Lavandula stoechas significantly alleviates cigarette smoke-induced acute lung injury via modulation of oxidative stress and the NF-κB pathway

Cigarette smoke (CS) is one of the major triggering factorsfor oxidative stress and contributes to development of acute lung injury and acute respiratory distress syndrome (ALI/ARDS), both of which are marked by severe lung inflammation. Due to the absence of viable treatment options for ALI/ARDS, methanolic extract of Lavandula stoechas (Ls.Met) was used to evaluate the protective effect against CS-induced ALI in both in vivo and in vitro settings. In order to prepare CS-induced ALI murine models, male Swiss albino mice were exposed to whole-body CS for 10 days. Normal saline (10?mL/kg), Ls.Met (250, 450, 750?mg/kg), and dexamethasone (1?mg/kg) were administered orally to respective animal groups (n?=?5/group) 1?h prior to CS-exposure. Twenty-four hrs following the last CS-exposure, bronchoalveolar lavage fluid (BALF) and lungs were harvested to examine the important aspects of ALI. Subsequently, in vitro protective effect of Ls.Met (10 and 100?μM) was assessed against 4% CSE (for 24?h)-stimulated RAW 264.7 macrophages. The presence of phenols and flavonoids was verified by HPLC analysis. Ls.Met dose-dependently and remarkably reduced macrophages and neutrophil invasion into the lungs, lung weight coefficient, albumin exudates into the alveoli, and improved hypoxemia and lung histopathological alterations. Notably, Ls.Met attenuated the CS-induced oxidative stress as evidenced by decreased levels of malondialdehyde, total oxidant status (TOS), and myeloperoxidas, alongside enhanced total antioxidant capacity (TAC) production. Moreover, Ls.Met demonstrated a marked reduction in CS-induced overexpression of proinflammatory cytokines (IL-6, IL-1β, and KC) and inhibited the activation of NF-κB, a key signalling pathway involved in inflammation. Lavandula stoechas could thus be a potential therapeutic option for the treatment of CS-induced ALI.

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