title: Cannabidiol improves lung function and inflammation in mice submitted to LPS-induced acute lung injury.
abstract: We have previously shown that the prophylactic treatment with cannabidiol (CBD) reduces inflammation in a model of acute lung injury (ALI). In this work we analyzed the effects of the therapeutic treatment with CBD in mice subjected to the model of lipopolysaccharide (LPS)-induced ALI on pulmonary mechanics and inflammation. CBD (20 and 80 mg/kg) was administered (i.p.) to mice 6 h after LPS-induced lung inflammation. One day (24 h) after the induction of inflammation the assessment of pulmonary mechanics and inflammation were analyzed. The results show that CBD decreased total lung resistance and elastance, leukocyte migration into the lungs, myeloperoxidase activity in the lung tissue, protein concentration and production of pro-inflammatory cytokines (TNF and IL-6) and chemokines (MCP-1 and MIP-2) in the bronchoalveolar lavage supernatant. Thus, we conclude that CBD administered therapeutically, i.e. during an ongoing inflammatory process, has a potent anti-inflammatory effect and also improves the lung function in mice submitted to LPS-induced ALI. Therefore the present and previous data suggest that in the future cannabidiol might become a useful therapeutic tool for the attenuation and treatment of inflammatory lung diseases.
authors.affiliation: Neuroimmunomodulation Research Group, Department of Pathology, School of Veterinary Medicine, University of São Paulo , São Paulo, SP , Brazil .
authors.forename: A
authors.initials: A
authors.lastname: Ribeiro
authors.forename: V I
authors.initials: VI
authors.lastname: Almeida
authors.forename: C
authors.initials: C
authors.lastname: Costola-de-Souza
authors.forename: V
authors.initials: V
authors.lastname: Ferraz-de-Paula
authors.forename: M L
authors.initials: ML
authors.lastname: Pinheiro
authors.forename: L B
authors.initials: LB
authors.lastname: Vitoretti
authors.forename: J A
authors.initials: JA
authors.lastname: Gimenes-Junior
authors.forename: A T
authors.initials: AT
authors.lastname: Akamine
authors.forename: J A
authors.initials: JA
authors.lastname: Crippa
authors.forename: W
authors.initials: W
authors.lastname: Tavares-de-Lima
authors.forename: J
authors.initials: J
authors.lastname: Palermo-Neto
mesh_terms: D055371:Acute Lung Injury / Q000139:chemically induced / Q000150:complications / Q000188:drug therapy* / Q000276:immunology; D000818:Animals; D000893:Anti-Inflammatory Agents / Q000008:administration & dosage / Q000627:therapeutic use*; D001992:Bronchoalveolar Lavage Fluid / Q000737:chemistry / Q000166:cytology / Q000276:immunology; D002185:Cannabidiol / Q000008:administration & dosage / Q000627:therapeutic use*; D002634:Chemotaxis, Leukocyte / Q000187:drug effects / Q000276:immunology; D016207:Cytokines / Q000097:blood; D004195:Disease Models, Animal; D004305:Dose-Response Relationship, Drug; D007274:Injections, Intraperitoneal; D007962:Leukocytes / Q000166:cytology / Q000276:immunology; D008070:Lipopolysaccharides / Q000494:pharmacology*; D008168:Lung / Q000187:drug effects / Q000276:immunology / Q000473:pathology; D008297:Male; D008810:Mice, Inbred C57BL; D009195:Peroxidase / Q000378:metabolism; D011014:Pneumonia / Q000209:etiology / Q000276:immunology / Q000517:prevention & control*; D012129:Respiratory Function Tests
chemical_list: D000893:Anti-Inflammatory Agents; D016207:Cytokines; D008070:Lipopolysaccharides; C482199:lipopolysaccharide, E coli O55-B5; D002185:Cannabidiol; D009195:Peroxidase
keywords: Cannabidiol; cannabinoids; inflammation; lipopolysaccharide; pulmonary mechanics