological process of asthma. Binding of PAF to its receptor triggers inflammatory downstream signal transduction, including activation of protein kinase C (PKC), causing an increase in cellular calcium levels. Inhibiting the PAF-induced inflammatory response represents an important means of relieving AHR and treating asthma
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