ArticleNaunyn-Schmiedeberg's archives of pharmacology2026
Myrtenol inhalation ameliorates lung injury induced by cigarette smoke in rats: the role of inflammation and oxidative stress.
Article in Naunyn-Schmiedeberg's archives of pharmacology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Cigarette smoke is a major contributor to chronic lung injury through oxidative stress, inflammation, and structural damage. Myrtenol, a natural monoterpene, exhibits anti-inflammatory and antioxidant properties. This study evaluated the protective effects of inhaled myrtenol against cigarette smoke-induced lung injury in rats. Twenty male Wistar rats were divided into four groups: control, cigarette smoke (CS), CS + myrtenol (50 mg/kg via inhalation), and CS + budesonide. Rats were exposed to cigarette smoke for 4 weeks. Inflammatory markers (tumor necrosis factor alpha [TNF-α] and interleukin-10 [IL-10]) and oxidative stress parameters (malondialdehyde [MDA], total antioxidant capacity [TAC], and superoxide dismutase [SOD]) in lung tissue and bronchoalveolar lavage fluid (BALF) were measured by ELISA. Gene expression of MUC5AC and matrix metalloproteinase 21 (MMP-21) in lung tissue was assessed by real-time PCR. Serum cotinine levels were measured, and histopathology was performed using H&E staining. Myrtenol significantly mitigated CS-induced lung injury. Treatment reduced TNF-α, MDA, MUC5AC, MMP-21, and serum cotinine levels, while increasing IL-10, TAC, and SOD compared with the CS group. Histological analysis showed decreased inflammatory infiltration and improved tissue structure. Effects were comparable to those of budesonide. Inhaled myrtenol exerts potent anti-inflammatory and antioxidant effects, reduces oxidative and inflammatory markers, and protects lung structure against chronic cigarette smoke exposure. These findings suggest myrtenol as a promising therapeutic agent for smoke-related pulmonary disorders.
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