Research Papers:

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

Kangfeng Jiang, Tao Zhang, Nannan Yin, Xiaofei Ma, Gan Zhao, Haichong Wu, Changwei Qiu and Ganzhen Deng _

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Oncotarget. 2017; 8:71038-71053. https://doi.org/10.18632/oncotarget.20298

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Kangfeng Jiang1, Tao Zhang1, Nannan Yin1, Xiaofei Ma1, Gan Zhao1, Haichong Wu1, Changwei Qiu1 and Ganzhen Deng1

1Department of Clinical Veterinary Medicine, College of Veterinary Medicine, Huazhong Agricultural University, Wuhan 430070, People’s Republic of China

Correspondence to:

Ganzhen Deng, email: [email protected]

Keywords: acute lung injury, geraniol, inflammation, apoptosis, NF-κB

Received: April 09, 2017     Accepted: July 19, 2017     Published: August 16, 2017


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. In vivo, 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). In vitro, 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.

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