title: Effect of Melilotus extract on lung injury via the upregulation of tumor necrosis factor-α-induced protein-8-like 2 in septic mice.
abstract: As a Traditional Chinese Medicine, Melilotus extracts have been reported to function as an anti‑inflammatory agent, antioxidant and inhibitor of capillary permeability. The present study aimed to identify the mechanisms by which Melilotus interferes with inflammation‑associated and oxidative stress pathways during sepsis. An animal model of cecal ligation‑perforation (CLP)‑induced sepsis was established. Two hours prior to surgery, animals in the treatment group were administered 25 mg/kg Melilotus extract tablets and subsequently every 8 h. At 24 h post‑administration, pathological modifications in lung tissue and expression levels of tumor necrosis factor‑α‑induced protein‑8‑like 2 (TIPE2) expression, nuclear factor (NF)‑κB, toll‑like receptor 4 (TLR4), heme oxygenase‑1 (HO‑1), inhibitor of κB kinase (IκB), pro‑inflammatory mediators (interleukin‑6 and tumor necrosis factor‑α), myeloperoxidase (MPO), malondialdehyde (MDA) and superoxide dismutase (SOD), were examined. The results showed that Melilotus extract had a marked effect on the pathological manifestation of lung tissue and lung inflammatory response, the upregulation of TIPE2, HO‑1 and IκB expression, and the inhibition of TLR4 and NF‑κB activities. In addition, following treatment with Melilotus extract, the model animals demonstrated decreased levels of MPO and MDA as well as increased levels of SOD. In conclusion, these results indicated that Melilotus extract may be a potential therapeutic agent for the treatment of CLP‑induced lung injury, the mechanism of which proceeded via inflammation‑ and oxidation‑associated pathways by increasing TIPE2 expression.
authors.affiliation: Department of Emergency, The First Hospital Affiliated to Kunming Medical University, Kunming, P.R. China.
authors.forename: Ming-Wei
authors.initials: MW
authors.lastname: Liu
authors.affiliation: Surgical Intensive Care Unit, The Second Hospital Affiliated to Kunming Medical University, Kunming, P.R. China.
authors.forename: Mei-Xian
authors.initials: MX
authors.lastname: Su
authors.affiliation: Department of Emergency, The First Hospital Affiliated to Kunming Medical University, Kunming, P.R. China.
authors.forename: Yun-Hui
authors.initials: YH
authors.lastname: Wang
authors.affiliation: Department of Emergency, The First Hospital Affiliated to Kunming Medical University, Kunming, P.R. China.
authors.forename: Chuan-Yun
authors.initials: CY
authors.lastname: Qian
mesh_terms: D000818:Animals; D016207:Cytokines / Q000378:metabolism; D004195:Disease Models, Animal; D005786:Gene Expression Regulation; D051547:Heme Oxygenase-1 / Q000378:metabolism; D018836:Inflammation Mediators / Q000378:metabolism; D047908:Intracellular Signaling Peptides and Proteins / Q000172:deficiency / Q000235:genetics*; D055370:Lung Injury / Q000188:drug therapy / Q000209:etiology* / Q000473:pathology; D029903:Melilotus; D051379:Mice; D018345:Mice, Knockout; D016328:NF-kappa B / Q000235:genetics / Q000378:metabolism; D009195:Peroxidase / Q000378:metabolism; D010936:Plant Extracts / Q000008:administration & dosage / Q000494:pharmacology*; D018805:Sepsis / Q000150:complications* / Q000235:genetics* / Q000378:metabolism; D013482:Superoxide Dismutase / Q000378:metabolism; D051197:Toll-Like Receptor 4 / Q000235:genetics / Q000378:metabolism; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
chemical_list: D016207:Cytokines; D018836:Inflammation Mediators; D047908:Intracellular Signaling Peptides and Proteins; D016328:NF-kappa B; D010936:Plant Extracts; C529002:TIPE2 protein, mouse; D051197:Toll-Like Receptor 4; D014409:Tumor Necrosis Factor-alpha; D009195:Peroxidase; D051547:Heme Oxygenase-1; D013482:Superoxide Dismutase