Protective effects of lavender oil on sepsis-induced acute lung injury via regulation of the NF-κB pathway

• Published in: Pharmaceutical biology Vol. 60; no. 1; pp. 968 - 978
• Main Authors: Xie, Qian, Wang, Yi, Zou, Guo-Liang
• Format: Journal Article
• Language: English
• Published: England Taylor & Francis 01.12.2022; Taylor & Francis Ltd; Taylor & Francis Group
• Subjects: Anti-inflammatory agents; Apoptosis; BAX protein; Bcl-2 protein; Caecal ligation and puncture; Caspase-3; Deactivation; Enzyme-linked immunosorbent assay; Glutathione; inflammation; Interleukin 6; Lungs; NF-κB protein; Nitric oxide; Nitric-oxide synthase; Oxidative stress; Peroxidase; Sepsis; Superoxide dismutase; Tumor necrosis factor-α; Tumors; Caecal ligation and puncture; apoptosis; inflammation; oxidative stress
• ISSN: 1388-0209; 1744-5116
• DOI: 10.1080/13880209.2022.2067570

Lavender oil (Lav) from Lavandula angustifolia L. (Lamiacease) exhibits antioxidative and anti-inflammatory properties against various diseases. The study explores the effect of Lav pre-treatment on sepsis-induced acute lung injury (ALI). Sprague-Dawley rats were assigned into Sham, caecal ligation and puncture (CLP), CLP + Lav (200, 400, and 800 mg/kg) groups. Lav was administered by gavage, once a day, for 7 days. Histological analysis was performed using haematoxylin and eosin staining. Cytokine and nitrite levels were detected by enzyme-linked immunosorbent assay kits and Griess reagent. Gene and protein expression were tested by quantitative real-time polymerase chain reaction and western blot. The levels of tumour necrosis factor-α (BALF: 64%, serum: 59%), interleukin (IL)-1β (BALF: 63%, serum: 66%) and IL-6 (BALF: 54%, serum: 59%), and nitrite (40%) and inducible nitric oxide synthase (51%), and the level of myeloperoxidase (66%) and malondialdehyde (59%), and cleaved-caspase 3 (84%) and Bax expression (74%) induced by CLP were decreased when given Lav. Additionally, the level of superoxide dismutase (211%) and glutathione (139%), and the expression of Bcl-2 (980%) induced by CLP were increased when given Lav. The increased p-nuclear factor (NF)-κB/NF-κB (72%) and p-inhibitor of κBα (IκBα)/IκBα (77%) induced by CLP could be reversed by Lav. Lav pre-treatment might protect rats from sepsis-induced ALI via deactivation of the NF-κB pathway. Our research demonstrated the regulatory mechanisms of Lav in sepsis-induced ALI and can provide a theoretical basis for the use of Lav in the treatment of sepsis-induced ALI.