Geraniol alleviates LPS-induced acute lung injury in mice via inhibiting inflammation and apoptosis

• Published in: Oncotarget Vol. 8; no. 41; pp. 71038 - 71053
• Main Authors: Jiang, Kangfeng, Zhang, Tao, Yin, Nannan, Ma, Xiaofei, Zhao, Gan, Wu, Haichong, Qiu, Changwei, Deng, Ganzhen
• Format: Journal Article
• Language: English
• Published: United States Impact Journals LLC 19.09.2017
• Subjects: Research Paper; NF-κB; apoptosis; geraniol; inflammation; acute lung injury
• ISSN: 1949-2553; 1949-2553
• DOI: 10.18632/oncotarget.20298

Geraniol (GOH), a special type of acyclic monoterpene alcohol, has been widely used to treat many diseases associated with inflammation and apoptosis. Acute lung injury (ALI) is a common clinical disease in humans characterized by pulmonary inflammation and apoptosis. In the present study, we investigated the protective effects of GOH in a mouse model of ALI induced by the intranasal administration of lipopolysaccharide (LPS) and elucidated the underlying molecular mechanisms in RAW 264.7 cells. , GOH treatment markedly ameliorated pathological injury and pulmonary cell apoptosis and reduced the wet/dry (W/D) weight ratio of lungs, myeloperoxidase (MPO) activity and the production of pro-inflammatory cytokines (IL-1β, IL-6, and TNF-α). , the levels of pro-inflammatory cytokines, iNOS and COX-2 were significantly increased in LPS-stimulated RAW 264.7 cells, an effect that was decreased by GOH treatment. Moreover, GOH treatment dramatically reduced the expression of Toll-like receptor 4 (TLR4) and then prevented the nuclear factor-κB (NF-κB) activation. GOH treatment also promoted anti-apoptotic Bcl-2 expression and inhibited pro-apoptotic Bax and Caspase-3 expression. Furthermore, knockdown of TLR4 expression exerted a similar effect and inhibited the phosphorylation of p65, as well as the Bax and Caspase-3 expression. Taken together, these results suggest that GOH treatment alleviates LPS-induced ALI via inhibiting pulmonary inflammation and apoptosis, a finding that might be associated with the inhibition of TLR4-mediated NF-κB and Bcl-2/Bax signalling pathways.