Citronellol exerts lung protective and anti‐inflammatory effects through hampering NF‐κB in lipopolysaccharide‐induced acute lung injury in mice

香茅醇 脂多糖 生理盐水 肺 医学 药理学 肿瘤坏死因子α 促炎细胞因子 炎症 恶化 免疫学 内科学 化学 精油 香叶醇 食品科学
作者
Samah M. Redha,Sarmed H. Kathem
出处
期刊:The FASEB Journal [Wiley]
卷期号:36 (S1)
标识
DOI:10.1096/fasebj.2022.36.s1.l7816
摘要

Acute lung injury (ALI) is one of the most serious conditions characterized by an exacerbation of inflammatory response in the lungs that can result from lung infection. Citronellol, a natural monoterpenoid found in citronella oil and other natural sources. In this study, the lung protective and anti-inflammatory effects of citronellol were investigated in ALI induced by Lipopolysaccharide (LPS) in mice.adult mice were allocated into groups, control mice received normal saline. Mice in the induction group received LPS 10mg/kg/day intraperitoneally and euthanized 2 hours later. Mice in the treatment groups received either 50mg or 100mg/kg/day of oral citronellol for 5 consecutive days prior to LPS injection.Pretreatment with citronellol (50mg/kg/day) attenuated lung inflammatory events as observed from the significant reduction of TNF-α (6.02±1.039 vs 29.20±4.77) and COX2 (4.12±0.23 vs 10.58±0.77) mRNA expressions in lung tissue compared to non-treated mice. Interestingly, increasing the dose of citronellol to 100mg/kg/day also resulted in a significant reduction in both TNF-α (3.30±0.745 vs 29.20±4.77) and COX2 (4.62±0.58 vs 10.58±0.77) mRNA expression compared to non-treated mice. Looking for the upstream events revealed that NF-κB gene expression was significantly hampered by citronellol 50mg/kg/day (5.11 ± 1.096 vs 11.88±1.57) and 100mg/kg/day (3.22± 0.253 vs 11.88±1.57) compared to non-treated mice. Analysis of the data revealed that the effect of citronellol were dose dependent in terms of TNF-α and NF-κB gene expression.This study clearly revealed that citronellol exerted anti-inflammatory and lung-protective effects in LPS-induced acute lung injury. The observed effects were dose-independent and resulted through hampering of NF-κB pathway.

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