Abstract
Coronavirus disease 2019 (COVID-19), caused by SARS-CoV-2, has induced a worldwide pandemic since early 2020. COVID-19 causes pulmonary inflammation, secondary pulmonary fibrosis (PF); however, there are still no effective treatments for PF. The present study aimed to explore the inhibitory effect of dihydroartemisinin (DHA) on pulmonary inflammation and PF, and its molecular mechanism. Morphological changes and collagen deposition were analyzed using hematoxylin-eosin staining, Masson staining, and the hydroxyproline content. DHA attenuated early alveolar inflammation and later PF in a bleomycin-induced rat PF model, and inhibited the expression of interleukin (IL)-1β, IL-6, tumor necrosis factor α (TNFα), and chemokine (C-C Motif) Ligand 3 (CCL3) in model rat serum. Further molecular analysis revealed that both pulmonary inflammation and PF were associated with increased transforming growth factor-β1 (TGF-β1), Janus activated kinase 2 (JAK2), and signal transducer and activator 3(STAT3) expression in the lung tissues of model rats. DHA reduced the inflammatory response and PF in the lungs by suppressing TGF-β1, JAK2, phosphorylated (p)-JAK2, STAT3, and p-STAT3. Thus, DHA exerts therapeutic effects against bleomycin-induced pulmonary inflammation and PF by inhibiting JAK2-STAT3 activation. DHA inhibits alveolar inflammation, and attenuates lung injury and fibrosis, possibly representing a therapeutic candidate to treat PF associated with COVID-19.
Highlights
On 11 March 2020 World Health Organization (WHO) declared Coronavirus Disease 2019 (COVID-19), a respiratory disease caused by the SARS-CoV-2 virus, as a pandemic [1]
As visualized by hematoxylin and eosin (H&E) staining (Figure 1A), the lung tissues from the control group of rats had intact alveoli, while the lung tissues from the rats stimulated with BLM exhibited obvious inflammatory cell infiltration in the alveolar cavity, pulmonary edema accompanying septal thickness, damage to the lung architecture, and alveolar disarray
The chemokine Ligand 3 (CCL3) level in the blood of rats treated with DHA2 decreased significantly. These findings suggested that CCL3 plays an important role in pulmonary inflammation and Pulmonary fibrosis (PF), and that DHA inhibits CCL3 expression to attenuate pulmonary inflammatory responses and PF
Summary
On 11 March 2020 World Health Organization (WHO) declared Coronavirus Disease 2019 (COVID-19), a respiratory disease caused by the SARS-CoV-2 virus, as a pandemic [1]. The latest figures from 12th December 2021 show that more than 270 million people have been infected with the virus, causing more than 5.32 million www.aging‐us.com deaths worldwide. SARS-CoV-2 crosses borders and races, and infects patients of any age via person-toperson transmission [2]. The disease causes a wide range of symptoms, from asymptomatic to respiratory failure [3, 4]. Pulmonary fibrosis (PF) is a possible complication of pulmonary involvement in COVID-19, which is a chronic, progressive, and fatal form of fibrosing interstitial pneumonia [5, 6]. The interstitial matrix widens during the progression of PF and the normal pulmonary parenchyma becomes compressed, leading to respiratory failure
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
