title: The ability of hydroxysafflor yellow a to attenuate lipopolysaccharide-induced pulmonary inflammatory injury in mice.
abstract: Hydroxysafflor yellow A (HSYA) is a component of the flower of Carthamus tinctorius L. The present study investigated whether HSYA could attenuate acute lung injury (ALI) induced by lipopolysaccharide (LPS) administration. Male Kunming mice were pretreated with HSYA 0.5 h prior to intraperitoneal application of LPS. Arterial blood gas, lung water content index, lung tissue myeloperoxidase (MPO) activity, mRNA expression of inflammatory cytokines, NF-κBp65, p38 mitogen-activated protein kinase (MAPK) and pathological changes in lung morphology were assessed. After LPS administration, all animals displayed increased arterial carbon dioxide partial pressure (PaCO₂), and decreased arterial oxygen partial pressure (PaO₂), arterial oxygen saturation (SO₂), HCO₃⁻ concentration and pH, which were ameliorated by pretreating the animals with HSYA. HSYA administration significantly attenuated inflammatory cell infiltration and alleviated pulmonary edema induced by LPS. Moreover, HSYA decreased NF-κB p65 nuclear translocation, inhibited proinflammatory cytokine TNF-α, IL-1β and IL-6 mRNA expression and promoted antiinflammatory cytokine IL-10 gene expression following LPS injection. Pulmonary p38 MAPK phosphorylation was upregulated 4 h after LPS treatment, which could be suppressed by pretreatment with HSYA. These findings demonstrated the protective effect of HSYA against LPS-induced acute lung injury, which is suggested to be associated with the inhibition of p38 MAPK, NF-κB p65 activation and alteration of inflammatory cytokine expression.
authors.affiliation: Department of Pharmacology, Beijing Institute of Heart Lung and Blood Vessel Diseases, Beijing Anzhen Hospital, Capital Medical University, Beijing, China.
authors.forename: Chun-Yan
authors.initials: CY
authors.lastname: Sun
authors.forename: Chong-Qiang
authors.initials: CQ
authors.lastname: Pei
authors.forename: Bao-Xia
authors.initials: BX
authors.lastname: Zang
authors.forename: Lin
authors.initials: L
authors.lastname: Wang
authors.forename: Ming
authors.initials: M
authors.lastname: Jin
mesh_terms: D055371:Acute Lung Injury / Q000139:chemically induced / Q000188:drug therapy*; D000818:Animals; D001784:Blood Gas Analysis; D002599:Chalcone / Q000031:analogs & derivatives* / Q000494:pharmacology; D016207:Cytokines / Q000378:metabolism; D008070:Lipopolysaccharides / Q000494:pharmacology; D008168:Lung / Q000187:drug effects / Q000473:pathology; D008297:Male; D051379:Mice; D009195:Peroxidase / Q000378:metabolism; D011809:Quinones / Q000494:pharmacology*; D051996:Transcription Factor RelA / Q000378:metabolism; D048051:p38 Mitogen-Activated Protein Kinases / Q000378:metabolism
chemical_list: D016207:Cytokines; D008070:Lipopolysaccharides; D011809:Quinones; C498144:Rela protein, mouse; D051996:Transcription Factor RelA; C085278:hydroxysafflor yellow A; D002599:Chalcone; D009195:Peroxidase; D048051:p38 Mitogen-Activated Protein Kinases