Ka Young Kim1, Hui Su Lee1, Geun Hee Seol1. 1. Department of Basic Nursing Science, School of Nursing, Korea University, Seoul, Republic of Korea.
Abstract
OBJECTIVES: The acute lung injury (ALI) model is characterised by a severe acute inflammatory response in the lungs that represents the pathogenesis of acute respiratory distress syndrome (ARDS). In this study, we sought to elucidate the anti-inflammatory mechanism of eucalyptol in relation to tissue remodelling in acute lung inflammation. METHODS: BALB/C mice were intraperitoneally injected with eucalyptol (100, 200 or 400 mg/kg) or dexamethasone (1 mg/kg) 1 h before intratracheal challenge with lipopolysaccharide (LPS; 1.5 mg/kg) and sacrificed after 4 h. The anti-inflammatory effects of eucalyptol were assessed by determining cell counts, measuring cytokine and nitric oxide production and performing Western blotting and histological analyses. KEY FINDINGS: Eucalyptol attenuated inflammation-associated increases in cell numbers, matrix metalloproteinase-9 (MMP-9) expression, production of cytokines (tumour necrosis factor-α and interleukin-6) and nitric oxide, and nuclear factor-kappa B (NF-κB) and phosphorylated extracellular signal-regulated kinase protein levels induced by LPS in bronchoalveolar lavage fluid from ALI mice. Furthermore, pretreatment with 400 mg/kg eucalyptol prevented LPS-induced histopathological changes. Collectively, these results indicate that eucalyptol acts through a mechanism involving decreased MMP-9 expression and an extracellular signal-regulated kinase-dependent NF-κB pathway to exert anti-inflammatory actions in acute lung inflammation. CONCLUSIONS: Thus, eucalyptol may be a potentially important agent in the treatment of pulmonary inflammation.
OBJECTIVES: The acute lung injury (ALI) model is characterised by a severe acute inflammatory response in the lungs that represents the pathogenesis of acute respiratory distress syndrome (ARDS). In this study, we sought to elucidate the anti-inflammatory mechanism of eucalyptol in relation to tissue remodelling in acute lung inflammation. METHODS: BALB/C mice were intraperitoneally injected with eucalyptol (100, 200 or 400 mg/kg) or dexamethasone (1 mg/kg) 1 h before intratracheal challenge with lipopolysaccharide (LPS; 1.5 mg/kg) and sacrificed after 4 h. The anti-inflammatory effects of eucalyptol were assessed by determining cell counts, measuring cytokine and nitric oxide production and performing Western blotting and histological analyses. KEY FINDINGS:Eucalyptol attenuated inflammation-associated increases in cell numbers, matrix metalloproteinase-9 (MMP-9) expression, production of cytokines (tumour necrosis factor-α and interleukin-6) and nitric oxide, and nuclear factor-kappa B (NF-κB) and phosphorylated extracellular signal-regulated kinase protein levels induced by LPS in bronchoalveolar lavage fluid from ALI mice. Furthermore, pretreatment with 400 mg/kg eucalyptol prevented LPS-induced histopathological changes. Collectively, these results indicate that eucalyptol acts through a mechanism involving decreased MMP-9 expression and an extracellular signal-regulated kinase-dependent NF-κB pathway to exert anti-inflammatory actions in acute lung inflammation. CONCLUSIONS: Thus, eucalyptol may be a potentially important agent in the treatment of pulmonary inflammation.
Authors: Ana I Caceres; Boyi Liu; Sairam V Jabba; Satyanarayana Achanta; John B Morris; Sven-Eric Jordt Journal: Br J Pharmacol Date: 2017-03-23 Impact factor: 8.739
Authors: Kahdr A Alatawi; Divyashree Ravishankar; Pabitra H Patra; Alexander P Bye; Alexander R Stainer; Ketan Patel; Darius Widera; Sakthivel Vaiyapuri Journal: Cells Date: 2021-10-01 Impact factor: 6.600