Vericiguat mitigates inflammation and oxidative stress in lung tissue of rats with experimental asthma

Asthma is a chronic inflammatory airway disorder characterized by bronchial obstruction, airway hyperresponsiveness (AHR), and structural remodeling. Immune mediators, including interleukin‑6 (IL‑6), interleukin‑10 (IL‑10), interleukin‑17 (IL‑17), and tumor necrosis factor‑α (TNF‑α), together with oxidative stress, contribute to disease progression. Vericiguat, a soluble guanylate cyclase (sGC) stimulator acting through the nitric oxide–sGC–cyclic guanosine monophosphate (NO–sGC–cGMP) pathway, promotes smooth muscle relaxation and reduces hypertrophy, inflammation, and fibrosis. This study evaluated the antioxidant and anti‑inflammatory effects of vericiguat in an ovalbumin (OVA)‑induced asthma model in rats. Twenty‑five adult male Wistar rats were assigned to five groups: control, Asthma, dexamethasone 2.5 mg/kg, vericiguat 1 mg/kg, and vericiguat 0.5 mg/kg. Asthma was induced by OVA sensitization (intraperitoneal) followed by inhalation challenge. After induction, animals received treatments for seven days. Twenty‑four hours after the final dose, rats were euthanized, and lung tissues were collected. Left‑lung homogenates were analyzed for oxidative stress markers—glutathione peroxidase (GPX), superoxide dismutase (SOD), malondialdehyde (MDA), and total antioxidant capacity (TAC) as well as cytokines (TNF‑α, IL‑6, IL‑10, IL‑17) and nitric oxide (NO). Right‑lung samples were processed for hematoxylin and eosin (H&E) histopathology. OVA exposure increased TNF‑α, IL‑6, IL‑17, MDA, and NO while reducing GPX, SOD, TAC, and IL‑10. Vericiguat significantly reversed these alterations and reduced airway inflammation histologically. Vericiguat at both doses improved oxidative and inflammatory parameters in asthmatic rats, supporting its potential therapeutic relevance.