(946.3) Citronellol exerts lung protective and anti-inflammatory effects through hampering NF-κB in lipopolysaccharide-induced acute lung injury in mice
Tuesday, April 5, 2022
10:00 AM – 12:00 PM
Location: Exhibit/Poster Hall A-B - Pennsylvania Convention Center
Poster Board Number: B210
Samah Redha (University of Baghdad), Sarmed Kathem (University of Baghdad)
Background: 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.
Method: 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.
Results: 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.
Conclusion: 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.
